Archive for the ‘Alzheimer’s’ Category

Sauna For Prevention of Cardiovascular & Alzheimer’s Disease & For Detoxification

 Approx. 25 Min.

Dr. Jari Laukkanen on Sauna Use For the Prevention of Cardiovascular & Alzheimer’s Disease

This podcast features Jari Laukkanen, M.D., Ph.D., a cardiologist and scientist at the Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio. Dr. Laukkanen has been conducting long-term trials looking at the health effects of sauna use in a population of over 2,000 middle-aged men in Finland. The results? Massive reductions in mortality and memory disease in a dose-response fashion at 20-year follow-up. In this almost 25-minute episode, we talk about…

  • 00:00:37 – The association between sauna use and fatal cardiovascular outcomes
  • 00:00:37 – The inverse association between cardiovascular-related deaths and all-cause deaths.
  • 00:02:00 – How men that used the sauna 2-3 times per week had a 27% lower cardiovascular-related mortality than men that used the sauna 1 time per week
  • 00:02:15 – How men that used the sauna 4-7 times per week had a 50% lower cardiovascular-related mortality than men that used the sauna one time per week.
  • 00:02:50 – The confounding factors Dr. Laukkanen and his colleagues had to adjust for, such as physical exercise, cholesterol, obesity, smoking, alcohol consumption, socioeconomic status.
  • 00:03:26 – The various types of cardiac-related deaths their reductions were shown in, including coronary artery disease, sudden cardiac death and more.
  • 00:05:00 – How one of the major mechanisms by which sauna use improves heart health is by reducing blood pressure and incident hypertension.
  • 00:05:40 – The mechanisms by which the sauna lowers blood pressure, which can occur via balancing of the autonomic nervous system, improvements in blood vessel function, decreases in arterial stiffness and compliance of arteries.
  • 00:06:17 – The increases in heart rate seen with sauna use that make it similar to moderate aerobic exercise in some ways (up to 150 beats/min!).
  • 00:06:56 – How time spent in the sauna was one of the more important factors for risk reduction with at least 20 minutes per session in a 174 F (79C) 4-7 times per week being a “sweet spot.”
  • 00:09:29 – The inverse, dose-response relationship between sauna use and all-cause mortality: 24% for 2-3 times per week, 40% for 4-7 times.
  • 00:10:00 – His newest study that now shows a reduction in risk in a similar dose-response fashion for dementia and Alzheimer’s disease by around 65% for the most frequent sauna users.
  • 00:10:18 – The way sauna use increases heat shock proteins which repair damaged proteins and prevent protein aggregates and how this could end up being at least one potential molecular mechanism at play.
  • 00:13:03 – How sauna use increases growth hormone by 200-330%.
  • 00:14:10 – The patterns of sauna use and especially whether to sauna before or after you weight train.
  • 00:15:55 – The effect of sauna on mood which may be from improvements in cardiorespiratory fitness and possibly endorphins as well.
  • 00:18:39 – How sauna improves heart rate variability.
  • 00:20:04 – Cold-water immersion after sauna and a few cautionary words for extreme contrast therapy in people with a pre-existing heart condition that is currently unstable.

Further, Dr. Mary Shackelton, MPH, ND talks about skin as a pathway for detoxification and how important it is to sweat on a weekly basis. Infrared saunas are one of the most effective ways of releasing toxins from deep within one’s tissues.

 Approx. 5 Min


For more:  Briefly, MSM stands for Methylsulfonylmethane and is 34% sulfur by weight. Sulfur plays a crucial role in detoxification and is an important antioxidant for producing glutathione. If you aren’t getting enough sulfur, glutathione can not work. Even if you have a diet rich in sulfur (think cabbage, onions, garlic, broccoli, etc – essentially the stinky veggies – and many other food items as well) your body still could use supplementation.  Besides helping sleep, melatonin is known for protecting the brain. Research has shown starting to supplement in middle age protects against Alzheimer’s, reduces the risk of Parkinson’s, shrinks the size of the infarct area in a stroke, minimizes brain swelling & dysfunction after head injury, and increases the “longevity protein” SIRT1.


The Diagnosis is Alzheimer’s. But That’s Probably Not the Only Problem.

Most people with dementia have a number of brain abnormalities, not just Alzheimer’s disease. The finding is forcing scientists to rethink the search for treatments.
A light micrograph of brain tissue of a person with Alzheimer’s disease, which shows the characteristic tangles (the dark teardrop shapes) and amyloid plaques (the rounded brown agglomerations).Credit Thomas Deerinck, NCMIR/Science Source

Allan Gallup, a retired lawyer and businessman, grew increasingly forgetful in his last few years. Eventually, he could no longer remember how to use a computer or the television. Although he needed a catheter, he kept forgetting and pulling it out.

It was Alzheimer’s disease, the doctors said. So after Mr. Gallup died in 2017 at age 87, his brain was sent to Washington University in St. Louisto be examined as part of a national study of the disease.

But it wasn’t just Alzheimer’s disease, the researchers found. Although Mr. Gallup’s brain had all the hallmarks — plaques made of one abnormal protein and tangled strings of another — the tissue also contained clumps of proteins called Lewy bodies, as well as signs of silent strokes. Each of these, too, is a cause of dementia.

Mr. Gallup’s brain was typical for an elderly patient with dementia. Although almost all of these patients are given a diagnosis of Alzheimer’s disease, nearly every one of them has a mixture of brain abnormalities.

For researchers trying to find treatments, these so-called mixed pathologies have become a huge scientific problem. Researchers can’t tell which of these conditions is the culprit in memory loss in a particular patient, or whether all of them together are to blame.

Another real possibility, noted Roderick A. Corriveau, who directs dementia research programs at the National Institute of Neurological Disorders and Stroke, is that these abnormalities are themselves the effects of a yet-to-be-discovered cause of dementia.

These questions strike at the very definition of Alzheimer’s disease. And if you can’t define the condition, how can you find a treatment?

In addition to plaques and tangles, other potential villains found in the brains of people with a diagnosis of Alzheimer’s include silent strokes and other blood vessel diseases, as well as a poorly understood condition called hippocampal sclerosis.

Potential culprits also include an accumulation of Alpha-synuclein, the abnormal protein that makes up Lewy bodies. And some patients have yet another abnormal protein in their brains, TDP-43.

No one knows how to begin approaching the multitude of other potential problems found in the brains of Alzheimer’s patients. So, until recently, they were mostly ignored.

“I wouldn’t say it’s a dirty little secret,” said Dr. John Hardy, an Alzheimer’s researcher at University College London. “Everybody knows about it. But we don’t know what to do about it.

In interviews, some experts said they had been reluctant to talk much about mixed pathologies for fear of sounding too negative. But “at a certain point we have to be somewhat more realistic and rethink what we are doing,” said Dr. Albert Hofman, chairman of the epidemiology department at Harvard’s T.H. Chan School of Public Health.

The problem began with the very discovery of Alzheimer’s disease. In 1906, Dr. Alois Alzheimer, a German psychiatrist and neuroanatomist, described a 50-year-old woman with dementia.

On autopsy, he found peculiar plaques and twisted, spaghetti-like proteins known as tangles in her brain. Ever since, they have been considered the defining features of Alzheimer’s disease.

But scientists now believe this woman must have had a very rare genetic mutation that guarantees a person will get a pure form of Alzheimer’s by middle age.

Patients with the mutation appeared to develop only plaques and tangles, and no other pathologies. So for decades, plaques and tangles were the focus of research into dementia.

The rare genetic mutations led to an overproduction of amyloid, it turned out, the abnormal protein in those plaques. To many scientists, that suggested that amyloid was the fundamental cause of Alzheimer’s disease.

More plaques usually meant more severe dementia, in both older and younger patients. So researchers tested drugs that could attack amyloid or stop its production in genetically engineered mice. The drugs worked beautifully.

Scientists recognized that mice were an imperfect model — they never develop dementia — but the studies were encouraging. So it was a huge disappointment when, over and over, those drugs failed in clinical trials in patients.

Tests of anti-plaque drugs continue, despite the increasing recognition that many factors may combine to cause dementia — or that, perhaps, the true cause has yet to be found.

“What motivates us is the depth of the unmet need,” said Dr. Dan Skovronsky, chief scientific officer of the drug company Eli Lilly, which continues to investigate anti-amyloid treatments.

“That’s why we keep going forward. But it is such a tough, tough problem, and made tougher because of the mixed pathology.”

What to do now? Scientists are struggling the reframe the problem. Some think research should be more focused on age.

“We can’t avoid the fact the number one risk factor for Alzheimer’s disease is age, and many of these other pathologies are age-associated,” said Dr. John Morris, a professor of neurology at Washington University in St. Louis. “We don’t see them in younger people.”

Carol Brayne, an epidemiologist at Cambridge University, has been saying as much for decades. There is something significant, she has found, about the obvious fact that the older a person gets, the more likely he or she is to develop dementia. By their 90s, one out of every two people has dementia.

A more optimistic view is that there may be something in the brain that sets off a cascade of multiple pathologies. If true, blocking that factor could stop the process and prevent dementia.

Dr. Hofman is convinced that the precipitating factor is diminished blood flow to the brain.

“Alzheimer’s disease is a vascular disease,” he said.

Supporting this view, he added, are data from nine studies in the United States and Western Europe consistently finding a 15 percent decline in the incidence of new Alzheimer’s cases over the past 25 years.

“Why is that? I think the only reasonable candidate is improved vascular health,” Dr. Hofman said. The most important factor is the decline in smoking, he believes, but people in rich countries also are more likely to better control high blood pressure and cholesterol levels.

Dr. Seth Love, professor of pathology at the University of Bristol in England, noted that a core feature of Alzheimer’s is a reduction in blood flow through the cerebrum of the brain.

That happens even in people with the genetic mutation that leads Alzheimer’s in middle age. Fifteen to 20 years before these people have dementia, blood to their brains slows.

“We don’t know why,” Dr. Love said.

Or perhaps it really is amyloid that begins the avalanche of other problems.

Some researchers still hold out hope that if anti-amyloid drugs are started early enough, they might prevent dementia. Clinical trials are testing the idea now in people genetically disposed to get Alzheimer’s disease.

But even if the drugs work, will they work in the elderly patients who make up the bulk of those with an Alzheimer’s diagnosis — but who don’t have anything resembling a pure form of the disease?

