Archive for the ‘Alzheimer’s’ Category

Lyme & Memory Loss

https://www.globallymealliance.org/blog/lyme-and-memory-loss

What causes memory loss specifically? And what does it feel like to experience it?

My long-term memory has always been sharp as a tack. I can repeat verbatim a conversation that happened two decades ago; I can tell you what a friend was wearing on the first day of third grade; I know what I ate at the restaurant my family went to on the last night of a vacation we took when I was in high school. People say, “It’s incredible that you can remember so much,” to which I often respond, “Just don’t ask me what I had for breakfast.”

The joke gets a good laugh, but it’s actually a serious matter: despite my unusually strong long-term memory, my short-term memory has been affected by the tick-borne illnesses Lyme disease, babesiosis, and ehrlichiosis. Some evenings I truly couldn’t tell you what I had for breakfast, and other times I need to look at my calendar to remember what I did that day. Once jogged, the memory comes back to me like a slow Google search, but the hang time between someone asking me about my day and my response can be embarrassingly long.

What causes memory loss specifically? And what does it feel like to experience it?

Though our central nervous systems are generally protected by the blood brain barrier, Lyme bacteria (spirochetes) are sneaky and smart, and can spiral their way across the border. Once that security breach occurs, a patient may experience “Lyme brain”, which can manifest as brain fog, word or song iteration, depression and anxiety, tremors, mini-seizures, headaches, burning extremities and memory loss.

As described in the book Conquering Lyme Disease: Science Bridges the Great Divide by Brian A. Fallon, MD and Jennifer Sotsky, MD, “Lyme disease can directly affect brain and sensorium in multiple ways: via direct infection, immune system effects, changes in neurotransmitter balance, and altered neural pathways.” Inflammation in the brain, as well as impaired oxygen flow to the brain as is often seen with babesiosis, can impact cognitive function. Drs. Fallon and Sotsky write that short-term memory problems are one of the most common cognitive effects of neurological Lyme disease. The book includes images of low blood flow in the brain of patients with memory impairment after Lyme disease (referred to as post-treatment Lyme encephalopathy).

In her book Lyme Brain, Nicola McFadzean Ducharme, ND, references studies in which Borrelia burgdorferi spirochetes were found in the brains of Alzheimer’s patients. While many Alzheimer’s patients don’t have Lyme, and many Lyme patients won’t develop Alzheimer’s, the studies show both how easily Lyme bacteria can cross the blood brain barrier, and how easily their presence can be misdiagnosed as dementia or Alzheimer’s when a chief symptom is memory loss.

The extent to which a patient’s memory is affected depends largely on their response to treatment.

When I started antibiotic therapy, some of my neurological systems worsened at first, as I experienced Herxheimer reactions, and the antibiotics chased those clever spirochetes deeper into my brain. After a couple months, my brain fog decreased, I had better concentration, and my memory improved. Sticking to an anti-inflammatory diet and taking supplements to help rid my brain of neurotoxins also helped. I learned to pace myself and to stay away from overstimulating activities (like big movie theaters or fireworks shows) that rile up my neurological symptoms, including memory loss.

Luckily, my long-term memory was never affected, which is a blessing as a writer. But while my short-term memory problems have improved, they are not fully gone. I especially notice them now when I am over tired or over worked. During those periods, I might leave someone a voicemail in the morning and then leave a similar message later in the day, forgetting about the first. I find myself asking friends, “Did I already tell you this story?” I’m hyper-aware of the deficit, but friends and family assure me that my lapses are relatively infrequent. Rest, quiet time away from screens, and relaxation usually have me back in “working order” in just a couple days.

If you are in an acute stage of neurological tick-borne illness, it’s possible that you’ve read this post and forgotten what it said; that you lost track of where you were whiling reading; or that you’ll tell someone about what you read more than once. Know that you’re not alone, and that with proper treatment through a Lyme Literate Medical Doctor (LLMD) and good self-care, a time will come when everything will seem much clearer.

[1] Fallon, Brian A., MD and Sotsky, Jennifer, MD. Conquering Lyme Disease: Science Bridges the Great Divide. New York: Columbia University Press (2018), 314.

