Archive for the ‘Parasites’ Category

Herpes Viruses Implicated in Alzheimer’s Disease

https://www.the-scientist.com/news-opinion/herpes-viruses-implicated-in-alzheimer-s-disease-64246#.W1VYqg-Tels.linkedin

Herpes Viruses Implicated in Alzheimer’s Disease

SAM GANDY, ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI

Herpes Viruses Implicated in Alzheimer’s Disease

A new study shows that the brains of Alzheimer’s disease patients have a greater viral load, while another study in mice shows infection leads to amyloid-β build up.

Jun 21, 2018, Anna Azvolinsky

 

The brains of Alzheimer’s disease patients have an abnormal build up of amyloid-β proteins and tau tangles, which, according to many researchers, drives the ultimately fatal cognitive disease. This theory is being challenged by a newer one, which posits that microbes may trigger Alzheimer’s pathology.

Two new studies, using different approaches, further bolster this pathogen theory. Analyzing the transcriptomes of post-mortem brain samples from patients with Alzheimer’s disease, one group of researchers finds that two strains of human herpesvirus are significantly more abundant than in the brains of people of the same age without Alzheimer’s disease. Gene networks in the brains of Alzheimer’s patients with these strains are also rewired such that disease-related genes are differentially expressed compared to controls.

In the other study, another team of investigators observed in mouse models and in a three-dimensional human neuronal cell culture that a Herpseviridae infection could seed amyloid-β plaques. 

“These two papers add to a weight of evidence that viruses—and pathogens in general—must now be seriously considered as causal agents in Alzheimer’s disease,” Chris Carter, who studies the genetics and epidemiology of Alzheimer’s and other neurological disorders at Polygenic Pathways in the U.K., tells The Scientist.

Over three decades, there have been accumulating data from human studies suggesting that certain microbes, namely, viruses bacteria and fungi, may trigger or promote Alzheimer’s pathology in the aging brain. 

See “Do Microbes Trigger Alzheimer’s Disease?”

The Mount Sinai group initially set out to mine their RNA and DNA sequencing data from Alzheimer’s brain samples for drug targets. Then they found these viral sequences that were difficult to ignore. “I recently gave a talk that I titled, ‘I went looking for drugs but all I found was these viruses,’” study coauthor Joel Dudley, a genomics researcher at the Icahn School of Medicine at Mount Sinai, tells The Scientist.

In their study of elderly human brains, Dudley and the team from Mount Sinai sequenced more than 1,400 post-mortem brain samples, finding the first evidence that human herpesviruses 6A (HHV-6A) and 7 (HHV-7) are in greater abundance in regions of the brain including the superior temporal gyrus, anterior prefrontal cortex, and dorsolateral prefrontal cortex.

These data suggest that multiple pathogens, and not just these viruses, likely contribute to Alzheimer’s disease. 

—Chris Carter, Polygenic Pathways

Using RNA and DNA sequencing data, the team computationally generated regulatory network models that implicated the presence these viruses in altering the activity of genes linked to Alzheimer’s risk.

The researchers turned to one of the microRNAs, miR-155, found in their analysis to be suppressed by HHV-6A in the human samples, to see what the functional consequence is of this interaction. They homed in on miR-155 because it was a novel microRNA and because it had been previously linked to herpes viruses. When they knocked out the gene for miR-155 in a mouse model of Alzheimer’s disease, the animals’ brains had larger amyloid plaques and higher levels of amyloid-β compared to the mouse model with a wildtype MIR155 gene.

“Conceivably, the viral proteins are acting as transcription factors that control expression of Alzheimer’s risk genes,” coauthor Sam Gandy, a professor of neurology who specializes in Alzheimer’s disease at Mount Sinai, writes in an email to The Scientist. “Perhaps this viral dysregulation of Alzheimer’s genes that we see promotes the Alzheimer’s pathology of amyloid beta aggregation, inflammation and tau tangles,” he says.

The results, published today (June 21) in Neuron, could pave the way to new intervention strategies. “If established that these viruses indeed play a role in the development of Alzheimer’s, retroviral agents should be tested as a potential therapy,” says Dudley.

In the other study, available as a preprint on the Cell website and in Neuron July 11, Rudolph Tanzi and Robert Moir, both researchers at Harvard Medical School and Massachusetts General Hospital, and their colleagues tested how amyloid-β in the brain—which these labs previously found to be an antimicrobial—reacts to herpes simplex virus 1 (HSV1), HHV6A, and HHV6B. These strains all tend to integrate into the genomes of neurons. They found that in a culture of human neuronal cells, amyloid-β could prevent HSV1 infection and can bind and aggregate the HSV1 and HHV6 viruses. Mice infected with HSV1—which can cause encephalitis—that also had genetically elevated amyloid-β expression were protected against encephalitis, but also had increased amyloid deposits.

“These studies further add to the steadily increasing number of papers that support a microbial role in Alzheimer’s disease,” Ruth Itzhaki, a molecular neurobiologist at the University of Manchester in the U.K. who studies the link between viruses and the development of Alzheimer’s disease, writes in an email to The Scientist.

A recent epidemiology study adds real-world credence to the microbial link to Alzheimer’s. A population study in Taiwan examined more than 33,000 individuals and found that those with a herpes simplex virus infection had a 2.5-fold greater risk of developing Alzheimer’s disease. The study authors found that in those people treated with antiherpes medications, the 2.5-fold risk dropped back down to baseline. 

“The conclusion you can draw is that the antiherpes medication reduced the risk of Alzheimer’s by keeping the herpes infection in check,” says Moir.

Itzhaki agrees. This study and two others, also from Taiwan, appear to link HSV1 causally to Alzheimer’s disease, she writes. “Despite various shortcomings, these Taiwan studies are the essential first steps to a proof that a microbe could be the cause of a non-infectious disease, in this case, Alzheimer’s.” Itzhaki and a colleague wrote about these studies recently in a commentary, which aimed to interpret the “important and surprising Taiwan data” on the effectiveness of the antiviral treatment, Itzhaki tells The Scientist.

Carter cautions that the new reports should not be interpreted to mean that there is likely a single, unique Alzheimer’s pathogen, if there is one at all. “These data suggest that multiple pathogens, and not just these viruses, likely contribute to Alzheimer’s disease. It is also likely that the pathogens may vary between Alzheimer’s patients.”

The Mount Sinai team will now be verifying whether HHV6 and HHV7 are actually integrated into the genomes of Alzheimer’s patients’ brains and testing for the presence of HHV6 and HHV7 in the bloodstream and central nervous system of Alzheimer’s patients. They would like to do a study comparing living patients and controls to see if the link they observed between the viruses’ presence and changes in gene regulation related to Alzheimer’s holds up.

Tanzi’s and Moir’s labs are focusing on the role of the brain microbiome in Alzheimer’s disease. Comparing the brains of older and younger individuals, including those with Alzheimer’s, their preliminary evidence shows that the brain microbiome—which contains hundreds of bacterial and fungal species—is shifted and linked to pro-inflammatory activity. “It’s analogous to what happens with the gut microbiome in individuals with irritable bowel syndrome,” says Moir. “Our model right now is that it’s not just a single microbe, but a disturbance in the brain microbiome that can lead to Alzheimer’s disease.”

B. Readhead et al., “Multi-scale analysis of independent Alzheimer’s cohorts finds disruption of molecular, genetic, and clinical networks by human herpesvirus,” Neuron, doi.org/10.1016/j.neuron.2018.05.023, 2018.

W.A. Eimer et al. “Alzheimer’s disease-associated β-amyloid is rapidly seeded by herpesviridae to protect against brain infection,” Neuron, in press, July 12, 2018.

Correction (June 21): We removed two sentences in paragraph seven. One noted the prevalence of virus in diseased brains, but did not note that the prevalence is the same in control brains. The other sentence misstated the regions of the brain where the viruses were in greater abundance compared to control brains and stated these brain regions were linked to Alzheimer’s disease. The Scientist regrets the error.