Perhaps those drugs will have only a small effect in patients with mixed pathologies, Dr. Hardy said. It would take gigantic trials going on for years to see such a tiny effect.

“Those aren’t the kind of medicines we are looking for,” said Dr. Skovronsky, of Eli Lilly. “We want something that has a big effect.”

Dr. Skovronsky has been forced to do some soul-searching. Trying anti-amyloid drugs in old people in the early or middle stages of Alzheimer’s just is not working.

But when is it best to intervene, and in whom? And do scientists need to find drugs for all the other pathologies in the brains of dementia patients, as well?

“It’s the right time to focus on these tough questions,” Dr. Skovronsky said.

Many Lyme/MSIDS patients are misdiagnosed with Alzheimer’s, dementia, ALS, MS, fibromyalgia, and other neurological diseases.
In this article, they find gum bacteria is implicated:
Researchers are reporting new findings on how bacteria involved in gum disease can travel throughout the body, exuding toxins connected with Alzheimer’s disease, rheumatoid arthritis and aspiration pneumonia. They detected evidence of the bacteria in brain samples from people with Alzheimer’s and used mice to show that the bacterium can find its way from the mouth to the brain.
This article shows a connection between aluminum, Alzheimer’s and Lyme:
Singer/actor Kris Kristofferson was misdiagnosed with Alzheimer’s – HAD LYME.


This article states that 50% of Alzheimer’s is caused by herpes simplex virus 1 (HSV1), the virus responsible for cold sores:

For more: researchers/


Alzheimer’s Association 2019 Facts & Figures

  Approx. 1 Min

More than 5 million Americans are living with Alzheimer’s disease. Share the facts and join the fight at

Dementia Deaths Have Doubled in Two Decades

By Dr. Mercola


  • Alzheimer’s disease — the most severe form of dementia for which there is no effective conventional treatment or cure — currently affects an estimated 5.8 million Americans. By 2050, that figure is projected to hit 14 million
  • The latest report from the National Center for Health Statistics reveals the rate of death from dementia more than doubled between 2000 and 2017, from 84,000 to 261,914
  • This data are based on death certificates, which the CDC admits (and a 2014 study demonstrated) underrepresents the true death toll
  • If changes in your memory or thinking skills are severe enough to be noticed by your friends and family you could be facing mild cognitive impairment, a slight decline in cognitive abilities that increases your risk of developing more serious dementia, including Alzheimer’s disease. Early warning signs are discussed
  • A high-fat, moderate-protein, low net-carb ketogenic diet is crucial for protecting your brain health and preventing degeneration that can lead to Alzheimer’s. Other risk factors and suggestions for how to minimize your risk are discussed

Alzheimer’s disease — the most common form of dementia for which there is no effective conventional treatment or cure — currently affects an estimated 5.8 million Americans,1 up from 5.4 million in 2016. By 2050, that figure is projected to hit 14 million.2

Research3 published in 2014 revealed Alzheimer’s had risen to the point of being the third leading cause of death in the U.S.4 For clarification, while the Centers for Disease Control and Prevention (CDC) continues to list Alzheimer’s as the sixth leading cause of death in the U.S.,5 this ranking is based on death certificates, and the study in question found Alzheimer’s was grossly underreported as a cause of death on death certificates.

Recalculations based on the evaluation of donated organs from the diseased put the actual death toll attributable to dementia at 503,400, making it the third leading cause of death, right behind heart disease and cancer.

According to CDC data, the death rate from Alzheimer’s rose 55 percent between 1999 and 2014.6,7Now, the latest report from the National Center for Health Statistics reveals the rate of death from dementia more than doubled between 2000 and 2017, from 84,000 to 261,914.8,9,10

Forty-six percent of dementia deaths in 2017 were attributed to Alzheimer’s. Other forms of dementia included vascular dementia, unspecified dementia and other degenerative nervous system diseases. But again, this data is based on death certificates, which the CDC admits (and the 2014 study above demonstrated) underrepresents the true death toll.

Could Your Memory Problems Be a Symptom of Alzheimer’s?

As noted by CNN, progression of Alzheimer’s disease varies, but often begin with short-term memory lapses that later progress to speech problems and trouble with executive functions.11

If changes in your memory or thinking skills are severe enough to be noticed by your friends and family you could be facing mild cognitive impairment (MCI). MCI is a slight decline in cognitive abilities that increases your risk of developing more serious dementia, including Alzheimer’s disease.

If your mental changes are so significant that they interfere with your ability to function or live independently, it could signal the onset of dementia. For instance, it’s normal to have trouble finding the right word on occasion, but if you forget words frequently and repeat phrases and stories during a conversation, there could be a problem.

The video above reviews 10 early warning signs of Alzheimer’s, and compares these signs with examples of typical age-related cognitive changes that are not a major cause for concern. You can also find a similar list compiled by the Alzheimer’s Association.12

Another red flag is getting lost or disoriented in familiar places (as opposed to needing to ask for directions on occasion). If you’re able to later describe a time when you were forgetful, such as misplacing your keys, that’s a good sign; a more serious signal is not being able to recall situations when memory loss caused a problem, even though your loved ones describe it to you. Other warning signs of MCI or dementia include:

Difficulty performing daily tasks like paying bills or taking care of personal hygiene
Asking the same question over and over
Difficulty making choices
Exhibiting poor judgment or inappropriate social behaviors
Changes in personality or loss of interest in favorite activities
Memory lapses that put people in danger, like leaving the stove on
Inability to recognize faces or familiar objects
Denying a memory problem exists and getting angry when others bring it up

If Your Memory Is Slipping, Switch to a Ketogenic Diet

If your memory slips often enough to put even an inkling of concern or doubt in your mind, it’s time to take action. A high-fat, moderate-protein, low-net-carb ketogenic diet is crucial for protecting your brain health and preventing degeneration that can lead to Alzheimer’s.

One of the most striking studies13 showing the effects of a high-fat/low-carb versus high-carb diets on brain health revealed that high-carb diets increase your risk of dementia by a whopping 89 percent, while high-fat diets lower it by 44 percent.

According to the authors, “A dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of mild cognitive impairment or dementia in elderly persons.” A ketogenic diet benefits your brain in a number of different ways. For example, it:

Triggers ketone production — A cyclical ketogenic diet will help you convert from carb-burning mode to fat-burning mode, which in turn triggers your body to produce ketones, an important source of energy (fuel) for your brain14 that have been shown to help prevent brain atrophy and alleviate symptoms of Alzheimer’s.15 They may even restore and renew neuron and nerve function in your brain after damage has set in.

Improves your insulin sensitivity — A cyclical ketogenic diet will also improve your insulin sensitivity, which is an important factor in Alzheimer’s.16 The link between insulin sensitivity and Alzheimer’s is so strong, the disease is sometimes referred to as Type 3 diabetes.

Even mild elevation of blood sugar is associated with an elevated risk for dementia.17 Diabetes and heart disease18 are also known to elevate your risk, and both are rooted in insulin resistance.

The connection between high-sugar diets and Alzheimer’s was also highlighted in a longitudinal study published in the journal Diabetologia in January 2018.19 Nearly 5,190 individuals were followed over a decade, and the results showed that the higher an individual’s blood sugar, the faster their rate of cognitive decline.

Studies have also confirmed that the greater an individual’s insulin resistance, the less sugar they have in key parts of their brain, and these areas typically correspond to the areas affected by Alzheimer’s.20,21

Reduces free radical damage and lowers inflammation in your brain — Ketones not only burn very efficiently and are a superior fuel for your brain, but also generate fewer reactive oxygen species and less free radical damage.

A ketone called beta hydroxybutyrate is also a major epigenetic player, stimulating radical decreases in oxidative stress by decreasing NF-kB, thus reducing inflammation and NADPH levels along with beneficial changes in DNA expression that improve your detoxification and antioxidant production.

I explain the ins and outs of implementing this kind of diet, and its many health benefits, in my new book “KetoFast.” In it, I also explain why cycling through stages of feast and famine, opposed to continuously remaining in nutritional ketosis, is so important.

What Do We Know About the Causes of Alzheimer’s Disease?

It’s often said that the underlying causes of Alzheimer’s disease are unknown, but there’s no shortage of theories. Insulin resistance, discussed above, appears to be a really significant factor, but it’s not the only one. Based on the available science, here are several other prominent or likely culprits that can raise your risk of Alzheimer’s disease, and suggestions for how to avoid them:

High-sugar, processed food diets — Insulin resistance is a direct result of a high-sugar diet. Processed foods also contain a number of other ingredients that are harmful to your brain, including gluten, vegetable oils, genetically engineered ingredients and pesticides.

Solution: Keep your fasting insulin levels below 3; minimize sugar consumption, boost healthy fat intake and focus on real food — If your insulin is high, you’re likely consuming too much sugar and need to cut back. Ideally, keep your added sugar to a minimum and your total fructose below 25 grams per day, or as low as 15 grams per day if you already have insulin/leptin resistance or any related disorders.

To get down to this level, you’ll have to eat real, whole food, as processed foods are chockfull of added sugars. It’s important to realize that your brain actually does not need carbs and sugars; healthy fats such as saturated animal fats and animal-based omega-3 are far more critical for optimal brain function.

Also remember to pay close attention to the kinds of fats you eat — avoid all trans fats or hydrogenated fats. This includes margarine, vegetable oils and various butter-like spreads.

Healthy fats to add to your diet include avocados, butter, organic pastured egg yolks, coconuts and coconut oil, grass fed meats and raw nuts such as pecans and macadamia. MCT oil is also a great source of ketone bodies.

Alcohol abuse — According to research22 published in 2018, alcohol use is a major risk factor for dementia. The study, the largest of its kind, concluded that alcohol use disorders “are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia,” Science News reports.23

Solution: Limit alcohol use, and get treatment for alcohol use disorder.

Vitamin D deficiency — The Scotland Dementia Research Centre has noted a very clear link between vitamin D deficiency and dementia.24 Indeed, studies have shown vitamin D plays a critical role in brain health, immune function, gene expression and inflammation — all of which influence Alzheimer’s. A wide variety of brain tissue contains vitamin D receptors, and when they’re activated by vitamin D, it facilitates nerve growth in your brain.