[1] McFadzean Ducharme, Nicola, ND. Lyme Brain. California: BioMed Publishing Group, LLC (2016), 15-16.

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jennifer crystal_2

Opinions expressed by contributors are their own.

Jennifer Crystal is a writer and educator in Boston. Her memoir about her medical journey is forthcoming. Contact her at lymewarriorjennifercrystal@gmail.com.

COVID-19 RNA Based Vaccines & The Risk of Prion Disease

https://scivisionpub.com/pdfs/covid19-rna-based-vaccines-and-the-risk-of-prion-disease-1503.pdf

Microbiology & Infectious Diseases

COVID-19 RNA Based Vaccines and the Risk of Prion Disease  

J. Bart Classen, MD*

Classen Immunotherapies, Inc., 3637 Rockdale Road, Manchester, MD 21102, E-mail: classen@vaccines.net.

Citation: Classen JB. COVID-19 RNA Based Vaccines and the Risk of Prion Disease. Microbiol Infect Dis. 2021; 5(1): 1-3. 

*Correspondence:

J. Bart Classen, MD, Classen Immunotherapies, Inc., 3637 Rockdale Road, Manchester, MD 21102, Tel: 410-377-8526.

Received: 27 December 2020; Accepted: 18 January 2021

ABSTRACT

Development of new vaccine technology has been plagued with problems in the past. The current RNA based SARS- CoV-2 vaccines were approved in the US using an emergency order without extensive long term safety testing. In this paper the Pfzer COVID-19 vaccine was evaluated for the potential to induce prion-based disease in vaccine recipients. The RNA sequence of the vaccine as well as the spike protein target interaction were analyzed for the potential to convert intracellular RNA binding proteins TAR DNA binding protein (TDP-43) and Fused in Sarcoma(FUS) into their pathologic prion conformations.

The results indicate that the vaccine RNA has specific sequences that may induce TDP-43 and FUS to fold into their pathologic prion conformations. In the current analysis a total of sixteen UG tandem repeats (ΨGΨG) were identifed and additional UG (ΨG) rich sequences were identifed. Two GGΨA sequences were found. Potential G Quadruplex sequences are possibly present but a more sophisticated computer program is needed to verify these.

Furthermore, the spike protein, created by the translation of the vaccineRNA, binds angiotensin converting enzyme 2 (ACE2), a zinc containing enzyme. This interaction has the potential to increase intracellular zinc. Zinc ions have been shown to cause the transformation of TDP-43 to its pathologic prion configuration. The folding of TDP-43 and FUS into their pathologic prion conformations is known to cause ALS, front temporal lobar degeneration, Alzheimer’s disease and other neurological degenerative diseases. The enclosed finding as well as additional potential risks leads the author to believe that regulatory approval of the RNA based vaccines for SARS-CoV-2 was premature and that the vaccine may cause much more harm than benefit.

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Important excerpt from the summary:

Many have raised the warning that the current epidemic of COVID-19 is actually the result of an bioweapons attack released in part by individuals in the United States government [10,11]. Such a theory is not far fetched given that the 2001 anthrax attack in the US originated at Fort Detrick, a US army bioweapon facility. Because the FBI’s anthrax investigation was closed against the advice of the lead FBI agent in the case, there are likely conspirators still working in the US government. In such a scenario the primary focus of stopping a bioweapons attack must be to apprehend the conspirators or the attacks will never cease. Approving a vaccine, utilizing novel RNA technology without extensive testing is extremely dangerous. The vaccine could be a bioweapon and even more dangerous than the original infection.