________________

**Comment**

  1.  Lyme/MSIDS patients often have viral involvement – particularly herpes strains
  2. The role of bacteria, viruses, and fungus is important and likely includes the very things Lyme/MSIDS patients have and are being treated for.
  3. This article points out another reason to take treatment for Lyme/MSIDS seriously.  If left unchecked, Lyme/MSIDS can possibly be a perfect storm for Alzheimer’s later.

For more:  https://madisonarealymesupportgroup.com/2017/01/18/a-bug-for-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/09/alzheimers-byproduct-of-infection/

https://madisonarealymesupportgroup.com/2016/11/17/antibiotics-and-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/03/borrelia-hiding-in-worms-causing-chronic-brain-diseases/

https://madisonarealymesupportgroup.com/2018/03/25/a-brief-history-of-neuroborreliosis-research-dementia-an-inside-look-at-two-researchers/

https://madisonarealymesupportgroup.com/2017/06/10/the-coming-pandemic-of-lyme-dementia/

https://madisonarealymesupportgroup.com/2016/11/17/alzheimers-lyme/

Dr. David Baewer discusses arboviruses & Lyme:  https://madisonarealymesupportgroup.com/2016/06/07/dr-david-baewer-coppe-labs/ Coppe Labs, in Wisconsin, provides advanced testing for leukotropic herpesviruses: EBV, CMV, HHV-6A and HHV-6B, as well as tick-borne pathogens, and their tests distinguish between latent and active infections.

 

 

Category:

Alzheimer's, Inflammation, Lyme, Parasites, Psychological Aspects, research, Treatment, Viruses

Tickborne Diseases – Confronting a Growing Threat

https://www.nejm.org/doi/full/10.1056/NEJMp1807870

Tickborne Diseases — Confronting a Growing Threat

Catharine I. Paules, M.D., Hilary D. Marston, M.D., M.P.H., Marshall E. Bloom, M.D., and Anthony S. Fauci, M.D.

July 25, 2018, at NEJM.org.

Every spring, public health officials prepare for an upsurge in vectorborne diseases. As mosquito-borne illnesses have notoriously surged in the Americas, the U.S. incidence of tickborne infections has risen insidiously, triggering heightened attention from clinicians and researchers.

nejmp1807870_f1

Common Ticks Associated with Lyme Disease in North America.

According to the Centers for Disease Control and Prevention (CDC), the number of reported cases of tickborne disease has more than doubled over the past 13 years.1 Bacteria cause most tickborne diseases in the United States, and Lyme disease accounts for 82% of reported cases, although other bacteria (including Ehrlichia chaffeensis, Anaplasma phagocytophilum, and Rickettsia rickettsii) and parasites (such as Babesia microti) also cause substantial morbidity and mortality. In 1982, Willy Burgdorfer, a microbiologist at the Rocky Mountain Laboratories of the National Institute of Allergy and Infectious Diseases, identified the causative organism of Lyme disease, a spirochete eponymously named Borrelia burgdorferi. B. burgdorferi (which causes disease in North America and Europe) and B. afzelii and B. garinii (found in Europe and Asia) are the most common agents of Lyme disease. The recently identified B. mayonii has been described as a cause of Lyme disease in the upper midwestern United States. Spirochetes that cause Lyme disease are carried by hard-bodied ticks (see graphic), notably Ixodes scapularis in the northeastern United States, I. pacificus in western states, I. ricinus in Europe, and I. persulcatus in eastern Europe and Asia. B. miyamotoi, a borrelia spirochete found in Europe, North America, and Asia, more closely related to the agents of tickborne relapsing fever, is also transmitted by I. scapularis and should be considered in the differential diagnosis of febrile illness occurring after a tick bite.

Patterns of spirochete enzootic transmission are geographically influenced and involve both small-mammal reservoir hosts, such as white-footed mice, and larger animals, such as white-tailed deer, which are critical for adult tick feeding. The rising incidence and expanding distribution of Lyme disease in the United States are probably multifactorial, but increased density and range of the tick vectors play a key role. The geographic range of I. scapularis is apparently increasing: by 2015, it had been detected in nearly 50% more U.S counties than in 1996.

Lyme disease’s clinical manifestations range from relatively mild, nonspecific findings and classic erythema migrans rash in early disease to more severe manifestations, including neurologic disease and carditis (often with heart block) in early disseminated disease, and arthritis, which may occur many months after infection (late disease). Although most cases are successfully treated with antibiotics, 10 to 20% of patients report lingering symptoms after receiving appropriate therapy.2 Despite more than four decades of research, gaps remain in our understanding of Lyme disease pathogenesis, particularly its role in these less well-defined, post-treatment symptoms.

Meanwhile, tickborne viral infections are also on the rise and could cause serious illness and death.1 One example is Powassan virus (POWV), the only known North American tickborne encephalitis-causing flavivirus.3 POWV was recognized as a human pathogen in 1958 after being isolated from the brain of a child who died of encephalitis in Powassan, Ontario. People infected with POWV often have a febrile illness that can be followed by progressive and severe neurologic manifestations, resulting in death in 10 to 15% of cases and long-term sequelae in 50 to 70% of survivors.3 An antigenically similar virus, POWV lineage II, or deer tick virus, was discovered in New England in 1997. Both POWV subtypes are linked to human disease, but their distinct enzootic cycles may affect their likelihood of causing such disease. Lineage II seems to be maintained in an enzootic cycle between I. scapularis and white-footed mice — which may portend increased human transmission, because I. scapularis is the primary vector of other serious pathogens, including B. burgdorferi. Whereas only 20 U.S. cases of POWV infection were reported before 2006,3 99 were reported between 2006 and 2016. Other tickborne encephalitis flaviviruses cause thousands of cases of neuroinvasive illness in Europe and Asia each year, despite the availability of effective vaccines in those regions. The increase in POWV cases coupled with the apparent expansion of the I. scapularis range highlight the need for increased attention to this emerging virus.

The public health burden of tickborne pathogens is considerably underestimated. For example, the CDC reports approximately 30,000 cases of Lyme disease per year but estimates that the true incidence is 10 times that number.1 Multiple factors contribute to this discrepancy, including limitations in surveillance and reporting systems and constraints imposed by available diagnostics, which rely heavily on serologic assays.4 Diagnostic utility is affected by variability among laboratories, timing of specimen collection, suboptimal sensitivity during early infection, imperfect use of diagnostics (particularly in persons with low probability of disease), inability of a single test to identify coinfections in patients with acute infection, and the cumbersome nature of some assays. Current diagnostics also have difficulty distinguishing acute from past infection — a serious challenge in diseases characterized by nonspecific clinical findings. Moreover, tests may remain positive even after resolution of infection, leading to diagnostic uncertainty during subsequent unrelated illnesses. For less common tickborne pathogens such as POWV, serologic testing can be performed only in specialized laboratories, and currently available tests fail to identify novel tickborne organisms.
Such limitations have led researchers to explore new technologies. For example, one of the multiplex serologic platforms that have been developed can detect antibodies to more than 170,000 distinct epitopes, allowing researchers to distinguish eight tickborne pathogens.4 In addition to its utility in screening simultaneously for multiple pathogens, this assay offers enhanced pathogen detection, particularly in specimens collected during early disease. Further studies are needed to determine such assays’ applicability in clinical practice.

Nonserologic platform technologies may also improve diagnostic capabilities, particularly in identifying emerging pathogens. Two previously unknown tickborne RNA viruses, Heartland virus and Bourbon virus, were discovered by researchers using next-generation sequencing to help link organisms with sets of unexplained clinical symptoms. The development and widespread implementation of next-generation diagnostics will be critical to understanding the driving factors behind epidemiologic trends and the full clinical scope of tickborne disease. In addition, sensitive, specific and, where possible, point-of-care assays will facilitate appropriate clinical care for infected persons, guide long-term preventive efforts, and aid in testing of new therapeutics and vaccines.

