Archive for the ‘Alzheimer’s’ Category

Ahead of the Curve Interview With Dr. Alan McDonald  Interview Here (Approx. 2 hours 13 min)

Episode 300: Ahead of the Curve – an interview with Dr. Alan McDonald

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Dr. Alan MacDonald is an Ivy League educated Medical Doctor who worked as a hospital pathologist in the eastern Long Island, New York area at the outset of the modern Lyme disease pandemic. He and his pioneering work were first featured on episode 171 of the Tick Boot Camp Podcast.

In this comprehensive interview, Dr. MacDonald discusses his groundbreaking and yet to be published research findings on topics such as the Lyme disease connection to suicide, brain cancer, Leukemia, dementia, Alzheimer’s disease, and Parkinson’s disease, in addition to how acute Lyme disease disrupts liver function and why and how Lyme disease testing is flawed.

PS you can also view an exclusive Tick Boot Camp presentation created by Dr. MacDonald with photos of Lyme under a microscope and descriptions highlighting the various topics discussed in this interview

Check out his GoFundMe page  to help him continue his groundbreaking work.

McDonald has truly done ground-breaking work but has been vilified by many of his own colleagues who seemingly can’t think outside the box or accept new information. Go here to watch other videos where he shows parasitosis (Neural Larval Migrans) within MS patients as he discovered nematode worms, eggs and both larval forms and mating adult pairs present in the brain and spinal fluid of MS patients.  These videos are circa 2016 and are revolutionary yet are quietly collecting dust and simply ignored in mainstream research.

At 5 min and 51 sec into the 2016 London lecture, you will see the discovery of worms in the brain and spinal fluid of EVERY MS patient tested.  He also explains the difficulty in finding these worms as they move from one area to another.

These worms cause inflammation and damage in the CNS on their own but also infect us with Lyme and other infections. 

CLICK HERE to view the research poster of Dr. MacDonald’s discovery of filarial (small roundworms) in the central nervous system of MS patients at their time of death.

CLICK HERE to view the research poster of Dr. MacDonald’s discovery of tapeworm larva and developing juvenile tapeworms in the central nervous system of MS patients at their time of death.

What this means regarding treatment, is that if you are one of those patients with these worms, you need to disable/kill the worms to get to the borrelia/MSIDS inside them.  Anthelminitics such as ivermectin and Albenza are used to kill worms as well as natural medicines; however, this must be done under the supervision of a doctor as the inflammation and herxheimer reactions can be very great. 

For some patients, addressing worms is a game-changer.  Consider talking to your LLMD about it.

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Bb Brain Infection & Lewy Body Dementia

Borrelia burgdorferi spirochetal brain infection and Lewy Body Dementia

Carl Tuttle

Hudson, NH, United States

Aug 2, 2022 — 

Latest email to the Federal Tick-Borne Disease Working Group…

———- Original Message ———-
To: “” <>
Cc: (All members of the TBDWG)
Date: 08/02/2022 9:40 AM
Subject: Borrelia burgdorferi spirochetal brain infection and Lewy Body Dementia

To the Tick-Borne Disease Working Group,

Please see the attached publication from Pathologist Alan MacDonald who has discovered borrelia burgdorferi spirochetal brain infection and Lewy Body Dementia.

Microbial DNA globular liquid crystal like deposits inside Lewy bodies in four Lewy dementia patients

Alan B MacDonald


Four autopsy brains demonstrated concurrent evidence of Diffuse Cortical Lewy Body Dementia and active Lyme neuroborreliosis in adjacent brain sites. Lewy bodies In DCLBD contain microbial DNA. Alpha Synuclein proteins, which intrinsically bind to human nuclear DNA also bind to microbial DNA deposits inside Lewy bodies in the cytoplasmic compartment of diseased neurons. This is the first report of an association between spirochetal brain infection and Lewy Body Dementia.

This is just one additional piece of evidence as identified in my Verbal Public Comment that there has been a 30yr deliberate mishandling/avoidance of Lyme disease while refusing to recognize its severity.

Now would be a good time to review how the deception was pulled off using taxpayer dollars through a grant issued by the CDC; an open checkbook handed to Gary Wormser to produce his junk science focusing on the acute stage of disease with bulls-eye rash and early treatment under Grant# RO1 CK 000152

2019 Communication Sent to the TBDWG:

———- Original Message ———-
Cc:,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, Alex.Azar@HHS.GOV,,,,,,,,,,,,,,,,,
Date: February 9, 2019 at 9:42 AM

Subject: Efficacy of a 14-day course of amoxicillin for patients with erythema migrans


Diagnostic Microbiology and Infectious Disease

Efficacy of a 14-day course of amoxicillin for patients with erythema migrans.

Wormser GP1, Brady KC2, Cho MS2, Scavarda CA2, McKenna D2.


“….findings provide additional evidence that a 14-day course of 500 mg amoxicillin given 3 times per day is highly effective therapy for patients with early Lyme disease.”

Feb 9, 2019

Division of Infectious Diseases,
New York Medical College,
Valhalla, NY 10595
Attn: Gary P. Wormser, MD

Dr. Wormser,

Once again, as previously stated in the email below; “Your fixation on the acute stage of disease [with bulls-eye rash] after early treatment has done nothing to advance our understanding of how Lyme disease disables its victim.”