Researchers also believe optimal vitamin D levels boost levels of important brain chemicals and protect brain cells by increasing the effectiveness of glial cells in nursing damaged neurons back to health. In a 2014 study,25 considered to be the most robust study of its kind at the time, those who were severely deficient in vitamin D had a 125 percent higher risk of developing some form of dementia compared to those with normal levels.

The findings also suggest there’s a threshold level of circulating vitamin D, below which your risk for dementia increases. This threshold was found to be right around 20 nanograms per milliliter (ng/ml) or 50 nanomoles per liter (nmol/L) for Europeans. Higher levels are associated with better brain health in general, and based on a broader view of the available science, 20 ng/ml is still far too low.

Solution: Optimize your vitamin D level — The bulk of the research suggests maintaining a vitamin D level between 60 and 80 ng/mL (150 to 200 nmol/L) year-round. Ideally, get your level checked twice a year, and if you’re unable to maintain a healthy level through sensible sun exposure alone, be sure to take an oral vitamin D3 supplement.

Low omega-3 level — According to neuroimaging research, low omega-3 may be a factor in Alzheimer’s,26 and omega-3 is certainly a crucial component for optimal brain health in general. People with higher omega-3 levels were found to have increased blood flow in areas of the brain associated with memory and learning.

The Journal of Alzheimer’s Disease also notes animal research showing omega-3 fatty acids have been shown to have anti-amyloid, anti-tau and anti-inflammatory activity in the brain.27

Solution: Optimize your omega-3 index — Ideally, get an omega-3 index test done once a year to make sure you’re in a healthy range. Your omega-3 index should be above 8 percent and your omega 6-to-3 ratio between 0.5 and 3.0.

Lack of sun exposure — While vitamin D deficiency is directly attributable to lack of sensible sun exposure, vitamin D production is not the only way sun exposure can influence your dementia risk. Evidence suggests sunlight is a beneficial electromagnetic frequency (EMF) that is in fact essential and vital for your health in its own right.

About 40 percent of the rays in sunlight is infrared. The red and near-infrared frequencies interact with cytochrome c oxidase (CCO) — one of the proteins in the inner mitochondrial membrane and a member of the electron transport chain.

CCO is a chromophore, a molecule that attracts and absorbs light. In short, sunlight improves the generation of energy (ATP). The optimal wavelength for stimulating CCO lies in two regions, red at 630 to 660 nanometers (nm) and near-infrared at 810 to 850 nm.

Solution: Get regular sun exposure and/or consider photobiomodulation therapy — I’ve interviewed two different experts on photobiomodulation, a term describing the use of near-infrared light as a treatment for Alzheimer’s. To learn more about this fascinating field, please see my interviews with Michael Hamblin, Ph.D., and Dr. Lew Lim. Both have published papers on using photobiomodulation to improve Alzheimer’s disease.

Prion infection — In addition to viruses, bacteria and fungi, an infectious protein called TDP-43, which behaves like infectious proteins known as prions — responsible for the brain destruction that occurs in mad cow and chronic wasting diseases — has been linked to Alzheimer’s.

Research presented at the 2014 Alzheimer’s Association International Conference revealed Alzheimer’s patients with TDP-43 were 10 times more likely to have been cognitively impaired at death than those without.28 Last year, researchers also found they could measure the distribution and levels of prions in the eye,29 thereby improving diagnosis of Creutzfeldt-Jakob disease (CJD), the human version of mad cow disease.

Solution: Avoid eating meat from animals raised in concentrated animal feeding operations (CAFOs) — Due to its similarities with mad cow disease, investigators have raised the possibility that Alzheimer’s disease may be linked to CAFO meat consumption. There are many reasons to avoid CAFO animal products, and this is yet another one, even if this particular risk is small.

Environmental toxins, including electromagnetic fields (EMF) — Experts at the Edinburgh University’s Alzheimer Scotland Dementia Research Centre have compiled a list of top environmental risk factors thought to be contributing to the epidemic, based on a systematic review of the scientific literature.30,31,32

As much as one-third of your dementia risk is thought to be linked to environmental factors such as air pollution, pesticide exposure and living close to power lines. The risk factor with the most robust body of research behind it is air pollution. In fact, they couldn’t find a single study that didn’t show a link between exposure to air pollution and dementia.

Particulate matter, nitric oxides, ozone and carbon monoxide have all been linked to an increased risk. Living close to power lines also has “limited yet robust” evidence suggesting it may influence your susceptibility to dementia.

Solution: Minimize exposure to environmental toxins and EMFs — In terms of air pollution, it’s worth remembering that your indoor air is often five times more polluted than outdoor air, and indoors, it’s something you can control, using a high-quality air purifier. Pesticides can be avoided by eating certified organic foods.

Non-native EMFs contribute to Alzheimer’s by poisoning your mitochondria, and this is not limited to living in close proximity to power lines. It also includes electromagnetic interference from the electric grid and microwave radiation from your cellphone, cellphone towers, Wi-Fi and more.

Radiation from cellphones and other wireless technologies trigger excessive production of peroxynitrites,33 a highly damaging reactive nitrogen species. Increased peroxynitrites from cellphone exposure will damage your mitochondria,34,35 and your brain is the most mitochondrial-dense organ in your body. To learn more about the mechanisms that place your health in jeopardy, and what you can do about it, see “Top 19 Tips to Reduce Your EMF Exposure.”

Inactivity / lack of exercise — Exercise has been shown to protect your brain from Alzheimer’s and other dementias,36 and also improves quality of life if you’ve already been diagnosed.

In one study,37,38 patients diagnosed with mild to moderate Alzheimer’s who participated in a four-month-long supervised exercise program had significantly fewer neuropsychiatric symptoms associated with the disease (especially mental speed and attention) than the inactive control group.

Other studies39 have shown aerobic exercise helps reduce tau levels in the brain. (Brain lesions known as tau tangles form when the protein tau collapses into twisted strands that end up killing your brain cells.) Cognitive function and memory40 can also be improved through regular exercise, and this effect is in part related to the effect exercise has on neurogenesis and the regrowth of brain cells.

By targeting a gene pathway called brain-derived neurotrophic factor (BDNF), exercise actually promotes brain cell growth and connectivity. In one yearlong study,41 seniors who exercised grew and expanded their brain’s memory center by as much as 2 percent per year, where typically that center shrinks with age.

Evidence also suggests exercise can trigger a change in the way the amyloid precursor protein is metabolized,42 thus slowing the onset and progression of Alzheimer’s. By increasing levels of the protein PGC-1alpha (which Alzheimer’s patients have less of), brain cells produce less of the toxic amyloid protein associated with Alzheimer’s.43 As noted in one 2016 paper on this topic:44

“Moderate and high intensities have demonstrated a neuroprotective effect through the production of antioxidant enzymes and growth factors such as superoxide dismutase, eNOS, BDNF, nerve growth factors, insulin-like growth factors and vascular endothelial growth factor and by reducing the production of ROS, neuroinflammation, the concentration of Aβ plaques in cognitive regions and tau pathology, leading to the improvement of cerebral blood flow, hyperemia, cerebrovascular reactivity and memory.”

Solution: Move regularly and consistently throughout the day, and implement a regular exercise routine.

Hypertension and heart disease — Arterial stiffness (atherosclerosis) is associated with a hallmark process of Alzheimer’s, namely the buildup of beta-amyloid plaque in your brain. The American Heart Association warns there’s a strong association between hypertension and brain diseases such as vascular cognitive impairment (loss of brain function caused by impaired blood flow to your brain) and dementia.45

Solution: Address high blood pressure and risk factors for heart disease — One of the most important all-natural remedies for high blood pressure is to raise your nitric oxide production, which can be done through high-intensity exercise (including the super-simple Nitric Oxide Dump exercise), high-nitrate foods such as beets and arugula.

For more information, see “Top 9 Reasons to Optimize Your Nitric Oxide Production” and “How to Successfully Control High Blood Pressure Without Medications.”

Genetic predisposition — Several genes that predispose you to Alzheimer’s have been identified.46 The most common gene associated with late onset Alzheimer’s is the apolipoprotein E (APOE) gene. The APOE e2 form is thought to reduce your risk while the APOE e4 form increases it.

That said, some people never develop the disease even though they’ve inherited the APOE e4 gene from both their mother and father (giving them a double set), so while genetics can affect your risk, it is NOT a direct or inevitable cause. Your risk for early onset familial Alzheimer’s can also be ascertained through genetic testing.47 In this case, by looking for mutation in the genes for presenilin 1 and presenilin 2.

Solution: Genetic testing to help ascertain your risk — People with one or more genetic predispositions are at particularly high risk of developing Alzheimer’s at a very young age.

Additional Alzheimer’s Preventive Strategies

In 2014, Bredesen published a paper that demonstrates the power of lifestyle choices for the prevention and treatment of Alzheimer’s. By leveraging 36 healthy lifestyle parameters, he was able to reverse Alzheimer’s in 9 out of 10 patients. This included the use of exercise, ketogenic diet, optimizing vitamin D and other hormones, increasing sleep, meditation, detoxification and eliminating gluten and processed food.

You can download Bredesen’s full-text case paper online, which details the full program.48 Following are a few lifestyle strategies that, in addition to those already mentioned above, can be helpful for the prevention of dementia and Alzheimer’s.

Optimize your gut flora To do this, avoid processed foods, antibiotics and antibacterial products, fluoridated and chlorinated water, and be sure to eat traditionally fermented and cultured foods, along with a high-quality probiotic if needed. Dr. Steven Gundry does an excellent job of expanding on this in his new book “The Plant Paradox.”
Intermittently fast — Intermittent fasting is a powerful tool to jump-start your body into remembering how to burn fat and repair the insulin/leptin resistance that is a primary contributing factor for Alzheimer’s.
Optimize your magnesium levels — Preliminary research strongly suggests a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Keep in mind that the only magnesium supplement that appears to be able to cross the blood-brain barrier is magnesium threonate.
Avoid and eliminate mercury from your body — Dental amalgam fillings are one of the major sources of heavy metal toxicity; however, you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.
Avoid and eliminate aluminum from your body — Common sources of aluminum include antiperspirants, nonstick cookware and vaccine adjuvants. For tips on how to detox aluminum, see “Top Tips to Detox Your Body.”
Avoid flu vaccinations — Most flu vaccines contain both mercury and aluminum.
Avoid statins and anticholinergic drugs — Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence and certain narcotic pain relievers.

Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10, vitamin K2 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.

Optimize your sleep — Sleep is necessary for maintaining metabolic homeostasis in your brain. Without sufficient sleep, neuron degeneration sets in, and catching up on sleep during weekends will not prevent this damage.49,50,51

Sleep deprivation causes disruption of certain synaptic connections that can impair your brain’s ability for learning, memory formation and other cognitive functions. Poor sleep also accelerates the onset of Alzheimer’s disease.52

Most adults need seven to nine hours of uninterrupted sleep each night. Deep sleep is the most important, as this is when your brain’s glymphatic system performs its cleanout functions, eliminating toxic waste from your brain, including amyloid beta. For a comprehensive sleep guide, see “33 Secret’s to a Good Night’s Sleep.”

Challenge your mind daily — Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of dementia and Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.


For more on the link between Lyme/MSIDS & Alzheimer’s/dementia:  Bacteria are usually ignored despite its historical and current significance in dementia research.  Today, the main bacterial threat to acquiring dementia comes from Lyme disease—a bacterium borrelia burgdorferi.  Kris Kristofferson was wrongly diagnosed with Alzheimer’s but had Lyme Disease. For years doctors told Kristofferson it was either Alzheimer’s or dementia, and may have been the result of blows to his head from boxing, football and rugby. The medication he was given gave him bad side effects and didn’t help.  Since starting treatment for Lyme Kristofferson “has made remarkable strides.” His wife Lisa said,

all of the sudden he was back.” Although he still has some bad days, there are other days when he is “perfectly normal,” she said.  According to reports by the Associated Press, the New York Times, and other news outlets, baseball Hall of Famer Tom Seaver has been diagnosed with dementia. This comes some 28 years after Seaver was first diagnosed with Lyme disease.




Researchers Identify Herpes 1, Chlamydia pneumoniae, & several types of spirochaete As Major Causes of Alzheimer’s

Researchers Identify Virus and Two Types of Bacteria as Major Causes of Alzheimer’s

A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.

This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.

Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.

Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.

“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.

Image shows an old lady looking out of a window.

Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said:

“The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”

The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.


Source: University of Manchester
Image Credit: The image is adapted from the University of Manchester press release.
Original Research: Full open access editorial for “Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152


Microbes and Alzheimer’s Disease

We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.

AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic.

“Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152






Anti-viral Therapy in Alzheimer’s- Clinical Trial

Anti-viral Therapy in Alzheimer’s Disease

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details. Identifier: NCT03282916

Recruitment Status : Recruiting

First Posted : September 14, 2017
Last Update Posted : January 25, 2019
National Institutes of Health (NIH)
National Institute on Aging (NIA)
Information provided by (Responsible Party):
Davangere P. Devanand, New York State Psychiatric Institute
Study Description
Brief Summary:
Anti-viral therapy in Alzheimer’s disease will investigate the efficacy of treating patients with mild Alzheimer’s disease with the U.S.A marketed generic anti-viral drug Valtrex (valacyclovir, 500mg oral tablet). Valacyclovir at 2 g to 4 g per day, repurposed to treat Alzheimer’s disease, will be compared to matching placebo in the treatment of 130 mild AD patients (65 valacyclovir, 65 placebo) who test positive for herpes simplex virus-1 (HSV1) or HSV2. The study will be a randomized, double-blind, 18-month Phase II proof of concept trial.
Condition or disease Intervention/treatment Phase
Alzheimer DiseaseHerpes Simplex 1Herpes Simplex 2 Drug: ValacyclovirDrug: Placebo Phase 2
Detailed Description:

Many viruses are latent for decades before being reactivated in the brain by stress, immune compromise, or other factors. After the initial oral infection, herpes simplex virus-1 (HSV1) becomes latent in the trigeminal ganglion and can later enter the brain via retrograde axonal transport, often targeting the temporal lobes.

HSV1 can also enter the brain via olfactory neurons directly. HSV1 (oral herpes) and HSV2 (genital herpes) are known to trigger amyloid aggregation and their DNA is commonly found in amyloid plaques. Anti-HSV drugs reduce Aβ and p-tau accumulation in brains of infected mice. HSV1 reactivation is associated with tau hyperphosphorylation in mice and may play a role in tau propagation across neurons. In humans, recurrent reactivation with newly produced HSV1 particles, ‘drop by drop,’ may produce neuronal damage and eventually lead to neurodegeneration and Alzheimer’s disease (AD) pathology, partly due to effects on amyloid and tau. Clinical studies show cognitive impairment in HSV seropositive patients in different patient groups and in healthy adults, and antiviral treatments show robust efficacy against peripheral HSV infection. The study team will conduct the first-ever clinical trial to directly address the long-standing viral etiology hypothesis of AD which posits that viruses, particularly the very common HSV1 and HSV2, may be etiologic or contribute to the pathology of AD.

In patients with mild AD who test positive for serum antibodies to HSV1 or HSV2, the generic antiviral drug valacyclovir, repurposed as an anti-AD drug, will be compared at oral doses of 2 to 4 grams per day to matching placebo in the treatment of 130 patients (65 valacyclovir, 65 placebo) in a randomized, double-blind, 78-week Phase II proof of concept trial. Patients treated with valacyclovir are hypothesized to show smaller decline in cognition and functioning compared to placebo, and, using 18F-Florbetapir PET imaging, to show less amyloid accumulation than placebo over the 78-week trial. Through the use of tau PET imaging with the tracer 18F-MK-6240 at baseline and 78 weeks, patients treated with valacyclovir are hypothesized to show smaller increases in 18F-MK-6240 binding than patients treated with placebo from baseline to 78 weeks. Apolipoprotein E genotype at baseline, as well as changes in cortical thinning on structural MRI, olfactory identification deficits, and antiviral antibody titers from baseline to 78 weeks, will be evaluated in exploratory analyses. In patients who agree to lumbar puncture, plasma and CSF acyclovir will be assayed to establish the degree of CNS penetration of valacyclovir in mild AD, and the investigators will obtain CSF Aβ42, tau, p-tau for subset exploratory analyses with changes in outcome measures.

If this trial is successful, the investigators will apply for funding to conduct a larger, multicenter, Phase III study using a study design that will be informed by the results of this Phase II trial. This innovative Phase II proof of concept trial clearly has exceptionally high reward potential for the treatment of AD.

Study Design
Study Type : Interventional  (Clinical Trial)
Estimated Enrollment : 130 participants
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Triple (Participant, Care Provider, Investigator)
Primary Purpose: Treatment
Official Title: Anti-viral Therapy in Alzheimer’s Disease
Actual Study Start Date : February 12, 2018
Estimated Primary Completion Date : August 2022
Estimated Study Completion Date : August 2022
Remember, Alzheimer’s is a label, nothing more.  They are still trying to figure out what causes it.
Dr. Klinghardt has gone on record stating that he’s not had one MS, ALS, or Parkinson’s patient NOT test positive for Lyme:

Dementia Misdiagnosed for PTLDS or Vice Versa? A Case Report

Frontotemporal Dementia Misdiagnosed for Post-Treatment Lyme Disease Syndrome or vice versa? A Treviso Dementia (TREDEM) Registry Case Report.

Di Battista ME, et al. J Alzheimers Dis. 2018.


We describe the case of a 61-year-old woman diagnosed with Borreliosis at the age of 57. Subsequently, the patient developed depression, anxiety, and behavioral disturbances. A lumbar puncture excluded the condition of Neuroborreliosis. The diagnostic workup included: an MRI scan, a 18F-FDG PET, a 123I-ioflupane-SPECT, an amyloid-β PET, a specific genetic analysis, and a neuropsychological evaluation.

Based on our investigation, the patient was diagnosed with probable behavioral-frontotemporal dementia (bvFTD), whereas in the previous years, the patient had been considered firstly as a case of Post-Treatment-Lyme Disease and, secondly, a psychiatric patient.

We believe that, in the present case, such initial symptoms of Borrelia infection may have superimposed on those of bvFTD rather than playing as a contributory cause.



Here we have a woman with an actual Lyme diagnosis who goes on to develop depression, anxiety, and behavioral disturbances.  (All common symptoms with neuro-Lyme:

Despite mainstream knowledge of absolute proof of abysmal testing, they state they ruled out infection despite a prior diagnosis based on a lumbar puncture.

In this informative read from Columbia University, we learn that there are specific steps to be followed for lumbar punctures regarding Lyme as well as the fact that patients may have neurologic Lyme Disease but still test negative on the Lyme index (an index used with cerebrospinal fluid in a lumbar puncture)

So this woman was handed a label and told, “Go home and be well.”

This scenario has played out so many times it’s like a skip in a record.

How about a clinical trial of antimicrobials known to have action against borrelia and then retest her (called a provocation test)?  Clinicians in the field understand how elusive this organism is.  A full work-up needs to be done on symptomology as it could possibly be a different pathogen altogether known to be transmitted by ticks and other bugs.  How about also testing for other tick borne pathogens known to give behavioral symptoms like Bartonella? (It could be one of 18 and counting pathogens spread by ticks)

You see, something is causing this “probable behavioral-frontotemporal dementia (bvFTD).”  

All they’ve done here is slap a name to it but they haven’t found the cause.  Without the cause they will not treat appropriately.  

Somebody get this woman to Columbia University!

How many more are going to slip through the cracks and loose their minds due to poor testing?

For more on the abysmal testing:

More on the relationship between Alzheimer’s, Dementia, ALS and Lyme:  Kris Kristofferson was wrongly diagnosed with Alzheimer’s but had Lyme Disease. For years doctors told Kristofferson it was either Alzheimer’s or dementia, and may have been the result of blows to his head from boxing, football and rugby. The medication he was given gave him bad side effects and didn’t help.  Since starting treatment for Lyme Kristofferson “has made remarkable strides.” His wife Lisa said,

“all of the sudden he was back.” Although he still has some bad days, there are other days when he is “perfectly normal,” she said.  Bacteria are usually ignored despite its historical and current significance in dementia research.  Today, the main bacterial threat to acquiring dementia comes from Lyme disease—a bacterium borrelia burgdorferi.