5 doctors state the injections are bioweapons & what you can do about it. (This was never a viral illness but blood poisoning due to a spike protein. The injections are NOT “vaccines” but cause YOU to manufacture spike proteins – perhaps indefinitely – the very thing causing illness. Those getting the injections are now transmitting this spike protein to those foregoing the injections.  Those getting the shots should be quarantined.) A lot is unknown.  (Within the 5 doctors link, Dr. Lee Merritt speaks about this “prion” disease within)

In-Depth Look at the Dangers of Mold Toxicity

https://holtorfmed.com/articles/immune-health/an-in-depth-look-at-the-dangers-of-mold-toxicity

In-Depth Look at the Dangers of Mold Toxicity

3/31/21

By Holtorf Medical Group

Mold is a type of fungus that grows in the form of multicellular filaments called hyphae. There are tens of thousands of mold species that have evolved to survive harsh conditions. Mold reproduces by means of small, lightweight spores that travel through the air. These spores contain toxic chemicals called mycotoxins that can be inhaled and lead to mold toxicity.

Mold toxicity is a very prevalent and underdiagnosed condition that can consist of a variety of symptoms. Although anyone can suffer from mold toxicity, 25% of the population is particularly vulnerable due to a genetic predisposition that inhibits the clearance of biotoxins.

Learn about sources of mold, how mold affects the body, and more below.

Sources

Because mold grows on organic matter, it is an increasingly common part of our environment and people can be exposed in a variety of ways. Mold is able to feed on the moisture and warmth of its surroundings, leading to the release of mold spores and volatile organic compounds (VOCs). In fact, research suggests that mold can surface anywhere after just two days of moisture exposure.

Outdoor sources of mold include:

  • Stagnant water sources
  • Forests, beaches
  • Playgrounds
  • Sidewalks

Unfortunately, mold is also commonly found indoors, which is typically more harmful as mold spores can accumulate in higher concentrations due to a lack of airflow. Mold spores can enter homes, schools, and workplaces by attaching to clothing, shoes, or pets. Additionally, homes in climates where it frequently rains or that reside near the water are more likely to develop mold as they are exposed to moisture more often. It is common for mold to be found in damp bathrooms, basements, carpets, tiles, drywall, washing machines, and dishwashers. Some of the most common varieties of indoor mold are Aspergillus, Cladosporium, and Stachybotrys atra, all of which are considered black mold.

There is a growing number of health problems caused by mold inhalation. This is thought to be, in part, due to the rise of people living in urban areas. Researchers at Hospital General Universitario Gregorio Maranon in Spain reported that Aspergillus spores in outdoor air are more common in urban than rural settings in the province of Madrid. The continuing rise in global population has also pushed more people into environments that are likely to breed mold such as coastal and riparian floodplains, other bottomlands, and hurricane-prone areas.

Other mold risk factors are on the rise due to poor building practices that have been accepted for convenience. For instance, poorly built roofs leave behind rainwater that fosters mold growth. It is also common for venting clothes dryers to be located in a spot where they direct moisture to vulnerable areas inside homes. Additionally, modern homes often have tighter building envelopes, slowing the escape of water vapor and allowing it to become trapped and grow mold.

It is important to note that the same conditions that allow for mold growth also foster bacteria, MVOCs, beta-glucans, live or dead spores, fungal fragments, endotoxins, dust mites, cockroaches, and other pests. This combination of toxins can trigger an immune response and exacerbate chronic illnesses.

How Mold Affects the Body

Fungal secondary metabolites or mycotoxins affect numerous bodily functions mainly through triggering an immune response that leads to chronic inflammation. Mycotoxins impact both the innate immune system (the first line of defense against invading pathogens) and the adaptive immune response (specified immune response that eliminates certain pathogens and prevents their growth).

Mycotoxins such as aflatoxins and ochratoxins (which are produced from Aspergillus) as well as fumonisins (produced by Fusarium) have immunomodulatory properties. Consequently, these mycotoxins alter the body’s inflammatory response. Specifically, they target the functionality and production of cytokines, macrophages, and neutrophils.

Mycotoxins bind with cytokines, leading to an increase in clot formation and arterial blockages. This can lead to headaches, muscle aches, lack of temperature regulation, and brain fog. Increased cytokine levels then trigger action from white blood cells such as macrophages and neutrophils. This inflammatory immune response can restrict blood flow and reduce the amount of oxygen transported to tissues, resulting in fatigue, shortness of breath, and muscle cramps.

Another contributing aspect to the chronic inflammation experienced with mold toxicity is due to the way in which mycotoxins impair the white blood cell’s regulation cytokines, which leads to an increase in infections and a slower recovery from these infections.