In the United States, prevention and management of tickborne diseases include measures to reduce tick exposure, such as avoiding or controlling the vector itself, plus prompt, evidence-based treatment of infections. Although effective therapies are available for common tickborne bacteria and parasites, there are none for tickborne viruses such as POWV.

The biggest gap, however, is in vaccines: there are no licensed vaccines for humans targeting any U.S. tickborne pathogen. One vaccine that was previously marketed to prevent Lyme disease, LYMErix, generated an immune response against the OspA lipoprotein of B. burgdorferi, and antibodies consumed by the tick during a blood meal targeted the spirochete in the vector.5 Nonetheless, the manufacturer withdrew LYMErix from the market for a combination of reasons, including falling sales, liability concerns, and reports suggesting it might be linked to autoimmune arthritis, although studies supported the vaccine’s safety. Similar concerns will probably affect development of other Lyme disease vaccines.5

Historically, infectious-disease vaccines have targeted specific pathogens, but another strategy would be to target the vector.5 This approach could reduce transmission of multiple pathogens simultaneously by exploiting a common variable, such as vector salivary components. Phase 1 clinical trials are under way to evaluate mosquito salivary-protein–based vaccines in healthy volunteers living in areas where most mosquito-borne diseases are not endemic. Since tick saliva also contains proteins conserved among various tick species, this approach is being explored for multiple tickborne diseases.5

The burden of tickborne diseases seems likely to continue to grow substantially. Prevention and management are hampered by suboptimal diagnostics, lack of treatment options for emerging viruses, and a paucity of vaccines. If public health and biomedical research professionals accelerate their efforts to address this threat, we may be able to fill these gaps. Meanwhile, clinicians should advise patients to use insect repellent and wear long pants when walking in the woods or tending their gardens — and check themselves for ticks when they are done.
________________

**Comment**

While this article repeats much of the same verbiage that’s been repeated for years, particularly the vaccine push, they are ignoring the following:

  1. Many TBI’s are congenitally transmitted:  https://madisonarealymesupportgroup.com/2018/06/19/33-years-of-documentation-of-maternal-child-transmission-of-lyme-disease-and-congenital-lyme-borreliosis-a-review/, https://madisonarealymesupportgroup.com/2018/07/24/congenital-transmission-of-lyme-myth-or-reality/, https://madisonarealymesupportgroup.com/2018/02/26/transplacental-transmission-fetal-damage-with-lyme-disease/
  2. There is a real probability of sexual transmission:  https://madisonarealymesupportgroup.com/2018/02/06/lyme-in-the-southern-hemisphere-sexual-transmission/, https://madisonarealymesupportgroup.com/2017/02/24/pcos-lyme-my-story/
  3. While they mention Ehrlichia, Anaplasma, Rickettsia, and Babesia, there are many other players that are hardly getting a byline.  For a list to date:  https://madisonarealymesupportgroup.com/2017/07/01/one-tick-bite-could-put-you-at-risk-for-at-least-6-different-diseases/.  This is an important issue because to date the medical world is looking at this complex illness as a one pathogen one drug illness when nothing could be further from the truth.  No one has done any research on the complexity of being infected with more than one pathogen.  It will reveal the CDC’s guidelines of 21 days of doxy to be utter stupidity.
  4. Also, worth mentioning is that only a few of these are reportable illnesses so there is absolutely no data on how prevalent any of this is.  Surveillance is a real problem.
  5. Regarding what ticks are where….this ancient verbiage needs to change.  Ticks are moving everywhere.  This is on record in numerous places:  https://madisonarealymesupportgroup.com/2018/07/16/ticks-that-carry-lyme-disease-are-spreading-fast/, https://madisonarealymesupportgroup.com/2018/07/10/we-have-no-idea-how-bad-the-us-tick-problem-is/, https://madisonarealymesupportgroup.com/2018/07/22/citizen-scientists-help-track-tick-borne-illness-exposure/
  6. No tick is a good tick.  They all need blood meals and have the potential to transmit disease.  
  7. This article is silent about the Asian Longhorned tick that propagates itself by cloning and can drain cattle of their blood.  Found in six states so far it was recently found on a child in New Jersey:  https://www.northjersey.com/story/news/environment/2018/07/24/bergen-county-nj-child-may-first-carrying-longhorned-tick-us/825744002/.  Word in the tick world is it had NOT bitten the child and tested negative for pathogens.  What is concerning is that it is known to transmit SFTS virus and Japanese spotted fever in Asia. This story is a reminder that this tick is NOT just a livestock problem and that a normal child going about a normal day with NO contact with livestock had this tick on her.  Another clear reminder that it is foolish to put any of this in a box.
  8. They need to emphasize that the “classic erythema migrans rash” while indicative of Lyme, is unseen or variable in many patients.
  9. Constraints in testing is a true problem but an even bigger problem is untrained and uneducated medical professionals.  This stuff may never test clearly.  Get over it.  Get trained to know what to look for!
  10. The Lyme vaccine was a bust.  It still is.  Unless safety concerns are dealt with we want nothing to do with any vaccine.
  11. All I know is that mosquitoes and Zika get more attention that this modern day 21st century plague that is creeping everywhere and is a true pandemic.  It still isn’t being seriously dealt with or researched.  What research is being done is same – o – same -o stuff we already know.  Study the tough stuff – the unanswered questions or things that are just repeated as a mantra for decades.
We need answers out here not repeated gibberish that isn’t helping patients.
Afterthought:

The one thing I didn’t deal with that I will point out now is this regurgitated number in the NEJM article of 10-20% of patients moving on to chronic/persistent Lyme. The following informative article written by Lorraine Johnson points out this number to be considerably higher which corresponds to my experience as a patient advocate: https://madisonarealymesupportgroup.com/2018/07/22/lyme-costs-may-exceed-75-billion-per-year/. Excerpt below:

Besides the staggering financial cost to this 21st century plague, this paper, based on estimates of treatment failure rates associated with early and late Lyme, estimates that 35-50% of those who contract Lyme will develop persistent or chronic disease.

Let that sink in.

And in the Hopkins study found 63% developed late/chronic Lyme symptoms.

For some time I’ve been rankled by the repeated CDC statement that only 10-20% of patents go on to develop chronic symptoms. This mantra in turn is then repeated by everyone else.

While still an estimate, I’d say 35 to over 60% is a tad higher than 10-20%, wouldn’t you? It also better reflects the patient group I deal with on a daily basis. I can tell you this – it’s a far greater number than imagined and is only going to worsen.

 

 

Category:

Anaplasmosis, Babesia, Borrelia Miyamotoi (Relapsing Fever Group), Lyme, Lyme Vaccine, Parasites, Testing, Ticks, Treatment, vaccines, Viruses

Recover From Brain Fog & Lyme Disease Naturally

https://www.linkedin.com/pulse/recover-from-brain-fog-lyme-disease-naturally-gary-blier/

Recover From Brain Fog & Lyme Disease Naturally

Published on June 26, 2018
Gary Blier
Founder, Advanced Cell Training

When most people think of Lyme disease, it conjures up thoughts of rashes, flu-like symptoms, and joint pain. However, there are a significant number of Lyme sufferers who also experience brain fog: agonizing neurological symptoms that leave them feeling drained, irritable, confused, and cognitively lagging.

Brain fog is one of the most common psychiatric manifestations of Lyme Disease. In fact, it’s estimated that 70% of individuals affected by Lyme show signs of cognitive decline or memory loss.

While you may be familiar with brain fog within the Lyme community, you may not be aware of what it is or why it happens. We’ll break it all down for you in this article and provide you with natural solutions you can carry out at home to lift the fog that robs you of a clear mind.

What is Brain Fog?

Brain fog is a term given by those whose brain function is underperforming compared to a normal, healthy brain. It can range from a mild case of “cloudiness” to a more severe case that makes it difficult to perform basic tasks.