Chronology of Research on Lyme Disease, Dementia, Alzheimer’s, Parkinsons, & Autism


Lapenta J1*, Lapenta JM2

1Lapenta, J. Medic Surgeon, Specialty Dermatology, 24 years of exercise. University of Carabobo,   Venezuela. Ceo Dermagic Express 2Lapenta, J.M. Medic Surgeon. University of Carabobo. Diplomat in Facial Aesthetics Occupational Medicine and Prehospital Auxiliary. Resident Doctor Ambulatorio Del Norte Maracay Aragua State. Coo Dermagic Express.

*Corresponding author: Lapenta J, Medic Surgeon, Specialty Dermatology, 24 years of exercise. University of Carabobo, Venezuela, Email:


The Lyme disease or Chronic Erythema Migrans whose first clinical description was made by the scientist Afzelius in the year 1908, and its causative agent the spirochete Borrelia Burgdorferi was discovered 73 years later by Willy Burgorfer in the year 1981, produced by the tick bite of the family Ixodidae, Ixodes scapularis and many others. Among the numerous species described, Borrelia Burgdorferi is disseminated mainly in the United States, Borrelia garinii and Borrelia Afzelii in Europe and Asia as the most involved and described in geographic and population studies. In addition to producing skin lesions in infected people, and multi-organ side effects it is able to reach the human brain and produce dementia, Alzheimer, Parkinson and Autism, events widely discussed today. In this investigation we will make a chronological description of the events that lead to definitely recognize that this spirochete as the spirochete of syphilis, Treponema pallidum which produces neurosyphilis in its tertiary stage, also the Borrelia is able to reach the brain, and produce collateral damage, a term called neuroborreliosis, and among its most lethal effects can cause dementia, Alzheimer, Parkinson and Autism and as a great sequel the so-called post-treatment syndrome of Lyme disease.

Keywords: Lyme disease, Neuroborreliosis, chronic erythema migrans, Borrelia burgdorferi, dementia, Autism, Alzheimer, Parkinson, post Lyme disease syndrome


The main objective of this research is to demonstrate that the Lyme disease produced by the spirochete Borrelia Burgdorferi and its different species, is not just a skin disease. It has been scientifically proven to produce numerous organic manifestations, and in this work we will demonstrate chronologically that this biological agent can conquer the brain, if it is not detected and treated in time produce lethal neurological effects such as dementia, Alzheimer’s, Parkinson, Autism and as a sequel, post Lyme treatment syndrome.


1.) Describe chronologically how it came to the definitive conclusion that the Borrelia Burgdorferi and its pathogenic species in humans can conquer the brain in several of its stages and produce diverse neurological manifestations ranging from meningitis to dementia, Alzheimer’s, Parkinsonism and Autism, including these terms in the so-called Neuroborreliosis.

2.) Describe the neurological clinical manifestations in positive Lyme patients: children of positive Lyme mothers, adults, and adolescents not treated in time, or those who received treatment and showed resistance to it.

3.) The World Health Organization (WHO) in the update of the ICD-11 year 2018 (International Classification of Diseases) included the codes for Lyme borreliosis related to this research: “Lyme neuroborreliosis”, “dementia due to Lyme disease” and “central nervous system demyelization due to Lyme borreliosis”. After our review, we will urge the recognition by this entity of the rest of the proposed codes.


The history of the term DEMENTIA produced by the spirochaete Borrelia Burgdorferi, is longstanding, beginning in the year of 1922 when the French Garin and Bujadoux described a patient with neurological symptoms and meningitis after the bite of a tick; The skin lesion was similar to the Erythema chronicum migrans (ECM), which was first described in 1908 by Afzelius. A similar case was published by Hellerstrom in 1930. [1-3]

Later in 1941 and 1944 Bannwarth described in 26 patients a clinical condition characterized by: lymphocytic meningitis, neuralgia and neuritis that mainly involved facial nerves; only 3 of them associated with stinging by ticks, but years later European researchers found that this syndrome was associated with tick bites and Erythema chronicum migrans (ECM). This condition was described under several names including meningopolineuritis by tick bite (Garin-Bujadoux-Bannwarth), remaining with the definitive name of Lymphocytic meningoradiculitis or Bannwarth Syndrome. [4-6]

To date there are more than 700 [144] articles published on the subject Lyme disease, we will focus on the most relevant, about 200 referring to the issue we are developing, to keep a chronological line in the exact time.



As we said previously, it was in the year 1922 when the French Garin-Bujadoux [1], described a patient with neurological symptoms and meningitis after a tick bite with skin lesion similar to Erythema chronicum migrans (ECM), and then confirmed by Bannwarth in 1941 and 1944 [4], [5], [6] with the description of 26 cases with a symptom characteristic triad: lymphocytic meningitis, neuralgia and neuritis, some associated with tick bites. This clinical picture was later named with the definitive name of meningopolineuritis or lymphocytic meningoradiculitis or Bannwarth syndrome.[1-6]

This fact was 60 years before the discovery of Borrelia Burgdorferi, but the first neurological symptoms related to the Erythema chronicum migrans (ECM) discovered by Afzelius in 1908 [2], [3], had already been described. [3-6]


The first confirmation that Erythema chronicum migrans (ECM) was and is produced by a living agent was discovered and published by Binder and Col. in 1955 who transplanted skin of three patients with ECM to 3 healthy volunteers and these, in the course of 1 to 3 weeks developed the disease. [7] This occurs 11 years after the description of Bannwarth [4], [5] and 33 years after the description of the first case by Garin and Bujadoux. [1]


In 1976 Lefevre JP, and Cols. [8], published 9 cases of meningoradiculitis after tick’s bites and compared them with 56 previously published cases. They found as predominant clinical symptoms:

  • Pain: radiculitis
  • Paralysis: more than 50% of cases: unilateral or bilateral paralysis of the 7th cranial nerve
  • Pyramidal signs
  • Signs of brain irritation: meningitis, neuralgia
  • Cerebrospinal fluid (CSF): pleocytosis.

This means that in these 20 years (1956-1976) about 65 cases of meningoradiculitis associated or not with ticks bite had already been published. [8]


In this year the French Goffinet AM, and Cols. publish a paper on meningoradiculitis produced by ticks, where confirm the previously described symptoms and launch the hypothetical theory that the etiology is a transmission of living agent, as Binder found in 1995 [7], and suggest that it is a virus transmitted by the tick bite. [9]

Still left 3 years for the discovery of the Borrelia Burgdorferi.


This year of 1981 marked a milestone, Wilheim “Willy” Burgdorfer discovered the causal agent of Chronic Erythema Migrans (ECM), a bacterium belonging to the family of spirochetes as Treponema pallidum (syphilis), studying the stomach of a tick of the genus Ixodes daminii collected in the town of Old Lyme Connecticut, United States, which was named Borrelia Burgdorferi in honor of its name. [10], [11]. From the location where the causative agent was discovered (Lyme village) the name of Lyme disease was born. [10], [11].

One year later in 1982. Hindfelt B, and Cols. [12], publish 11 more cases of meningoradiculitis of Bannwarth, of which 50% was associated with tick bites, describing the classic symptoms of this syndrome, (meningitis, neuritis and radiculopathies); and in addition in the cerebrospinal fluid (CSF): mononuclear pleocytosis (lymphocytes), defect of the blood-brain barrier and intrathecal IgG synthesis, expanding the clinical findings of this pathology.

All patients recovered almost completely from their neurological symptoms in 1-2 months, regardless of treatment. [12]


This year was also very important because researchers Skoldenberg B, and Cols. [13], published 21 cases of chronic persistent meningitis of which 4 (19%) had Chronic Erythema Migrans as antecedent and 4 (19%) had been bitten by ticks; neurological symptoms included:

  • Aseptic meningitis
  • Cranial neuropathy (mostly paralysis of the facial nerve)
  • Peripheral motor and sensory radiculopathies
  • Myelitis
  • Cerebrospinal fluid alterations: mononuclear pleocytosis, protein increase, intrathecal IgG synthesis

The symptoms coincide with those previously described for Bannwarth meningoradiculitis [4], [5]. [6], [8], [9], [12], but the authors report a dramatic improvement in all cases when treated with penicillin G for 14 days [13]. This fact confirmed what was stated by previous studies that it was a living agent that caused the disease. [1-13] Spirochetes (Treponema pallidum, syphilis) are sensitive to this antibiotic [17], [18], [19], and Borrelia Burgorferi is a spirochete. [10], [11].


In the year 1984 keep going the publication of cases of meningoradiculitis of Bannwarth associated with Lyme disease, and Pachner AR. and Cols. [14] published a study of 38 cases, emphasizing the neurological aspects from those patients studied between 1976 and 1983. Already began to speak of “Lyme meningitis” with the same characteristics of Bannwarth syndrome (meningitis, neuropathy and radiculoneuritis); in addition to it, among other symptoms already described: headache, stiff neck, and lymphocytic pleocytosis in cerebrospinal fluid (CSF), unilateral or bilateral facial paralysis and weakness of the extremities. [14]

That same year Pfister and Cols. published 4 cases of meningoradiculitis of Bannwarth in Germany, Munich [15], where demonstrate the presence of antibodies against spirochetes of the Ixodes daminii tick in 100% of cases. In three patients, the antibodies were also present in the cerebrospinal fluid (CSF). In one patient, they isolated CSF spirochetes, and demonstrated specific IgG antibodies in serum and CSF against spirochetes. In one case, the spirochete of cerebrospinal fluid (CSF) was isolated morphologically equal to the spirochete of the tick Ixodes daminii; and postulate that Lyme disease and Bannwarth meningoradiculitis have the same etiology: spirochetes. [10], [11], [15].

This study was confirmed by researcher Rayberg B. [16] that same year of 1984 published in Sweden 9 more cases of Bannwarth syndrome where 6 cases (66%) had high titers of antibodies against the Lyme spirochete (Borrelia) and reaffirm the published previously: Bannwarth syndrome and Lyme disease are caused by spirochetes. [10], [11], [15], [16]

This year of 1984 also marks a milestone in the study of Lyme disease and its relationship with spirochetes when the German scientist Weber K. [17], published 4 cases of this disease that presented the reaction of Jarisch-Herxheimer after being treated with antibiotic therapy. This reaction was first described by the Austrian dermatologists Adolf Jarisch and the German Karl Herxheimer in 1895 and 1902 respectively, when they treated cases of syphilis with mercurial. [18], [19]. This reaction only occurs in cases of spirochetosis (syphilis, leptospira and others), and now the newly discovered spirochete Borrelia Burgdorferi [10], [11], [15], [16], [18], [19]

The reaction occurs a few hours after administration of the antibiotic and is produced by endotoxins released by spirochetes at death, and is characterized by: malaise, hypotension, chills, muscle spasms, headache, tachycardia, hyperventilation and exacerbation of lesions in skin. [18], [19]. This reaction was confirmed in later years in the treatment of Lyme spirochetosis. [32], [55], [138], [146], [168]

That same year of 1984, 117 cases were described in New Jersey, studied between 1976 and 1982, of which 86 were adults and 31 children with Lyme disease. Chronic erythema migrans was present in 93% of the cases. The most common late neurological manifestations, in addition to the immediate organic ones (arthritis 26%, and febrile syndrome 45%), were meningitis (10%) and facial paralysis (8%) of the cases. [20]

In the year 1985 the Germans Christen HJ, and Cols. describe 3 cases of meningoradiculitis of Garin-Bujaudox-Bannwarth in children, confirming the previous description, that the Erythema chronicum migrans (ECM) and its neurological manifestations can also affect children. [20], [21]

This same year 1985 the researchers Stiernstedt GT, and Cols. in 41 out of 45 cases of spirochetal meningitis (91%), prove that the enzyme-linked immunosorbent assay (ELISA) was highly sensitive to the diagnosis of spirochetal meningitis. Also the indirect immunofluorescence method in serum and cerebrospinal fluid (CSF) with 98% of positivity. [22]

It was in this decade that the term “Neuroborreliosis” began to be used in relation to the neurological manifestations of Erythema chronicum migrans (ECM) or newly “named” Lyme disease, when the causative agent was discovered; and many of the works had already been described about meningoradiculitis or Bannwarth syndrome associated with tick bites, and its neurological manifestations. But really the term “Neuroborreliosis” was born in the year 1922 (63 years before) when Garin and Bujadoux described the first case [1], later confirmed by Bannwarth in 1941 and 1944. [4], [5].

This fact that the French Garin and Bujadoux were the first to describe Lyme neuroborreliosis has tried to be disqualified by some authors [172], but definitely the majority of the scientific community does recognize them.

Still left a year before the description of the first cases of dementia associated with Lyme disease [23], fact that marked a milestone and revealed that the neurological damage produced by Borrelia Burgdorferi went beyond the meningoradiculitis of Garin-Bujadoux-Bannwarth Classically described. [1], [4], [5]. [6], [8], [9], 12]


Another important year in the timeline of this research on the association of Lyme disease with dementia. The scientist MacDonald A.B. [23], published for the first time two cases where spirochetes were identified in brain tissue subcultures in the autopsy of two patients who died from dementia, using indirect immunofluorescence and monoclonal antibodies specific for Borrelia species, which had previously been identified by ”dark field” light microscopy.

The cases were a 74-year-old woman with mild dementia of less than 1 year’s duration living in Florida and New York, and the other a 69-year-old man who died in a nursing home in Texas after a history of progressive dementia. 4 to 5 years; him also presents symptoms of Parkinson’s. [23]

This fact was confirmed that same year (1986) by Willy Burgdorfer (discoverer of the spirochete) and Reik L. Jr. [24], who published 8 positive Lyme cases with neurological abnormalities where they found high titers against Borrelia species. Neurological symptoms included:

  • Aseptic meningitis
  • Encephalitis
  • Cranial neuritis
  • Motor and sensory radiculitis
  • Myelitis
  • Severe encephalitis that resulted in dementia in two (2) of these patients
  • Irreversible myelopathy in one (1) patient

These last two findings enlarged the neurological spectrum already known by Borrelia Burgdorferi infection; [12-24].

On the other hand no patient showed the classic marker of the disease that is the Chronic erythema migrans (ECM) and only 3 had arthritis, which is the other clinical marker of this pathology. This fact led them to conclude that Lyme disease can present as pure neurological forms, without extra neural characteristics [24].


In 1987, articles on Bannwarth’s meningoradiculitis and its relation to tick bite, enlargement of the neurological spectrum, (chronic encephalomyelitis, late neuroborreliosis, and findings of IgG anti Borrelia antibodies in the cerebrospinal fluid by ELISA) continue to be published; [26-32] but in addition to this, another important fact occurs:

This year in the timeline of Lyme Neuroborreliosis and its relationship with Alzheimer’s disease was demonstrated, because the researcher MacDonald A.B and Col. [25], published a case of a patient who died of Alzheimer’s which I performed an autopsy of the brain tissue and found the spirochetes of Borrelia in the cerebral cortex. The authors propose that, as in tertiary or late syphilis, Borrelia species invade the brain and remain there for years, subsequently causing dementia; state that an undetermined number of patients with Alzheimer’s disease have late tertiary neuroborreliosis. [25].

This fact: Lyme’s relationship with Alzheimer’s was later shown in other studies that we will mention later [79], [81], [87], [107], [128], [135], [165], [170], [186].

Also this year of 1987 Moore JA, reports again the reaction of Jarisch-Herxheimer in the treatment of Lyme Borreliosis. [32]


For this year, the French Dupuis MJ. [33] published a study describing the three stages of Lyme disease and its neurological manifestations, making a summary of the symptoms, mostly already described previously:

Stage 1 during the first month is characterized by Chronic erythema migrans and associated manifestations.

Stage 2 includes neurological symptoms:

  1. Classic meningoradiculitis. (Garin-Bujadoux-Bannwarth syndrome)
  2. Lymphocytic meningitis with acute or recurrent course.
  3. Facial paralysis
  4. Neuritis of other cranial nerves
  5. Cranial polyneuritis
  6. Sign of Argyll-Robertson
  7. Affectation of peripheral nerves
  8. Acute transverse myelitis
  9. Severe encephalitis
  10. Myositis

Stage 3 of the disease: neurological symptoms, months or years after the disease has started:

  1. Chronic neuropathy with mainly sensory or motor signs
  2. Recurrent cerebrovascular accidents
  3. Cerebral angiopathy
  4. Progressive encephalomyelitis
  5. Ataxic and spastic March. (Parkinson’s symptoms)
  6. Dysfunction of the cranial nerve that includes optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy
  7. Simulation of other diseases: multiple sclerosis
  8. Lesions of the multifocal and mainly peri-ventricular white substance
  9. Psychic disorders: acute presenile dementia.

The author states that high doses of the antibiotic penicillin can stop the disease and sometimes induce regression. [33]; also affirms the great similarity between Borrelia burgdorferi and Treponema pallidum (syphilis) [17], [18], [19], considering it as the “great imitator” of other diseases. [33]


This year of 1989 the researcher Pachner AR and Col. [34], contribute in the classification of the neurological spectrum of Lyme disease by publishing an article where they consider that Borrelia Burgdorferi and its species are highly neurotropic and classify neuroborreliosis in two types:

– Lyme meningitis in the second stage of the disease, which resembles aseptic meningitis; it is often associated with facial paralysis, peripheral nerve involvement and / or radiculopathies and may be the first manifestation of the disease even without the presence of Chronic erythema migrans (ECM)

– The third stage: parenchymal disease which causes a multitude of nonspecific manifestations of the central nervous system (CNS) that can be confused with conditions such as multiple sclerosis, brain tumor and psychiatric disorders.

The authors consider that the “new great imitator” of the diseases is “Lyme borreliosis”, a term attributed ancestrally to another spirochete, Treponema pallidum, causal agent of syphilis; confirming what was stated in the previous study [33], [34] and also in relation to the fact that the neurological manifestations of Lyme disease occurs in stages 2 and 3 of the disease fundamentally.

The scientist Kristoferitsch W. and Cols. describe in that year the characteristics of the neuroborreliosis, type meningoradiculitis of Bannwarth in Europe and affirm that the characteristics are very similar to those presented by the American patients (US) [35].

Pizzarello LD, MacDonald and Cols. [36], published a case of loss of vision in a 71-year-old patient due to temporal arteritis, biopsy and blood culture were performed where spirochetes compatible with Borrelia spices were found. After treatment with iv ceftriaxone the patient showed a moderate improvement. The authors considered this case as the first one where Borrelia is found in a biopsy of the temporal artery. [36]

That same year the Germans Bialasiewicz AA, and Cols. [37] published a case of a 25-year-old female patient who presented with a neurorretinitis in the left eye, later confirmed by Borrelia Burgdorferi, presenting affectation of both eyes, finding advanced atrophy of the optic nerve, visual acuity decrease; magnetic resonance shows multiple demyelinating lesions for ventricular and subcortical areas. This case was considered by the authors to be the first in the literature describing demyelinating lesions in the brain with bilateral optic neuritis verified serologically. The patient improved after receiving treatment with doxycycline. [37]

This fact of the demyelination caused by the Borrelia Burgdorferi was confirmed that same year of 1.989 when Meier C, and Cols. [38], publish a work on 8 patients with neurological complications of the peripheral nervous system produced by Lyme Borreliosis. More than 60% of the patients presented the classic meningoradiculitis of Garin-Bujadoux-Bannwarth. In the biopsy of the nerves it was found:

– Macroscopic infiltrations of epineural vasa nervorum and small infiltrations around of endoneurial capillaries: lymphocytes, histiocytes and plasma cells.

– Thrombosis and recanalization in some epineural vessels.

– Seven biopsies showed a significant loss of myelinated axons due to axonal degeneration.

– In one biopsy they observed segmental demyelination with axonal degeneration.

The authors conclude that the peripheral neurological manifestations of Lyme Borreliosis are angiopathic due to vasa nervorum vasculitis and mainly caused by axonal degeneration. [38] This fact, demyelination of the nerves, also in the brain appears for the first time in our timeline [37], [38] and further broadens the clinical spectrum of neuroborreliosis.

Still left nearby 3 decades in our timeline and already by this date (1.989) the term “Neuroborreliosis” of Lyme had been recognized and among the neurological manifestations of our research: dementia [23], [24], [33], Alzheimer [25], Parkinson [23], [33], they were already described; and in addition to this: central and peripheral demyelination of nerve cells [37], [38] associated with Borrelia Burgdorferi.