Early treatment of strep throat prevents patients from advancing to rheumatic fever which as you know causes irreversible heart damage. If we focused on the acute stage of strep we would never have realized that missed early treatment caused serious life-altering/life-threatening health consequences.

-Ignoring the late stage horribly disabled Lyme population which could total in the millions worldwide.

I noticed that your manuscript did not include the following reference:

July 2017- In Vitro Susceptibility of the Relapsing-Fever Spirochete Borrelia miyamotoi to Antimicrobial Agents.


“We were able to show that both B. miyamotoi strains and B. hermsii demonstrated greater susceptibility to doxycycline and azithromycin, equal susceptibility to ceftriaxone and proved to be resistant to amoxicillin in vitro as compared to the B. burgdorferi s.l. isolates.” 

Your retirement Dr. Wormser is highy, highly anticipated.

Carl Tuttle
Lyme Endemic Hudson, NH

NOTE: Wormser’s study was funded directly from the US Centers for Disease Control

Funding: RO1 CK 000152 which appears to be an open checkbook for his junk science.

(Wasteful taxpayer spending)

Cc: Tick Borne Disease Working Group

Assistant Secretary for Health, ADM Brett P. Giroir, M.D.

On January 4, 2019 at 10:48 AM CARL TUTTLE <> wrote:


Shapiro ED, Wormser GP. Lyme disease in 2018: what is new (and what is not).

Jan 4, 2019

Division of Infectious Diseases,
New York Medical College,
Valhalla, NY 10595
Attn: Gary P. Wormser, MD

Dr. Wormser,

In reference to your response to my letter to the Editor published in the December 18th issue of JAMA, it would appear that you and your coauthor Dr. Shapiro conveniently ignored my question highlighted below:

Excerpt from my letter to the editor:

Controversies About Lyme Disease

-Carl Tuttle

“It is well known that untreated streptococcal pharyngitis can progress to rheumatic fever, causing irreversible heart damage. Untreated syphilis leads to progressive disability and dementia, and untreated HIV infection progresses to AIDS with significant disability and death. What happens to the patient with Lyme disease who goes months, years or decades before diagnosis because of a false negative serological test?”

Untreated Lyme is destroying lives, ending careers while leaving the patient in financial ruin as reported by the disabled Lyme community for the past three decades. The absence of a bulls-eye rash after tick bite allows patients to progress to severe neurological disease instead of obtaining a prompt diagnosis and early treatment.

I would like to call attention to the following quote taken from an interview with Professor Willy Burgdorfer, the discoverer of the Lyme disease spirochete:

“The controversy in Lyme disease research is a shameful affair. I say that because the whole thing is politically tainted. Money goes to people that have for the past thirty years produced the same thing. Nothing.  – Willy Burgdorfer

Source: (Live interview)

Prof. Willy Burgdorfer Talks About Lyme Disease

Your fixation on the acute stage of disease after early treatment Dr. Wormser has done nothing to advance our understanding of how Lyme disease disables its victim.

For example:

Subjective symptoms after treatment of early Lyme disease.

Gary Wormser, New York Medical College

(Financed by the U.S. Centers for Disease Control)


“At 12 months after enrollment, only 5 (2.2%) of 230 evaluable patients reported new or increased symptoms, and in none of the patients were these symptoms of sufficient severity to be functionally disabling”


Summary of Wormser’s study: Anyone experiencing symptoms after the one-size-fits-all treatment approach is just experiencing nothing more than the “aches and pains of daily living.”

So basically Wormser’s results are then assumed to apply to the entire patient population; in other words, Lyme is no big deal which has wrongly influenced our nation’s response to this serious life-altering health threat. The research into how Lyme disables should have been completed by now but the misclassification of Lyme as a simple nuisance disease (hard to catch and easily treated) has paralyzed the response to this runaway plague.

Many infections as I continue to point out evolve into an entirely different and serious life-altering/life-threatening disease when left untreated.

Post Treatment Lyme Disease Syndrome (PTLDS) after early treatment and untreated Lyme of months, years or decades are two entirely different disease states; the latter being ignored for three decades. Patients who have had a prolonged exposure to the pathogen are almost always incapacitated.

Purposely avoiding the advanced stage of disease hides the horribly disabled and anyone unable to see this is somewhat naive.

So I ask the question Dr. Wormser, What is the motivation for downplaying the severity of Lyme disease while ignoring patient outcry for thirty years?

A prompt response to this inquiry is requested.

Please hit Reply-All as I have carbon copied the Tick Borne Disease Working Group and Assistant Secretary for Health, ADM Brett P. Giroir, M.D.