Brain fog symptoms include:

Memory loss
Slowed processing
Difficulty thinking or making decisions
Poor concentration
Mood swings
Confusion
Sleep disturbances
Decreased problem-solving abilities
Easily overwhelmed
Low energy or fatigue
Headaches
Depersonalization or dissociation (i.e., loss of emotional connection to others and life)
Other brain fog indicators may include feeling fuzzy-headed, unmotivated, melancholy, or irrational for no apparent reason. It’s also not uncommon for anxiety and depression to accompany brain fog, especially in cases of prolonged illness.

Additionally, brain fog symptoms can wax and wane during periods of high stress, exposure to electromagnetic frequencies and overly stimulating environments, hormonal changes, and during a herxheimer reaction. Symptoms can even intensify with certain moon cycles.

Your Brain on Lyme

Scientists are still trying to understand Lyme disease and how it affects the brain, but several studies have already concluded that Lyme bacteria can impact every aspect of the brain. Medical experts also agree that Lyme and coinfections cause the brain to swell, which can result in neurological or neuropsychiatric symptoms such as brain fog.

One of the most common causes of brain fog are the Lyme pathogens themselves, otherwise referred to as spirochetes. These corkscrew-shaped bacteria deeply embed themselves inside tissues, neurons, and cells. They can cross over the blood-brain barrier and wreak havoc on brain receptors and neural pathways.

When these pathogens die off, they excrete harmful endotoxins and exotoxins that inhibit brain function. If you do not detox properly, these toxins can accumulate and cause brain fog or damage brain tissue. The very presence of such toxins trigger the immune system to go into hyperdrive, releasing more cytokines into the blood, fueling inflammation within the brain and body. Cytokines are small proteins that are instrumental in cell signaling.

To overcome Lyme disease and brain fog, it’s crucial to address all underlying inflammation by making modifications to one’s diet and lifestyle.

Natural Brain Fog Recovery Tips

Get on the road to recovery from Lyme brain fog by taking inventory of the following areas:

Restful Sleep

One of the most significant neurological challenges for people with Lyme is insomnia. More than just a frustrating symptom, disturbed sleep patterns can interfere with healing by damaging the immune system, allowing toxins or pathogens to take root in the body. Insufficient sleep can also raise cytokine chemicals and quinolinic acid in the body that can lead to inflammation and worsen neurological symptoms.

Getting adequate sleep is key to Lyme recovery. Remember, it’s not just about the hours you clock every night, but also the quality of sleep that matters. Your brain and immune system do most of their healing when you are in a deep sleep, so it’s advised to get sleep around 10:00 pm and wake after about 7-8 hours of good sleep.

Need extra help in this department? Ask a medical practitioner about checking your hormones or thyroid levels to see what could be preventing you from getting enough zzz’s.

Anti-Inflammatory Diet

To support your brain health, try an anti-inflammatory diet to give your brain and body the nutrients it needs to heal. Buy organic as often as possible because toxic GMOs and pesticides can cause inflammation and put unnecessary stress on your body.

Eliminate these common offenders from your diet: caffeine, alcohol, refined carbohydrates, gluten, and sugar. All of these are enemies of brain fog and can impair brain function. It’s also best to avoid these substances until after your Lyme recovery.

Click here to read a great article on the top 15 anti-inflammatory foods that can transform your health:  https://draxe.com/anti-inflammatory-foods/

Also, cut out neuro-inflammatory saturated fats and instead up your intake of good or monounsaturated fats. Olive oil, nuts, avocado, and some types of fish have been shown to enhance memory and cognitive function, according to Harvard Medical School.

De-Stress Your Brain

High levels of cortisol, the body’s “stress hormone” have been linked to brain fog. Chronically elevated cortisol can disrupt your symphony of hormones that work intrinsically to keep your body in check. When one hormone falls too low, another one overcompensates to restore harmony.

Routinely check your cortisol levels (preferably via a saliva test) to ensure your levels are in balance. Actively pursue activities that reduce stress and declutter your mind, whether it be meditation, prayer, music, or your favorite hobby. Give yourself permission to unplug from the grid and relax.

Detox, Detox, Detox

Brain fog is often a sign of built-up toxins–Lyme, mold, parasites, or yeast–in the blood and intestines. Consider infrared sauna sessions, or doing light exercise or yoga to stimulate your lymphatic system. Get those toxins moving out of your body!

You may also speak to your healthcare providers about supplements you can take to support your detox pathways. Bentonite clay, activated charcoal, and juice cleanses are generally safe options for cleaning out the sludge.

Another way to help flush toxins out is to stay well-hydrated throughout the day. Multiply your body weight by 67%. The resulting number is the number of ounces of water you should drink daily. For example, a 100-pound person would need 67 ounces of water. Divide that by 8 – the number of ounces in a glass of water – and the result is roughly 8 glasses of water per day. Most of us fall far short of this amount.

Self-Healing for Lyme Disease and Brain Fog

You might also need extra support recovering from Lyme disease and brain fog. Advanced Cell Training (ACT) offers a self-healing program that enables your body’s own awesome ability to kill microorganisms – even in the brain. With ACT, you can train your own immune system to respond appropriately to spirochetes, parasites, and coinfections. This simple training process has helped thousands over the last 20 years overcome health issues. Basically, we point out where your body is going wrong and show it how to self-correct and get things back on track.

For more on ACT:  https://advancedcelltraining.com

 

Category:

Activism, Detoxing, diet and nutrition, Inflammation, Lyme, Parasites, Psychological Aspects, Treatment

Panel Says TBI’s Have Reached Epidemic Levels

https://m.medicalxpress.com/news/2018-04-tick-borne-diseases-epidemic-panel.html

Tick-borne diseases reach epidemic levels, panel says

April 16, 2018
by Delthia Ricks, Newsday
Lyme disease
Adult deer tick, Ixodes scapularis. Credit: Scott Bauer/public domain

Tick-borne infections have reached epidemic proportions on Long Island, where children are disproportionately affected by Lyme disease and other infections transmitted by the eight-legged creatures, a panel of top scientists announced recently.

“Lyme disease is mostly a disease of children and curiously mostly a disease of boys,” Jorge Benach said at a recent symposium at Stony Brook University School of Medicine. Benach, who discovered the bacterium that causes Lyme disease, is a molecular geneticist at Stony Brook University School of Medicine.

His observation that Lyme disease is mostly an  of children was corroborated by Dr. Christy Beneri, a pediatrician at Stony Brook Children’s Hospital. She said her institution encountered a wide range of tick-borne illnesses annually and that boys tended to outnumber girls in the number of infections. The most likely reason for the disparity, Beneri said, is the tendency among boys to play outdoors in wooded areas where ticks thrive.

In the extensive pediatric research Beneri presented at the symposium was evidence of some children developing Bell’s palsy, a temporary facial paralysis that occurs when the Lyme bacterium affects a cranial nerve. The paralysis resolves with antibiotic treatment, Beneri said.

Beyond the Lyme bacterium, ticks on Long Island have been found to harbor babesia and anaplasma.

Babesia are protozoa, or parasitic, infectious agents that hone in on red blood cells, similar to the way a malaria parasite invades the same cells.

Anaplasmosis is an infection caused by the bacterium Anaplasma phagocytophilum. It can trigger aches, fever, chills and confusion.

Beneri and Benach were among five leading Stony Brook experts, including university president Dr. Samuel Stanley, who addressed what they described as a mounting epidemic of infections caused by the ever-expanding range of ticks. Stanley, who was the first speaker, is a specialist in infectious diseases.

“New York bears a disproportionate impact from tick-borne diseases,” Stanley said at the symposium, which was held in a lecture hall in the university’s health sciences building. “This is a regional and state problem.”

New York has the highest number of confirmed Lyme  cases nationwide, according to the U.S. Centers for Disease Control and Prevention, which has cataloged more than 95,000 Lyme infections in the state since 1986. Suffolk County has long been ground zero for the ailment on Long Island, studies consistently have shown.

“Cases in Suffolk County hover between 500 and 700 and this is just for the reported cases,” Benach said, noting that Suffolk has among the highest rates of many tick-transmitted infections because of the dense infiltration of the insects in county.