Many studies were carried out this decade [39-62], since the potential damage that Borrelia can cause in both the central nervous system (CNS) and the peripheral nerves was already known, so the scientists focused their studies in this line; we will mention the most outstanding ones.

The investigator Judith Miklossy in 1990 [39] describes the neuropathological findings of a case with Lyme neuroborreliosis, manifested as chronic meningitis; there were meningovascular and parenchymal occlusive changes similar to those that occur in tertiary syphilis or neurosyphilis; and suggest that the case described represents the meningovascular form of Lyme or tertiary neuroborreliosis, confirming previous studies [25], [33], [34].

In the year 1991 Krupp, L.B, and Cols. [42], describes 15 patients treated for Lyme Borreliosis who complained of persistent cognitive difficulty after 6 to 7 months of treatment with antibiotic therapy; they were compared with 10 healthy controls. Post-Lyme patients showed a marked deterioration in cognitive tests: memory loss mainly in selective recognition; attributed this finding to chronic encephalopathy produced by Borrelia. This study was confirmed in 1995 by Benke T. and Cols. [50], in 1997 by Gaudino EA. and Cols. who also made a differentiation between this syndrome and chronic fatigue syndrome (SCF). [55] In 1999 Elkins LE. and Cols. also confirmed this fact. [61]

Perhaps this represents the first study [42], about what later was and is called post-treatment Lyme disease syndrome (PTLDS), or Post-Lyme syndrome (PLS) because patients were evaluated months after receiving treatment and presented neurological damage symptomatology in this case chronic encephalopathy. [42], [50], [55], [61]

In the year 1993 Fallon B.A. and Cols. [44], published three cases (3) of neuroborreliosis associated with depression, previously described [33], but patients showed panic attacks and mania; considering these last symptoms as the first reported associated with Lyme neuroborreliosis. [44]

In the year 1994 Schaeffer S, and Cols. publish an article on Lyme disease associated with dementia [48], in 1995 Waniek C, and Cols., report another neuropsychiatric case [49] with fatal outcome of progressive frontal lobe dementia, where pathologically severe subcortical degeneration was found, and reaffirm the fact that Lyme disease can present as pure neurological forms. [24], [48]; the patient improved with antibiotic treatment, but then relapsed.

Now we will put a summary of the neurological findings described in this decade related to Lyme Borreliosis, apart from the classic triad of lymphocytic meningoradiculitis or Garin-Bujadoux-Bannwarth syndrome (meningitis, neuritis and radiculopathies), and the detection of spirochete in cerebrospinal fluid (CSF) and its changes, already widely discussed:

1.) Progressive dementia. [48, [49]

2.) Depression: 26-66% of cases. [43] [46], [54], mania. [44], panic attacks. [44], [60]

3.) Memory disorders [43], [50], [54], [58], [59]: verbal memory, mental flexibility, associative, verbal and articulation functions; decreased consciousness, mental confusion.

4.) Encephalitis, encephalomyelitis, isolated transverse myelitis, vasculitic cerebral disorders. [43], [49], [50], [54]

5.) Paranoia, schizophrenia, bipolar disorders, obsessive-compulsive disorders. [46]

6.) Hallucinations, nightmares, hypersexuality. [52]

7.) Sleep disorders, fatigue. [54], [59]

8.) Jarisch-Herxheimer reaction, post-treatment with antibiotics (amoxicillin). [56]

9.) Hemiparesis, hemianopsia, stenosis of cerebral arteries. [58]

10.) Sensitivity to light, touch and sounds. [60]

The highlights in this decade were the appearance of new neurological symptoms associated with Borrelia Burgdorferi infection, which led to it being considered a “neuropsychiatric” disease, the appearance of the Post-treatment syndrome of the disease (PTLDS) or (PLS) ), and the appearance of new laboratory techniques to detect the causative agent [62].


Already for this decade Lyme neuroborreliosis was widely recognized by scientists worldwide. There were numerous studies [63 – 97] of which we will highlight the most important in relation to our research.

In the year 2001 Tager F.A. and Cols. published a study on 20 children with a history of cognitive complaints after having Lyme disease compared with 20 healthy children. The Lyme positive children presented more cognitive and psychiatric disorders than the healthy ones, being the most relevant: anxiety, depression and fatigue. [66]

In the year 2003, Cassarino D.S. And Cols. [72] published a case of a 63-year-old male patient who presented Erythema Migrans rash, which was detected against Borrelia Burgdorferi antibodies in serum and cerebrospinal fluid (CSF). Clinically I present joint pains and tremors. He was diagnosed with clinical Parkinsonism by several neurologists and subsequently had a fatal outcome. In the cerebral autopsy it was found:

– Mild atrophy of the basal ganglia.

– Depigmentation of the substantia nigra.

– Extensive neuronal loss.

– Extensive loss of the neuronal black substance.

– Astrogliosis

– Absence of Lewy bodies.

– Ubiquitin-positive glial cytoplasmic inclusions in striatal and nigral oligodendroglia.

The authors considered this case as the first report of striatonigral degeneration in a patient with Borrelia burgdorferi infection of the central nervous system and clinical Parkinsonism associated with Lyme. [72] Already the symptoms of Parkinson’s had been previously reported [23], [33].

In the year 2005, Jones CR. and Cols. [76] present a study on the clinical manifestations of 102 children born to Lyme-positive mothers, the most notable neurological clinical symptoms being the following:

1.) Fatigue and lack of resistance: 72%

2.) Orthopedic disorders: sensitivity (55%), pain (69%) spasms and generalized muscle pain (69%), rigidity and / or retarded motion (23%).

3.) Neurological disorders:

A- Headaches: 50%

B-) Irritability: 54%.

C-) Bad memory: 39%

4.) Delay in development: 18%

5.) Seizure disorder: 11%

6.) Vertigo: 30%

7.) Tic disorders: 14%

8.) Involuntary athetoid movements: 9%.

9.) Earning disorders and humor changes: 80%

A-) Cognitive speaking: 27%

B-) Speech delay: 21%

C-) Reading-writing problems: 19%

D.) Problems of vocal articulation: 17%.

E-) Auditory / visual processing problems: 13%

F-) Word selection problems: 12%

G-) Dyslexia: 8%

10.) Suicidal thoughts: 7%

11.) Anxiety: 21%

12.) Anger or rage: 23%

13.) Aggression or violence: 13%

14.) Irritability: 54% -80%

15.) Emotional disorders: 13%

16.) Depression: 13%

17.) Hyperactivity: 36%

18.) Photophobia: 40-43%

19.) Ocular problems: posterior cataracts, myopia, stigmatism, conjunctive erythema (Lyme eyes), optical nerve atrophy and / or uveitis: 30%

20.) Sensitivity of skin and noise (hyperacuity): 36-40%

21.) Autism: (9%). [41]

Autism related to Lyme disease appears in the timeline (2.005), which was confirmed by subsequent studies [93], [95], [117], [124], [125], [130], [179]

Bransfield, R.C. and Cols. publish a study in the year 2008 where they state that chronic infections, including Borrelia burgdorferi and others transmitted by ticks, produce a weakened state in children, either in fetal development or during development that may promote an autistic state. Positive reactivity was found in several patients with autism spectrum disorder for Borrelia Burgdorferi in several studies of 22%, 26%, 20% – 30% and 50% for Mycoplasma, [93]; later the same author published in the year 2009 another work confirming this event and names as possible causal agent of this infectious spectrum:

Babesia, Bartonella, Borrelia burgdorferi, Ehrlichia, Human herpesvirus-6, Chlamydia pneumoniae and Mycoplasma (in particular Mycoplasma fermentans). [95]

In the year 2006, MacDonald A.B. [79], publishes a paper in which he hypothesizes that the rounded forms of Borrelia Burgdorferi are the main cause of rounded structures called “plaques” in the brain affected with Alzheimer’s disease (AD); these are emblematic and are observed as rounded amyloid forms of brain damage in Alzheimer’s. [79]

The same author (MacDonald) in the year 2007 publishes another study where he reaffirms his theory that the “neurofibrillary tangles” present in Alzheimer’s disease are produced by a chronic infection, in this case the Borrelia burgdorferi, mentioning a pilot study where it was demonstrated that seven (7) out of ten (10) Alzheimer’s cases showed positive signs for infectious DNA in the neurons analyzed. [81]; remember that this author in 1987 found Borrelia Burgdorferi in the brain of one patient who died of Alzheimer’s disease. [25]

In the year 2008, Judith Miklossy reaffirms what MacDonald presented, publishing a paper that concludes that bacteria, including spirochetes (Borrelia, Treponema) contain amylodogenic proteins; that cortical deposition of beta-amyloid-peptide (Abeta) and tau phosphorylation can be induced after chronic infections, which produce inflammation of the brain, cytokine release, apoptosis, generation of free radicals, release of nitric oxide and activation of complement, which generate a cascade of events that finally produce the amyloidogenesis typical of Alzheimer’s disease. The author proposes that the treatment with antibiotics and anti-inflammatories in these cases is vital to avoid dementia. [87]

In that year of 2008, Judith Miklossy herself published another work on the neuropathology of dementia in syphilis and Lyme disease, where she emphasizes and reaffirms that both Treponema pallidum (syphilis) and Borrelia burgdorferi (Lyme), both spirochetes, in later stages cause dementia, cortical atrophy and deposition of amyloid in the brain. These manifestations may occur years or decades after the primary infection and in the tertiary stage is where the dementia develops apart from other neurological symptoms. [88]

Other studies conducted in this decade reported associated with neuroborreliosis: spontaneous hemorrhage of the temporal lobe [64], posterior column dysfunction [65], headache, loss of sleep, mild ataxia, dysfunction of perception, abnormality in the tendon reflexes, disturbances of sensory responses, memory deterioration, alteration of thoughts [67], personality disorders, anxiety and affect changes [91, paranoid and depressive syndrome. [92]

Summary of this decade with Lyme neuroborreliosis: neurological manifestations in children, association with Alzheimer’s, Parkinson’s and Autism. The so-called post-treatment Lyme disease syndrome (PTLDS) also appears in the timeline.


In this last decade, Lyme disease became known worldwide and studies in relation to it and its consequences in the affected population increased markedly. [98-208]

The dementia associated with Lyme neuroborreliosis was confirmed in several studies [105], [128], [160], [193], corresponding to the years: 2011, 2014, 2016 and 2018.