Carl Tuttle
Lyme Endemic Hudson, NH


For more:

Infectious Agents and Alzheimer’s Disease

Infectious agents and Alzheimer’s disease

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*Correspondence:; (Jolanta Dorszewska)
Academic Editor: Rafael Franco
J. Integr. Neurosci. 2022, 21(2), 73;
Submitted: 8 March 2021 | Revised: 25 March 2021 | Accepted: 29 April 2021 | Published: 28 March 2022

Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Individuals affected by the disease gradually lose their capacity for abstract thinking, understanding, communication and memory. As populations age, declining cognitive abilities will represent an increasing global health concern. While AD was first described over a century ago, its pathogenesis remains to be fully elucidated. It is believed that cognitive decline in AD is caused by a progressive loss of neurons and synapses that lead to reduced neural plasticity. AD is a multifactorial disease affected by genetic and environmental factors. The molecular hallmarks of AD include formation of extracellular amyloid (A) aggregates, neurofibrillary tangles of hyperphosphorylated tau protein, excessive oxidative damage, an imbalance of biothiols, dysregulated methylation, and a disproportionate inflammatory response.

Recent reports have shown that viruses (e.g., Herpes simplex type 1, 2, 6A/B; human cytomegalovirus, Epstein-Barr virus, hepatitis C virus, influenza virus, and severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), bacteria (e.g., Treponema pallidum, Borrelia burgdorferi, Chlamydia pneumoniae, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcmitans, Eikenella corrodens, Treponema denticola, and Helicobacter pylori), as well as eukaryotic unicellular parasites (e.g., Toxoplasma gondii) may factor into cognitive decline within the context of AD. Microorganisms may trigger pathological changes in the brain that resemble and/or induce accumulation of Apeptides and promote tau hyperphosphorylation. Further, the mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss.

Here we review the influence of infectious agents on the development of AD to inspire new research in dementia based on these pathogens.


For more:

7 Conditions Masquerading As Dementia

7 Conditions Masquerading As Dementia

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
© [5/30/22] GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here //

Tulane Researcher Asks, “Could Chronic Lyme Contribute to Alzheimer’s Dementia?” avatar
Focus – Opinions and Features
15 APR 2022

Tulane researcher asks, “Could chronic Lyme contribute to Alzheimer’s dementia?”

By Kris Newby, Invisible International

In 2019, the late-great-science-writer Sharon Begley wrote an insightful article, “The maddening saga of how an Alzheimer’s ‘cabal’ thwarted progress toward a cure for decades.”

Begley’s reporting described how a powerful group of researchers became fixated on one theory of Alzheimer’s causation at the expense of all others.

Their hypothesis: that Alzheimer’s cognitive decline was caused by neuron-killing, beta-amyloid protein clumps in the brain, and that if you dissolved the clumps, the disease process would stop.

As this theory hit a brick wall, Begley showed how the actions of the cabal harmed patients: “…for decades, believers in the dominant hypothesis suppressed research on alternative ideas: They influenced what studies got published in top journals, which scientists got funded, who got tenure, and who got speaking slots at reputation-buffing scientific conferences.”

Decades later, with no cure or effective drugs for Alzheimer’s dementia, some researchers are gathering evidence on a different causation theory — that dementia could be triggered by any number of chronic infectious diseases, and that amyloid plaques are a byproduct of an active infection, not the cause.

One of these researchers is Monica Embers, PhD, an associate professor of microbiology and immunology at the Tulane National Primate Research Center. She’s also the leading expert in identifying treatments that can eradicate Lyme bacteria infections in nonhuman primates, our closest mammalian relatives.

CME course on infection and dementia

In her new continuing medical education course, “Chronic Infection and the Etiology of Dementia,” she lays out the evidence that the Lyme bacteria could be one possible cause of dementia.

Her theory is this: When pathogens like the Lyme bacteria sneak past the blood-brain barrier, the immune system doesn’t allow protective killer cells from the entering the inflexible brain cavity, because resulting brain inflammation and swelling could lead to death.

Instead, it encapsulates invading microbes with protein clumps, called beta-amyloid plaques or Lewy bodies, to stop the infection. As a person ages, the bodily processes that clean up this “brain gunk” slows, resulting in protein accumulation that impedes brain signaling and kills neurons.

In her 31-minute course, Dr. Embers describes the clinical symptoms of Alzheimer’s and Lewy body dementia, the impact on public health, genetic risks, and the list of infections associated with dementia-like symptoms.

The course also reviews a well-documented case study about a 54-year-old woman who was treated for the Lyme bacteria (Borrelia burgdorferi), developed dementia, then died 15 years after the initial infection. After death, B. burgdorferi was identified by PCR (DNA detection) in her brain and central nervous system (CNS) tissues, and by immunofluorescent staining of the bacteria in the spinal cord. (For more, read this peer-reviewed study.)

Dr. Embers and her study’s co-authors conclude, “These studies offer proof of the principle that persistent infection with the Lyme disease spirochete may have lingering consequences on the CNS. Published in postmortem brain autopsy images and extensive pathology tests are a compelling reason to pursue this line of scientific inquiry.”

You can watch this free CME course here.

Kris Newby is Communications Director of Invisible International, a 501(c)(3) nonprofit foundation dedicated to reducing suffering from invisible illnesses. The organization offers 24 free, online Continuing Medical Education (CME) courses on the diagnostics, epidemiology, immunology, symptoms, and treatment of Lyme disease, bartonellosis, and other vector-borne infections. 

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