Moreover, some mycotoxins inhibit the production of messenger cells, leukotriene B4, by targeting the enzyme, LTA4 hydrolase. This interrupts communication between the immune cells and minimizes the body’s defense mechanism. Because the first line of defense is impaired, it is difficult to develop adaptive immunity and eliminate the mycotoxins. As a result, the body is likely to experience chronic inflammation and a host of other issues.

Respiratory Impact

Mold enters the body through the skin and through inhalation, making respiratory function a primary target of mold. Once inhaled, mold can quickly colonize the lungs and sinuses as they are optimal growing conditions. This leads to the continual release of mycotoxins. Moreover, biofilms can form around the mold colonies, protecting them from the body’s immune system.

The sinuses are particularly susceptible to mold colonies and many species of Aspergillus have been identified in the sinuses of those with chronic sinus inflammation. Aspergillosis is known to be able to colonize in the lungs of both humans and animals, which causes invasive fungal infections. Because of the respiratory tract’s susceptibility to mold, mold exposure often mirrors allergy symptoms such as coughing, runny nose, sneezing, itchy eyes, and asthma.

Neurological Impact

Once mycotoxins are inhaled, they are stored in the body’s fatty tissue. Given that the brain is approximately 60% fat, mold toxicity can have profound neurological effects. Mycotoxins trigger an inflammatory immune response and this inflammation in the brain can impair cognitive function and lead to symptoms such as fatigue, memory loss, headaches, insomnia, dizziness, anxiety, depression, and more.

Chronic inflammation in the brain, especially when caused by toxins, can cause long-lasting damage. This is because when the brain is in a chronic state of inflammation, glial cells can no longer support neuron health and neural communication. When inflammation is present, glial cells change their cell morphology significantly and activate rapidly. These cells generate reactive oxygen species and release signals to trigger immune cells, which results in a continuation of the body’s inflammatory response. Over time, this leads to the degradation of tissue and of the blood–brain barrier and neurocognitive issues.

Alzheimer’s specialist, Dr. Bredson, MD, has found that one-third of Alzheimer’s Disease patients are considered “Inhalational Alzheimers,” which means their Alzheimer’s is a result of chronic inflammation caused by mold or other toxins. Other diseases that can be caused by mycotoxins include: ADHD, migraines, Parkinson’s, Chronic Fatigue Syndrome, and more.

The Role of Mold in Lyme Disease and Chronic Illness

Mold has a significant negative impact on the immune system, making those with chronic illnesses such as Lyme disease more at risk for developing serious health issues.

Because those with a chronic illness often have a weakened immune system, their body is less likely to be able to fight off mold spores and toxins. When the mold then begins to colonize in the body, patients experience chronic mycotoxin exposure, which reduces the body’s ability to fight infection due to mycotoxins immuno-suppressant effect. Thus, the body’s weakened immune system is forced to fight the chronic illness in addition to mycotoxins, leading to a worsening of symptoms associated with both conditions. Additionally, mold exposure and toxicity elicit an inflammatory response, which worsens chronic conditions such as Lyme, Fibromyalgia, gut dysfunction, and more.

Warning Signs of Mold Toxicity

Mold illness can cause a wide variety of symptoms. Often, it is only the respiratory symptoms that are recognized but it is important to be aware of its profound effects:

  • Fatigue
  • Anxiety
  • Depression
  • Light sensitivity
  • Headaches
  • Blurred vision
  • Dizziness
  • Vertigo
  • Brain fog
  • Memory loss (typically short-term)
  • Chronic congestion or sinus infections
  • Coughing
  • Abdominal pain
  • Muscle pain and/or joint pain
  • Hormone deficiency
  • Adrenal dysfunction
  • Nose bleeds
  • Environmental sensitivity (chemical sensitivity)
  • Chronic colds, flus, acute infections
  • Nausea
  • Itchy/ red eyes
  • Insomnia
  • Night sweats
  • Temperature dysregulation
  • Weight gain
Seeking Treatment

For over a decade, there has been a consensus in the medical community that regular exposure to mold significantly increases people’s risk for disease. This public health hazard has still not been addressed with the concern it should be as governmental agencies, such as the Institute of Medicine report commissioned by the CDC and released in 2004, have concluded that the primary health concerns with mold are solely respiratory. However, mold can have long-lasting health effects, especially for those dealing with a chronic illness.