In relation to Autism associated with Lyme disease, studies were published in this decade in 2012, 2013, 2014, 2017, 2018 with evident evidence that infection by the spirochete Borrelia burgdorferi predisposes children of Lyme positive mothers to present the spectrum autistic, because it has been scientifically demonstrated that this spirochete crosses the placenta [203], [207], and can conquer the fetal brain producing neurological damage in the short and long term in pregnant women, who did not receive adequate treatment, and even after receiving treatment with moderate answers; [117], [24], [125], [130], [179] this fact had already been previously described. [76], [93], 95]

Regarding the association of Alzheimer with Neuroborreliosis, highlight the researcher Judith Miklossy, who published 3 studies, years 2011, 2015, 2016, shows convincing evidence that infection by spirochetes such as Treponema pallidum (syphilis) and Borrelia Burgdorferi, (Lyme) chronically infecting the brain, produce the Beta-Amyloid peptide characteristic of this disease. [107], [135], [165]

In 2017 we published a paper in which we demonstrated the effectiveness of the antibiotic Minocycline in Alzheimer’s disease and other neurological disorders, such as Parkinson’s and Multiple Sclerosis, which would confirm the infectious theory as part of the etiology of these diseases [192]; Other neurological disorders where Minocycline proves to be effective are: schizophrenia, bipolar disorders and autoimmune encephalomyelitis [192]. Here the reflection is unique: if an antibiotic improves a neurological condition, it is because you have an infection (bacteria) in your bloodstream and brain.

Lyme disease showed over time that it does not respect creeds, races, sports and professions by infecting movie celebrities, singers, presidents of nations, and athletes; we present them in this decade, because most of them were in recent years that manifested their illness when Lyme disease was already a notorious event in society. Among them are: Thalia (Mexican singer), 2007; Richard Gere (actor) 1999; Alec Baldwin (actor) 2011; Avril Lavigne (Canadian Singer); 2012; George W Bush Jr. (Former President of U.S.) (2007); Jennifer Capriati (tennis player) 2013; Yolanda Hadid (TV Actress) 2012; Ben stiller (Actor) 2010; Kris Kristofferson (Actor and singer) 2006; Ashley Olsen (Actress) 2012, and many more. [155], [156, [157], [158], [169]. These people are human beings; in no previous study they have been mentioned, they were omitted.

Of these cases, the singer and actor Kris Kristofferson deserves special mention. Since the year 2006 he was bitten by a tick and later developed neurological disorders that led him to present loss of memory; He was missdiagnosed with Alzheimer’s disease and received treatment with two medications without improvement. Later he was diagnosed with Lyme and after receiving antibiotic therapy began to “recover” the memory, considered by some as a true “miracle” and “come back”. It was not a “miracle” his bloodstream and brain were infected with Borrelia Burgdorferi. Today recovered, is 82 years old and continues to sing. [170], [171]

In year 2017, the Ad-Hoc Committee for the recognition of the ICD-11 codes (International Classification of Diseases year 2018) of Lyme disease was established by the social activist Luché-Thayer, J. and recognized scientists [177], who in March of that year describe the first spectrum of all the clinical manifestations of the disease. Subsequently, in august of the same year, published “The situation of human rights defenders of patients with Lyme disease and Recurrent fever.” For that moment I joined the crew as an expert reviewer. [208]

This fact led us to publish in January 2018 the full spectrum of Lyme disease under the name of “Understanding Lyme Disease, classification and codes” [190]; which we expanded with a second publication where we included aspects that were missing such as the post-treatment Lyme disease syndrome (PTLDS), [191] described in the 90’s, [42], [50], [55], [61], and subsequently reviewed in numerous studies [101], [109], [119], [126], [136], [159], [162], [180], [183]; and immunological aspects related to the HLA antigens (major histocompatibility complex), which shows the relationship of the HLA-DR-4, HLADR-2, and HLA DRB1 alleles, with greater susceptibility to Lyme disease, Lyme arthritis and resistance to treatment with antibiotic therapy [45], [68], [75], [80], [118], [191].

In august of 2018 Bransfield Robert. C. publishes a compilation of practically the entire neuropsychiatric spectrum of Lyme disease, [203] already described by him in other studies [83], [90], [93], [95], [115], [116] , [117], [125], [130], [132], [144], [163], [164], [176], [185], [203]. He concludes that there are three ways in which Borrelia Burgdorferi infects the brain causing neuropsychiatric symptoms:

1.) The meningovascular form associated with cerebral vascular infarcts.

2.) Infection within the central nervous system (CNS) which is the atrophic form of Lyme meningoencephalitis and is associated with cortical atrophy, gliosis and dementia.

3.) Infection outside the central nervous system (CNS) that causes immunological effects within the central nervous system (CNS) and other effects that contributes to neuropsychiatric symptoms [203], among those who stand out:

Developmental disorders, autism spectrum disorders, schizoaffective disorders, bipolar disorder, depression, anxiety disorders (panic disorder, social anxiety disorder, generalized anxiety disorder, posttraumatic stress disorder, intrusive symptoms), eating disorders, decreased libido, sleep disorders, addiction, opioid addiction, cognitive impairment, dementia, seizure disorders, suicide, violence, anhedonia, depersonalization, dissociative episodes, derealization [203]; most of them described previously.

This year of 2018 the World Health Organization recognized in the ICD-11 (International Classification of Diseases year 2,108) the following codes for Lyme disease: [206]

– IC1G.0: Early Lyme cutaneous borreliosis.

– IC1G.1: Disseminated Lyme borreliosis.

– IC1G.10: Lyme neuroborreliosis.

– IC1G.11: Carditis due to Lyme.

– IC1G.12: Ophthalmic Lyme Borreliosis.

– IC1G.13: Lyme arthritis.

– IG1G.14: Late cutaneous Lyme borreliosis.

– IC1G.1Y: Other specified disseminated Lyme Borreliosis.

– IC1G.1Z: Disseminated Lyme borreliosis unspecified.

– IC1G.2: Congenital Lyme Borreliosis.

– IC1G.Y: Other specified Lyme Borreliosis.

– 6D85.Y: Dementia due to Lyme disease.

– 9C20.1: Infectious panuveitis in Lyme disease.

– 9B66.1: Infectious intermediate uveitis in Lyme disease.

– 8A45.0Y: Central nervous system demyelination due to Lyme borreliosis.


– Lyme “neuroborreliosis” was not born in the 80s when it began to be mentioned in scientific studies after its causative agent, the Borrelia Burgdorferi was discovered by Willy Burgoderfer in 1981 and its presence in the human brain was later confirmed. He was born in 1922 when the French Garin and Bujadoux described for the first time the meningoradiculitis lymphocytic with its neurological manifestations.

– We demonstrate chronologically and scientifically that Borrelia Burgdorferi and its species can conquer the human brain and produce dementia, Parkinson’s, Alzheimer’s and Autism.

– Unlike Treponema pallidum, which only in the tertiary stage of syphilis is when it produces dementia (neurosyphilis); Borrelia Burgdorferi (Lyme) in its secondary and tertiary stage produces neuropsychiatric manifestations (neuroborreliosis).

– Lyme disease can present as pure neurological forms, without the presence of Erythema chronicum migrans (ECM); this fact is what in many cases makes the diagnosis difficult.

– Several highly specific diagnostic tests appeared to detect Borrelia Burgdorferi, even surpassing those proposed by the CDC.

– The World Health Organization (WHO) recognized the code “Lyme Neuroborreliosis”, “Dementia due to Lyme” this year of 2018 in the ICD-11 and the “demyelination of the central nervous system due to Lyme borreliosis”

– Clinical diseases not recognized: “Alzheimer due to Lyme”, “Parkinson due to Lyme”, but assuming that “dementia” is a common symptom of Alzheimer’s, its tacit recognition is understood; like the case of Parkinson’s, because the demyelination of the central nervous system and the chronic infection of the brain by Borrelia species can cause symptoms of Parkinsonism. Also the “Autism due to Lyme” was not recognized but like the previously described, it is supposed to be included in the term “neuroborreliosis due to Lyme”

– The post-treatment Lyme disease syndrome (PTLDS), was not recognized by the WHO; it was extensively reviewed in this research and which was described more than 20 years ago, will be the subject of a forthcoming investigation.

– Finally, the Lyme disease, now it is not only a dermatological disease, is a neuropsychiatric illness that can easy destroy your brain, if it is not detected and treated at time.


If we include Alzheimer’s disease, Parkinson’s disease and Autism within the spectrum “Lyme neuroborreliosis” code, only post-treatment Lyme disease syndrome (PTLDS) will be left out in this investigation.


To the scientists who with their consecration to the investigation since this disease were described, have managed to reach the bottom and clarify many questions about this disease.

To organizations that struggle every day for society to understand how dangerous this disease is, the need for early diagnosis and adequate treatment; and how to prevent the tick bite.

To my son, and father, motors of the  real “machine” Dermagic Express of these investigations, which we dedicate to the entire world population.


**Comment from me**

The chronology of how this has played out is important for two reasons – 1) Research has shown for decades how serious this illness(es) is.  Again, prudence would err on the side of caution and further research on ALL of these areas should have been conducted long ago.  If this were Zika (a big money maker) trust me, research would be conducted with abandon.  2) The paper trail with tangible proof only supports the belief that there are reasons WHY all of this continues to be ignored allowing thousands and thousands to suffer alone.  

My only other comment is that we still don’t know many things and would be amiss in putting it all in a nice box with a bow on it.

For instance, while there are 3 stages of Lyme, people can hop around within these stages in no certain order.  One little girl within 4-6 hours of tick bite couldn’t walk or talk:  It didn’t take her days, weeks, or months to have this cross into the central nervous system.  We need studies showing if tick bite LOCATION has anything to do with this.  She was bitten above her eye.  Since that’s in close proximity to her brain, it would make logical sense for her to potentially have neurological symptoms quickly but no research to date spells this out.  YET WE NEED TO KNOW.

My own personal story is that of gynecological symptoms first which then radiated out everywhere:

Many claim to be infected in untero, yet the authorities deny, deny, deny this, despite much evidence:



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156.) La Nacion 1 de julio de 2015  • 17:29. Otros famosos que padecieron la rara enfermedad de Avril Lavigne. Source:

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