Typical Lyme symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans, said Dr. Luis Marcos, a specialist in internal medicine and infectious diseases.

Marcos presented data showing the wide range of illnesses caused by ticks throughout the region, including Borrelia miyamotoi, a corkscrew-shaped bacterium identified in recent years as the cause of a relapsing fever.

Dr. Eric Spitzer, a pathologist, discussed the many laboratory tests that Stony Brook used to arrive at a diagnosis of a tick-transmitted illness. He said that for years, doctors nationwide sent specimens to the university for analysis because of its well-known precision. Testing of those specimens earned the university $32 million over a 20-year period, he said.

Panelists identified the most prevalent ticks on Long Island as the American dog tick; the invasive lone star tick, which migrated from Southern states; and the blacklegged tick, known as deer tick.

_______________

For more:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/

https://madisonarealymesupportgroup.com/2016/03/08/anaplasmosis/

http://danielcameronmd.com/best-antibiotics-treat-borrelia-miyamotoi/ The study authors demonstrated that B. miyamotoi is susceptible to doxycycline, azithromycin, and ceftriaxone but resistant to amoxicillin in vitro. The next step would be to show whether these drugs work in patients.

 

]

 

Category:

Activism, Anaplasmosis, Babesia, Borrelia Miyamotoi (Relapsing Fever Group), Lyme, Parasites, Ticks

A Brief History of Neuroborreliosis Research & Dementia – An Inside Look at Two Researchers

https://www.facebook.com/thomas.grier1/posts/10214592863122717?notif_id=1521692245045022&notif_t=notify_me&ref=notif

A Brief History of Neuroborreliosis Research & Dementia – an Inside Look at Two Researchers

Part 1
by
Thomas Grier

Two Ends of the Same Spirochete
How Dr. Judith Mikklossy and Dr. Alan MacDonald approached the role that Borrelia play in Alzheimer’s Dementia from two different perspectives. Dr. Mikklossy looked at the initial disease formation and the effects of Borrelia on Brain-Cell-Cultures, Dr. Alan MacDonald looked at the end process of this infection by observing borrelia in Brain autopsies from Alzheimer’s patients.

I first started becoming seriously ill in 1989 and by the Spring of 1991 I was diagnosed with Multiple Sclerosis. After months of despair at the lack of concern by my physicians, I finally collapsed in the street. I was unable to walk, drive, read a book, or control my body contortions.

I was sent to the neurology ward of the closest hospital St. Luke’s. This hospital employed different neurologists than the clinic where I had been doctoring for two years. I had poorly controlled atrial fibrillation, an enlarged heart, severe pressure in my head, and a visual field where my eyesight was reduced to a fuzzy disk with completely distorted peripheral vision. I was racked with pain, fevers, sweats, and was having both auditory and visual hallucinations.

The doctors were at a loss. What had been considered as Multiple Sclerosis was now an unknown mystery disease.

After a week waiting for answers to various tests, I was put on a waiting list for a nursing home. My doctors gave me nothing but dire news of my prognosis. My personal family doctor and the neurologist I had been seeing were on vacation all week. (This turned out to be a blessing.)

I entered the hospital on a Friday and by Monday I had not seen any take charge doctor. After three days of being bed ridden and given supportive care by well-meaning nurses, the on-duty neurologist that saw me, visited me Monday morning and looked bone tired. This was the first time Dr. Barbara Martyn had ever seen me. (I had been diagnosed at the clinic across town with “MS” for over a year and had seen dozens of doctors and a half dozen specialties at a cost of over $100,00)

This doctor had seen me all of 10 minutes and suggested to me that I did not have MS but rather that I had Lyme disease. She ordered that a 20 day course of intravenous Rocephin be started immediately. But she also continued with the MS tests that had been ordered over the weekend.

I was told there was a long wait to get a brain MRI. Out hospital patients had a four month wait and in-hospital patients had to wait 10 days. Within a few hours of seeing this doctor I had both a CAT-Scan and an MRI.

Dr. Martyn MD (Now deceased from breast cancer) had over the weekend been attending the International Lyme Disease Conference in Arlington Virginia, and only had 4 hours sleep because her flight was delayed. Yet because of that conference she was able to look at my chart and in five minutes decided that Lyme disease was now the most likely cause of my multitude of multi-systemic maladies.

But all of this is a story for another time.

My misdiagnosis with Multiple Sclerosis galvanized my commitment to learn more about the spirochetal disease that was literally swimming inside my brain. As a graduate student 10 years earlier I had worked at the next door specialty hospital and worked with a Tertiary Sphillis patient that had failed three attempts of ever increasing doses of IM Penicillin. So having spirochetes in my brain was not a comforting thought.

Through my association with a Nurse Educator (Barbara Jones RN, MS) it became clear to me in 1991 that other MS patients just like me also had been misdiagnosed and actually had Lyme disease. I felt that what I was experiencing, felt like an infection of my brain, but it also manifested much like dementia.

I could not think clearly. When I spoke I now substituted easy words for hard words, reading black text on white paper gave me seizures, I got lost easily, I was both seeing and hearing things that weren’t real. Emotionally it was like I had a lobotomy that had cut all the feeling out of my brain. I had intellect, but no emotions. Other than uncontrollable urges to cry, I felt as though I had no emotional contact to the world.

That first day of antibiotic therapy, the IV Rocephin caused every muscle in my body to twitch and my body to spasm. The pressure in my head doubled, my entire body perspired and I spiked high fevers. It was this first few hours of agony that I became committed to better understand Lyme disease, and its affects on the human brain. At this time I did not know that my decades of running in the woods and meadows had exposed me to many tick-borne diseases.

As part of my journey I attended every medical conference that I could get to, and by 1997 I had attended well over a dozen conferences, and I tried my best to make sense out of what the CDC and Yale Medical were reporting: It didn’t make any sense?

I kept asking myself “Where are the pathology studies? Why aren’t they looking in the brain.”

I didn’t know then that human pathology studies would never be done with any American tax-payer dollars, and that the CDC and NIH would shoot down all requests for brain-autopsies done in America that would look for spirochetes in the brain.

My first encounter with the CDC hiding information:

I had been a graduate student at the U of MN School of Medicine for two years, and after I was able to walk again. (I didn’t drive much for the next five years) I visited my old mentor at the Medical School to talk to him about this misunderstood disease. Dr. Eugene Cotton was the head of the medical school, and he immediately became enthralled with what I was saying.

I was a Lyme patient who could speak to him in medical terms of what I was going through and explain the odd contradictions that I was encountering with medical experts. Gene immediately spoke up. His friend was the head of the CDC and he had just seen a study by Dr. Judith Miklossy that showed the presence of Borrelia burgdorferi in the brains of 13 consecutive Alzheimer’s patients in Switzerland.

He was so concerned with these findings that he ordered a brain-autopsy study to be done with American dollars, but that the work be done in secret in Canada and no results to be published or reported without going through the CDC.

No results were ever released.

So I called the graduate assistant to the doctor and was met with nothing but hostility and his repeating that all results were proprietary and were never meant to be pubished.

WHAT? We paid for this study! What good is a public health study if the results aren’t shared with the medical community?

Miklossy J, Kasas S, Janzer RC, Ardizzoni F, Van der Loos H. Further ultrastructural evidence that spirochaetes may play a role in the aetiology of Alzheimer’s disease. 1994 Neuroreport. 2;5(10):1201-4.

How research on Lyme is hindered by poor science: It astounded me that all research conducted on animals used only strain B-31 a laboratory strain of Borrelia not found in ticks. More disturbing was that every far-reaching conclusion about diagnosis, and treatment success was based entirely on antibody serology tests created using lab strain B-13.

Over and over repeatedly these antibody tests had been proven unreliable and several published studies pointed out how nebulous these tests were and how flipping a coin was just as accurate. All conclusions about neuroborreliosis were based almost entirely on unreliable antibody-serology tests! Diagnosis was made by serology, and cure was determined by a drop in antibodies. No one at the CDC or major medical institutions seemed to have interest in cracking a few heads open and looking for spirochetes with better tools.

[See photo of testing failures]

The few incidents of culture positives in patient’s after receiving antibiotic treatment, were being purposely ignored and never acknowledged or referenced in papers by the CDC. By 1995 it was clear to me that when it came to the pathology of neuroborreliosis, the Lyme-patient community was completely on their own.

JUST LIKE MEDICAL ADVANCES IN THE 19TH CENTURY, INDIVIDUALS WERE NOW TAKING IT UPON THEMSELVES TO DO THE RESEARCH THAT THE PAID EXPERTS REFUSE TO DO.

In 1994 I had administrated an antibiotic treatment study in Pine County Minnesota for MS patients. I enrolled 26 MS patients diagnosed by both MRI and spinal fluid findings. We only enrolled seronegative patients using either the IGenix Lyme ELISA test or Marshfield Clinic Lyme serology tests. I insisted that only seronegative patients be enrolled and treated. I chose negative patients with clinical symptoms, because these were the patients that were slipping through the cracks in the medical system and not receiving treatment simply because the Lyme antibody tests were inaccurate.

We fell short of our goal of 40+ patients and a big part of that was I felt, the lack of cooperation by the MS Society. Not only could I not speak at their local MS Support Groups to enroll patients, but the MS Support groups would not even distribute our consent forms and brochure. One MS Support Group leader told me that all Lyme disease did was offer false hopes.

Most MS patients were told that Lyme disease had no connection to MS, and in one instance where I spoke to MS patients at the Houghton Michigan MS support group, the MS society flew out a representative one week later for a special meeting with the group, and she spoke very harshly to the support group who had allowed me to speak. Eight members of that group were so outraged that the very next month they splintered off from the MS support network, and formed the first Houghton-Hancock LDSG. After I spoke I arranged for a LLMD near Green Bay WI to treat any and all of the MS patients who could not get treated in Michigan. In all, eight of the MS patients had dramatically improved on antibiotics.

One of those patients enrolled in our LEAMS study (Lyme Endemic Area MS Study) and went from crutches to walking and made cognitive improvements to the point of renegotiating his divorce settlement and getting total custody of his kids. He even appeared on a local talk show and encouraged other MS patients to get treated with antibiotics. The backlash by the Upper Peninsula Health Department was swift and completely unyielding in their opinion that treating Lyme disease long-term or treating MS with antibiotics was a waste of time and dangerous.

Of the 26 MS patients in our antibiotic trial, only three seroconverted and had positive serologic evidence of having Lyme disease. But a total of 8 of the 26 patients overall responded favorably to three months of antibiotics. Unfortunately, 17 of 26 did not respond at all.

After a one year follow-up, we discovered that one patient in our treatment failure group had stayed on amoxicillin for 15 months and made a nearly total recovery.

What I concluded from our MS antibiotic treatment study was this:

  • # of Patients Conclusion Length of Rx w/Amox/doxy/Biaxin
  • 3 Had Lyme disease and made partial recoveries 3 months
  • 5 5 patients had improvement but were not seropositive 3 months
  • 17 Had no response to antibiotics either doxy/amox/or Biaxin 3-months Rx
  • 1 One MS patient had 15 months of amoxicillin and made a near full recovery

I found the results disappointing and had hoped for better. My thoughts on our results are: Not all MS is caused by the Lyme bacteria, and that our treatment length was far too short. It would be years later in 2004 when Alan MacDonald would discover an association in MS with nematode parasites and that these parasites were often associated with Borrelia and found in the human brain in many dementia cases.

It may well be that as many as half the cases of MS and dementia are caused by mixed infections. Also we knew nothing of other Borrelia species like Borrelia myamotoi that also enters the brain, and is seronegative on lyme tests.

I was very frustrated. Our study was ignored by the Minnesota health department and they would not even consider a study of their own. When I presented my proposal to State Representative Mary Murphy, Dr. Michael Osterholm PhD the state epidemiologist crashed the meeting insisting that he talk with her alone. (She got very angry.) Osterholm said it was ridiculous to even report MS in surveillance reports because it wasn’t an infectious disease.

He also repeatedly said that hunters cannot get Lyme disease in the Fall because the female ticks won’t feed on humans in those months??? He made these comments because I had helped pass a bill to distribute Lyme information to hunters. Of course he lied.His own paper that he gave Representative Murphy stated that Lyme disease can be contracted in any month of the year and cases had been reported in all months in Minnesota.

It was clear that the State Health department wasn’t going to be any help in a human pathology Lyme Study. It was now 1995 and I had run out of medical sources to get for better answers and better studies? But this was the year that I met Dr. Alan MacDonald.

I first met Dr. Alan MacDonald (pathologist) at an LDF conference. Between talks he was carrying a small boy on his shoulders and he joyfully talked about creating a CD-ROM of various forms of spirochetes and pontificated about the role of variant forms. Almost simultaneously we remarked on the extraordinary work by Dr. Gabriel Steiner in Germany and his findings of “crescent-like” forms in the brains of MS patients.

As luck would have it Dr. Vincent Marshall the expert on Gabriel Steiner was at this conference and his insights on spirochetes in the human brain in MS patients were invaluable to me.

No one else in America had been looking back 75 years in the European Literature for a spirochete connection to MS. While it is easy to dismiss any one published study on MS and spirochetes, it is complete denial to dismiss over 30 pre-WWII published studies by a dozen different researchers in four different countries.

I knew when I met Alan and Vincent that I had found researchers who had the same mindset and goals as me.

In late 1996 we discussed doing brain autopsies on actual patients. It was a patient in our LDSG that led us to our our first candidate. This patient was from a very endemic area of Wisconsin, and he too was all about finding answers through better science.

Jim’s father was a lifelong farmer, hunter and outdoorsman. Unfortunately this vibrant active man was now wasting away in a nursing home, he had dementia later confirmed by autopsy and the presence of amyloid plaques as Alzheimer’s disease. In addition to dementia this patient also had about a dozen symptoms of Lyme disease. More importantly he had two sons with Lyme disease that had been misdiagnosed with rheumatoid arthritis and MS who both recovered on long-term antibiotics (two years). The brothers both recovered on antibiotics and were now asking if their dying father could also have Lyme disease? And more to the point: did Lyme disease cause his dementia?

Jim Forris from Ashland WI battled with his family to do this autopsy. Like most families they just wanted this dark chapter in their lives to be closed and doing an autopsy was a lot of work, it was expensive, the process seemed morbid, and what guarantee was there that he would have spirochetes in his failing brain?

But Jim had the power of attorney over his father’s affairs, and without any more consultation he had his father’s brain harvested at death, and then shipped it to New York to Dr. Alan MacDonald.

The results were beyond our expectations. Jim’s father had Borrelia burgdorferi in every cross section of his brain. More importantly in 1997 Dr. MacDonald was the first to capture Borrelia intracellular inside neurons and had serial sections showing the spirochete could transit brain cells with apparent ease. Spirochetes were found attached to glial cells and many were seen in extracellular spaces.

Unfortunately at this time it was not even a consideration to stain for amyloid and Borrelia on the same slide. Alan would do this a decade later with spectacular results!

In medicine this should have been a huge deal.A major discovery. But inexplicably it was completely ignored. We even kept the stored unstained paraffin blocks available to the patient’s doctors and others to see for them selves. No one was willing to test the tissues for themselves.

When Jim approached his father’s doctors with the offer to share the formalin fixed brain with them for their own research, their response to Jim Forris’s sincere and generous offer was to get a restraining order. A restraining order! This was no longer just denial or ignorance, this was now obfuscation and obstruction of medical science. In medicine not only can ignorance be bliss, but it can also be used as plausible deniability.

Once it was determined that this dementia patient actually had Lyme disease and they had repeatedly denied even testing for Lyme: The response was that the clinic in Duluth MN wanted nothing more to do with this case or the family of the patient. All discussions were squashed!

These images below should have been regarded as a medical breakthrough just as important as finding the cause of Legionaire’s disease or the true cause of ulcers by H. pylori. Instead like all great finds in Lyme disease research, it was either ignored or met with disdain.

Intracellular Borrelia inside brain neurons and glial cells explained a lot about what we had been seeing in patients.

• Neuro Lyme patients often had severe neurologic symptoms
• Few bacteria were ever seen in the blood
• Blood tests were often negative due to low infection load in blood
• Patients often relapsed after recommended lengths of antibiotics
• Treatments required higher dose of antibiotics, that are dosed longer and often in combinations to reach therapeutic/bactericidal levels in the brain

We were excited at this finding, but had no idea of how much more convoluted the pathology would become. It became clear we had to better understand the interactions of Borrelia with brain cells.

We were elated when in 2006 the CDC funded study by doctors Jill Livengoode and Dr. Robert Gilmore. They confirmed our finding of Borrelia having the ability to penetrate both glial cells and human neurons. But inexplicably the very study that the CDC funded was almost immediately suppressed by the CDC, and several administrators even disparaged their work as though to contradict their findings by saying: “…this was a test tube study and means nothing.”

Neither Gilmore or Livengoode appear to be speaking openly about their collaboration? And to my knowledge do not publically make comments about its importance. A similar situation appears to be happening in Canada where researchers have photographed live Borrelia swimming through blood vessels with ease. What is going on?
What is the ultimate agenda with these denialists? It certainly isn’t science or they would fund a multi-national brain autopsy study to deny or confirm Alan’s and Livengoode’s work on intracellular penetration in-vivo.

Microbes Infect. 2006 Nov-Dec;8(14-15):2832-40. Epub 2006 Sep 22.

Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.

Livengood JA, Gilmore RD Jr.
Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA.

So now with the CDC all but denying the existence of Livengoode and Gilmore’s work things looked even more bleak in the world of lyme disease pathology research.

=========================================

Enter Dr. Judith Mikklossy

Where my quest led me was to attend every science based Lyme conference that Tom Forschner and Karen Forschner of the LDF planned and administrated. (I believe the Lyme Disease Foundation conferences were for over a decade the most medically sound, research based Lyme conferences I ever attended.)

It was in 1997 when I first met Dr. Judith Miklossy a Neuro-Pathologist who had been researching dementia for several years. Judith presented her Swiss study of brain-autopsies on 13 Alzheimer’s patients. All 13 had spirochetes and her aged matched controls (no dementia) were negative for Borrelia.

Judith even isolated live bacteria from one of the subjects. This would lead to several more studies including using that isolate to measure the effects on rat-brain cultures. Dr. Mikklossy continues to focus on Borrelia and its role in causing dementia, and its prevalence in Alzheimer’s brains.

https://jneuroinflammation.biomedcentral.com/…/1742-2094-8-…

But there was another pathologist presenting at the same conference and he also had been working with the idea that Borrelia was playing a role on the pathology of Alzheimer’s Dementia. His name was Dr. Alan MacDonald MD, and he had a keen interest in not only the spiral form, but also the spherical forms of Borrelia, and felt they had a role in the pathogenesis of dementia.

MacDonald AB: Borrelia in the brains of patients dying with dementia. JAMA. 1986, 256: 2195-2196.

While Judith was concentrating on the mechanism of pathogenesis by looking at Rat-Brain model, Alan’s method was to work backwards: Alan chose to look at hundreds of brain sections from hundreds of Alzheimer’s patients, and to look at what the end process of neuroborreliosis looks like, and to attempt to explain the mecahnisms of changes seen in the Alzheimer’s brain.

When we combine Mikklossy’s work and Alan MacDonald’s work, we see that they meet in the middle reaching similar conclusions and findings.

McGeer PL, Itagaki S, Tago H, McGeer EG: Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR. Neurosci Lett. 1987, 79: 195-200. 10.1016/0304-3940(87)90696-3.

Mikklossy

Dr. Judith Mikklossy investigated how Borrelia interacts with specific brain cells, and developed what for all intents is a petri dish model of Alzheimer’s disease. All the markers we look to see in Alzheimer’s brain is found withing mere weeks of adding Borrelia burgdorferi to rat brain cultures.

With the addition and enrichment with brain-microglia cells, the various cells immediately produced its first marker: precursor amyloid protein.

These are the other markers she observed in just eight weeks.

1 Precursor Amyloid Protein APP production
2 Cleavage of APP to Beta Amyloid
3 Conversion to Beta sheet amyloid
4 Hyperphosphoralation of microtubule protein Tau
5 Neurofibrillary tangles
6 Vacuole-like spaces

Everything we expect to see in an Alzheimer’s brain was seen except true plaques.

MacDonald

Alan took a different approach to Alzheimer’s research and the role of spirochetes.

Registering more living patients for brain autopsies is an extremely slow process with poor success rate because family members will often go against the patient’s wishes and at the last minute will cancel the tissue harvest. Also the process is expensive without an institution with the equipment and funding to do the work.

Here is what is involved with registering patients for a brain autopsy:

• A family discussion and agreement to pursue pathology research
• Legal consent forms must be signed
• Costs per brain are $1,000-5,000 depending on what is done
• A large enough patient sample across many states is needed to be statistically relevant.
• Expert techniques are needed in: sectioning, staining, and fluorescent microscopy using individually designed DNA probes
• Storage of samples
• Data analysis

As a way to speed up the process and reduce costs and legal concerns, Alan ordered brain samples (both frozen and paraffin blocks) from Alzheimer’s Brain Banks like Harvard.

Alan sectioned and stained hundreds of samples and found some amazing things that I have listed below.

• Borrelia often forms biofilms within the human Alzheimer’s brain
• More than one species of Borrelia is involved
• The spirochetes either attract amyloid or helps produce it as the bacteria biofilms are found interspersed inside the amyloid plaques
• Nematode worms are sometimes seen in the diseased brain of both MS and Alzheimer’s patients
• The nematode gut stains positive by DNA probes for Borrelia
• The nematodes destroy brain tissue and deposits feces and eggs in the brain
• Borrelia biofilms are seen in fatal glioblastoma tumors
• Both Borrelia burgdorferi and Borrelia mayonii have been found within the testicle of one patient
• In severe dementia, amyloid can sometimes be detected in the blood using amyloid stains, this might be a blood test for Alzheimer’s?

So while Dr Mikklossy looks for the genesis of Alzheimer’s disease, Alan MacDonald looks at the end state of the disease process and asks what the role Borrelia play?

They have reached similar conclusions:

• Borrelia can form “colonies or biofilms” in the brain.
• Borrelia can penetrate blood vessels and weaken blood vessels possibly leading to strokes
• Borrelia bacteria have a tropism (attraction) for the brain and for specific brain cells.
• Borrelia is found both intracellular and extracellular in the brain
• While the bacteria is detected in the brain by autopsy, the blood can remain negative for the associated antibodies
• The blood-brain-barrier represents a therapeutic challenge to treat effectively and maybe considered a treatable but incurable condition
• Borrelia may well be part of the biochemical process that leads to amyloid production
• The debate over whether Borrelia like Syphilis can cause dementia is now overwhelmingly supportive of a new category of dementia: “Borrelia Associated Dementia”

END PART ONE

https://jneuroinflammation.biomedcentral.com/…/1742-2094-8-…

MacDonald AB: Borrelia in the brains of patients dying with dementia. JAMA. 1986, 256: 2195-2196.

MacDonald AB, Miranda JM: Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987, 18: 759-761. 10.1016/S0046-8177(87)80252-6
MacDonald AB: Concurrent neocortical borreliosis and Alzheimer’s Disease. Ann N Y Acad Sci. 1988, 539: 468-470. 10.1111/j.1749-6632.1988.tb31909.x.
Pappolla MA, Omar R, Saran B, Andorn A, Suarez M, Pavia C, Weinstein A, Shank D, Davis K, Burgdorfer W: Concurrent neuroborreliosis and Alzheimer’s disease: analysis of the evidence. Hum Pathol. 1989, 20: 753-757. 10.1016/0046-8177(89)90068-3.

Miklossy J, Kuntzer T, Bogousslavsky J, Regli F, Janzer RC: Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis. Acta Neuropathol. 1990, 80: 568-572. 10.1007/BF00294622.

Miklossy J: Alzheimer’s disease – A spirochetosis?. Neuroreport. 1993, 4: 841-848. 10.1097/00001756-199307000-00002.

Baker HF, Ridley RM, Duchen LW, Crow TJ, Bruton CJ: Evidence for the experimental transmission of cerebral beta-amyloidosis to primates. Int J Exp Pathol. 1993, 74: 441-454.

Baker HF, Ridley RM, Duchen LW, Crow TJ, Bruton CJ: Experimental induction of beta-amyloid plaques and cerebral angiopathy in primates. Ann N Y Acad Sci. 1993, 695: 228-231. 10.1111/j.1749-6632.1993.tb23057.x.

Baker HF, Ridley RM, Duchen LW, Crow TJ, Bruton CJ: Induction of beta (A4)-amyloid in primates by injection of Alzheimer’s disease brain homogenate. Comparison with transmission of spongiform encephalopathy. Mol Neurobiol. 1994, 8: 25-39. 10.1007/BF02778005.

MacDonald, Alan in European Journal of Clinical Microbiology 32(8) · March 2013 with 32 Reads

Alzheimer’s disease Braak Stage progressions: Reexamined and redefined as Borrelia infection transmission through neural circuits Medical Hypotheses 68(5):1059-64 · February 2007
Alzheimer’s neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochete in Medical Hypotheses 68(4):822-5 · February 2007 with
MacDonald, Alan Alzheimer’s & dementia: the journal of the Alzheimer’s Association 2(3) · July 2006

Spirochetal cyst forms in neurodegenerative disorders,… hiding in plain sightArticle in Medical Hypotheses 67(4):819-32 · February 2006
Gestational Lyme borreliosis. Implications for the fetusArticle · Literature Review in Rheumatic Disease Clinics of North America15(4):657-77 · December 1989
Miklossy J, Kasas S, Janzer RC, Ardizzoni F, Van der Loos H: Further morphological evidence for a spirochetal etiology of Alzheimer’s Disease. NeuroReport. 1994, 5: 1201-1204.
Schaeffer S, Le Doze F, De la Sayette V, Bertran F, Viader F: Dementia in Lyme disease. Presse Med. 1994, 123: 861
Fallon BA, Nields JA: Lyme disease: a neuropsychiatric illness. Am J Psychiatry. 1994, 151: 1571-1583.
Miklossy J: The spirochetal etiology of Alzheimer’s disease: A putative therapeutic approach. Alzheimer Disease: Therapeutic Strategies. Proceedings of the Third International Springfield Alzheimer Symposium. Edited by: Giacobini E, Becker R. 1994, Birkhauser Boston Inc., 41-48. Part I
Miklossy J, Gern L, Darekar P, Janzer RC, Van der, Loos H: Senile plaques, neurofibrillary tangles and neuropil threads contain DNA?. J Spirochetal and Tick-borne Dis (JSTD). 1995, 2: 1-5.
Miklossy J, Darekar P, Gern L, Janzer RC, Bosman FT: Bacterial peptidoglycan in neuritic plaques in Alzheimer’s disease. Azheimer’s Res. 1996, 2: 95-100.
Miklossy J: Chronic inflammation and amyloidogenesis in Alzheimer’s disease: Putative role of bacterial peptidoglycan, a potent inflammatory and amyloidogenic factor. Alzheimer’s Rev. 1998, 3: 45-51.
Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ: Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis and may be associated with Alzheimer disease. J Alzheimer’s Dis. 2004, 6: 1-11.
Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K: Beta-amyloid deposition and Alzheimer’s type changes induced by Borrelia spirochetes. Neurobiol Aging. 2006, 27: 228-236. 10.1016/j.neurobiolaging.2005.01.018.

Miller LM, Wang Q, Telivala TP, Smith RJ, Lanzirotti A, Miklossy J: Synchrotron-based infrared and X-ray imaging shows focalized accumulation of Cu and Zn co-localized with beta-amyloid deposits in Alzheimer’s disease. J Struct Biol. 2006, 155: 30-37. 10.1016/j.jsb.2005.09.004.

MacDonald AB: Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete. Med Hypotheses. 2006, 67: 592-600. 10.1016/j.mehy.2006.02.035.

Larsen P, Nielsen JL, Dueholm MS, Wetzel R, Otzen D, Nielsen PH: Amyloid adhesins are abundant in natural biofilms. Environ Microbiol. 2007, 9: 3077-3090. 10.1111/j.1462-2920.2007.01418.x.

Meer-Scherrer L, Chang Loa C, Adelson ME, Mordechai E, Lobrinus JA, Fallon BA, Tilton RC: Lyme disease associated with Alzheimer’s disease. Curr Microbiol. 2006, 52: 330-332. 10.1007/s00284-005-0454-7.
Miklossy J: Chronic inflammation and amyloidogenesis in Alzheimer’s disease – role of spirochetes. J Alzheimer’s Dis. 2008, 13: 381-391.

Honjo K, van Reekum R, Verhoeff NP: Alzheimer’s disease and infection: do infectious agents contribute to progression of Alzheimer’s disease?. Alzheimers Dement. 2009, 5: 348-360. 10.1016/j.jalz.2008.12.001.
Loeb MB, Molloy DW, Smieja M, Standish T, Goldsmith CH, Mahony J, Smith S, Borrie M, Decoteau E, Davidson W, McDougall A, Gnarpe J, O’DONNell M, Chernesky M: A randomized, controlled trial of doxycycline and rifampin for patients with Alzheimer’s disease. J Am Geriatr Soc. 2004, 52: 381-387. 10.1111/j.1532-5415.2004.52109.x.PubMedGoogle Scholar
Tsai GE, Falk WE, Gunther J, Coyle JT: Improved cognition in Alzheimer’s disease with short-term D-cycloserine treatment. Am J Psychiatry. 1999, 156: 467-469.PubMedGoogle Scholar
Kim HS, Suh YH: Minocycline and neurodegenerative diseases. Behav Brain Res. 2009, 196: 168-179. 10.1016/j.bbr.2008.09.040.
Miklossy J, Kasas S, Zurn AD, McCall S, Yu S, McGeer PL: Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis. J Neuroinflammation. 2008, 5: 40-10.1186/1742-2094-5-40.

McGeer PL, McGeer EG: Local neuroinflammation and the progression of Alzheimer’s disease. J Neurovirol. 2002, 8: 529-538. 10.1080/13550280290100969.

Guo JP, Arai T, Miklossy J, McGeer PL: Abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer disease. Proc Natl Acad Sci USA. 2006, 103: 1953-1938. 10.1073/pnas.0509386103.

Miklossy J, Rosemberg S, McGeer PL: Beta amyloid deposition in the atrophic form of general paresis. Alzheimer’s Disease: New advances. Proceedings of the 10th International Congress on Alzheimer’s Disease (ICAD). Edited by: Iqbal K, Winblad B, Avila J. 2006, Medimond, International Proceedings, 429-433.

Miklossy J: Biology and neuropathology of dementia in syphilis and Lyme disease. Dementias. Edited by: Duyckaerts C, Litvan I. 2008, Edinburgh, London, New York, Oxford, Philadelphia, St-Louis, Toronto, Sydney: Elsevier, 825-844. Series Editor Aminoff MJ, Boller F, Schwab DS: Handbook of Clinical Neurology vol. 89

 _________
For More:

Category:

Activism, Alzheimer's, Biofilm, Borrelia Miyamotoi (Relapsing Fever Group), Lyme, Parasites, research