If you feel you are suffering from mold toxicity or would like to get tested, contact Holtorf Medical Group today. At Holtorf Medical Group, our physicians are trained to provide you with cutting-edge testing and innovative treatments to properly diagnose and treat your condition, optimize your health, and improve your quality of life.


Resources

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For more:

Are Infections Seeding Some Cases of Alzheimer’s Disease?

https://www.nature.com/articles/d41586-020-03084-9

Are infections seeding some cases of Alzheimer’s disease?

A fringe theory links microbes in the brain with the onset of dementia. Now, researchers are taking it seriously.

Some scientists think that microbes such as the herpes simplex virus 1 (shown here on an epithelial cell) could trigger some cases of Alzheimer’s disease. Credit: SPL

Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ.

The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. (See link for article)

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**Comment**

Important quote:

Several microbes have been proposed as triggers of Alzheimer’s, including three human herpes viruses and three bacteria: Chlamydia pneumoniae, a cause of lung infections; Borrelia burgdorferi, the agent of Lyme disease; and, most recently, Porphyromonas gingivalis, which leads to gum disease. In theory, any infectious agent that can invade the brain could have this trigger role (there’s no good evidence, however, that SARS-CoV-2, the virus behind COVID-19, has this ability).

It’s also sad that Alzheimer’s research has been pigeon-holed for so long:  https://madisonarealymesupportgroup.com/2020/01/05/the-maddening-saga-of-how-an-alzheimers-cabal-thwarted-progress-toward-a-cure-for-decades/,  https://madisonarealymesupportgroup.com/2020/01/14/what-causes-alzheimers-not-toxic-amyloid-new-study-suggests/

This article contains Norrins’ paper in the comment section. The article above states there are 40 studies in the cue vying for the 1 million cash prize in March, when the challenge results will be announced:  https://madisonarealymesupportgroup.com/2019/12/23/a-turning-point-in-alzheimers-disease-microbes-matter/

https://madisonarealymesupportgroup.com/2019/12/23/a-turning-point-in-alzheimers-disease-microbes-matter/

Can Lyme Disease Cause Dementia?

https://danielcameronmd.com/can-lyme-disease-cause-dementia/

CAN LYME DISEASE CAUSE DEMENTIA?

can lyme disease cause dementia

There have been reports of Borrelia burgdorferi (Bb), the bacterial agent of Lyme disease, triggering primary dementia, such as Alzheimer’s disease. Researchers who examined the records of 1,594 patients with dementia found that 1.25% had a positive intrathecal anti-Borrelia antibody index (AI), specific for neuroborreliosis. They concluded,

“Pure Lyme dementia exists and has a good outcome after antibiotics.” 1

In a retrospective study, entitled “Secondary dementia due to Lyme neuroborreliosis,” Kristoferitsch and colleagues describe several case reports of patients diagnosed with dementia-like syndromes due to Lyme neuroborreliosis or Lyme disease.2

Rapid improvement with antibiotic treatment

The authors’ case report featuring a 76-year-old woman demonstrates how Lyme disease can cause dementia-like symptoms. The patient developed progressive cognitive decline, loss of weight, nausea, gait disturbance and tremor over a 12-month period. She was referred to a neurology clinic for evaluation.

Three months earlier, the woman had been diagnosed with tension headaches and a depressive disorder. Medications, however, did not improve her symptoms.

Further testing revealed bilateral white matter lesions and an old lacunar lesion located at the left striatum. Extensive neurocognitive testing found “a severe decline of attention, memory and executive functions corresponding to subcortical dementia,” the authors write.

“LNB [Lyme neuroborreliosis] was diagnosed when further CSF [cerebral spinal fluid] examinations disclosed a highly elevated Bb-specific-AI indicating local intrathecal Bb-specific antibody synthesis,” Kristoferitsch writes.

After a 3-week course of treatment with ceftriaxone, the woman “recovered rapidly,” the authors write.

“In a telephone call in February 2018 at the age of 82 years, the patient reported no gait problems or cognitive impairment and had just returned from a trip to Cuba,” the authors write.

Woman admitted to psychiatric ward with severe dementia

A 71-year-old woman with rapidly progressing dementia and short periods of altered consciousness was admitted to a psychiatric hospital. Six months earlier, she was having mild forgetfulness.

MRI results, which indicated slight mesiotemporal atrophy, along with neurocognitive testing supported an initial diagnosis of primary dementia.

“Later, the patient’s daughter reported a tick bite followed by a widespread rash,” the authors write. “Thus, LNB [Lyme neuroborreliosis] was suspected and confirmed by CSF investigations.”

After 2 weeks of antibiotic treatment with ceftriaxone, the woman’s symptoms subsided and her cognition improved.

READ MORE: 80-year-old man with Lyme encephalopathy instead of dementia

At her 5-year follow-up visit, the woman’s “cognition was stable” and memory tests indicated a score above the mean for females her age, “which strongly argued against any dementing process,” the authors write.

In reviewing the literature, Kristoferitsch et al. identified several signs and symptoms that may indicate that Lyme neuroborreliosis (or Lyme disease) is causing dementia in a patient.

Distinguishing features of Lyme-induced dementia

  • Most of the patients or family members did not recall previous tick bites, an EM rash or symptoms of Lyme disease. Therefore, when “EM or other characteristic symptoms of early LB 1–2 years before the onset of dementia may if untreated serve as an indicator for chronic LNB.”
  • Unlike most neurodegenerative dementias, dementia caused by Lyme disease appears to progress rapidly, the authors write.
  • Weight loss is another symptom observed in LNB [Lyme neuroborreliosis],” the authors explain. “It is also compatible with the diagnosis of AD [Alzheimer’s disease] but when it occurs in chronic LNB, it can be more pronounced, reaching up to 20 kg/year.” Weight loss in patients with Alzheimer’s disease is less prominent, the authors explain.
  • Headache, nausea, malaise and vomiting are typically not symptoms of degenerative dementias, the authors explain. But, “might be associated with secondary dementia and thus also with chronic LNB [Lyme neuroborreliosis].”
  • Gait disturbances at the onset or early in the disease which was observed in all cases of this study, makes the diagnosis of a probable AD [Alzheimer’s disease] uncertain or unlikely.”

Additionally, “In most patients, improvement of symptoms was reported already within a few days of antibiotic treatment,” Kristoferitsch writes.

Early recognition and treatment is important

The authors stress the importance of recognizing Lyme-induced dementia-like syndromes.

“It is essential to be aware of this manifestation of Lyme neuroborreliosis, because early antibiotic treatment will prevent permanent sequelae that may occur throughout the further course of the untreated disease,” the authors conclude.

References:
  1. Blanc F, Philippi N, Cretin B, et al. Lyme neuroborreliosis and dementia. J Alzheimers Dis. 2014;41(4):1087-1093. doi:10.3233/JAD-130446
  2. Kristoferitsch W, Aboulenein-Djamshidian F, Jecel J, et al. Secondary dementia due to Lyme neuroborreliosis. Wien Klin Wochenschr. 2018;130(15-16):468-478. doi:10.1007/s00508-018-1361-9

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**Comment**

The proof is in the pudding. These patients were given treatment and they immediately improved. This is noted again and again with chronic Lyme patients – yet according to mainstream medicine led by the CDC and IDSA, this is a figment of our imaginations – otherwise known as PTLDS, an acronym they give complicated cases so they don’t have to deal with persistent infection, and therefore lengthy treatment.

It also allows them to continue to attempt to peddle their lucrative vaccine they continue to pull out of the hat every couple of years.

For more:  https://madisonarealymesupportgroup.com/2020/05/16/lyme-disease-awareness-month-kris-kristofferson-was-misdiagnosed-with-alzheimers-memory-loss-was-due-to-ticks/

For more: