Archive for the ‘Alzheimer’s’ Category

Finding Link Between Infection & Alzheimer’s Disease Could Be Worth $ 1 Million–Public-Health/Article/10-19/Finding-Link-Between-Infection-and-Alzheimer-s-Disease-Could-Be-Worth-1-Million/56312  Full article here

Finding Link Between Infection and Alzheimer’s Disease Could Be Worth $1 Million

OCTOBER 15, 2019

By Tom Rosenthal

WASHINGTON—If you can present persuasive evidence that a particular microbe causes Alzheimer’s disease, there’s a $1 million prize waiting for you.

“This is an award for achievement; it is not a grant,” said Leslie N. Norins, MD, PhD, FIDSA, the founder and CEO of Alzheimer’s Germ Quest, Inc. ( The nonprofit group is funding the award to encourage more intensive research on the possibility that microorganisms are the root cause of the incurable disease afflicting 47 million people worldwide, including 5.6 million Americans aged 65 years and older.

“I’ve closely reviewed the scientific literature and personally believe it’s clear that one germ, possibly not yet discovered, is the root cause of most Alzheimer’s disease,” Dr. Norins said. “But we’ll see what researchers find out.”



I posted on this a year ago when Leslie Norins, Ph.D. wrote this fantastic paper:

Alzheimer’s has had a Cabal similarly to Lyme in that research has been hijacked by a group of individuals with blinders on.  According to Norins, the 2017 Alzheimer’s Association had a conference in London where researchers from 70 countries could share progress.  A keyword index of the presentations showed the largest entries, 110, were for amyloid/APP.The next most common item was tau, the tangled protein, with 85 entries. Inflammation—the body’s reaction to something—had 45 mentions.  Presentations of germ importance had only single digit presence: prion proteins (8 entries), infectious disease (4 entries), bacteria (1 entry). Virus was not even listed as a keyword.

Yet numerous researchers have doggedly fought against the myopic focus and have found spirochetes in the brains of Alzheimer’s patients:, and Kris Kristofferson was diagnosed with Alzheimer’s but actually had Lyme disease:  Fantastic read by microbiologist Tom Grier.

New Alzheimer’s Blood Test 94% Accurate

New Alzheimer’s Blood Test 94% Accurate

Megan Brooks

August 02, 2019

A new blood test to detect brain changes emblematic of early Alzheimer’s disease (AD) has moved one step closer to reality and could be a “game changer” for the field.

Researchers found that measuring the ratio of β-amyloid (Aβ) 42 and Aβ40 in blood using a high-precision assay is 94% accurate in diagnosing brain amyloidosis, using amyloid PET or CSF phosphorylated (p-tau) 181/Aβ42 as reference standards.

“Right now we screen people for clinical trials with brain scans, which is time-consuming and expensive, and enrolling participants takes years,” senior investigator Randall J. Bateman, MD, professor of neurology, Washington University School of Medicine in St. Louis, said in a statement.

“But with a blood test, we could potentially screen thousands of people a month. That means we can more efficiently enroll participants in clinical trials, which will help us find treatments faster, and could have an enormous impact on the cost of the disease as well as the human suffering that goes with it,” he added.

The study was published online August 1 in Neurology.

Easy Screening Tool

Using an immunoprecipitation and liquid chromatography–mass spectrometry assay, the researchers measured Aβ42/Aβ40 in plasma and CSF samples from 158 older, mostly cognitively normal individuals (94% with Clinical Dementia Rate [CDR] = 0) that were collected within 18 months of an amyloid PET scan.

Plasma Aβ42/Aβ40 correlated highly with amyloid PET status (receiver operating characteristic area under the curve [AUC], 0.88; 95% confidence interval [CI], 0.82 – 0.93) and CSF p-tau181/Aβ42 (AUC, 0.85; 95% CI, 0.79 – 0.92), the researchers report.

The combination of plasma Aβ42/Aβ40, age, and apolipoprotein (APOE) ε4 status had “very high” correlation with amyloid PET (AUC, 0.94; 95% CI, 0.90 – 0.97), “suggesting that plasma Aβ42/Aβ40 may be used as a screening tool for those at risk of AD dementia,” the researchers write.

In addition, individuals with a positive plasma Aβ42/Aβ40 but negative amyloid PET scan have a 15-fold higher risk of converting to amyloid PET-positive (P = .01).

“The sensitivity of the plasma Aβ42/Aβ40 assay to amyloid PET-negative individuals who convert to amyloid PET-positive suggests that plasma Aβ42/Aβ40 becomes positive earlier than the established amyloid PET threshold used for this study,” Bateman and colleagues note in their report.

“Therefore, a positive plasma Aβ42/Aβ40 with a negative amyloid PET scan may represent early amyloidosis rather than a false-positive result in some individuals,” they add.

As reported by Medscape Medical News, the study builds on earlier work by the same researchers.


For more: researchers/

The Dementia Letters Project

Kathryne Fassbender of the Dementia Letters Project

Brittany Klaus Jul 26, 2019


Kathryn Fassbender

A passion for serving the elderly has led Kathryne Fassbender to start a dialogue about dementia to help both those living with the condition and their care partners.

At, the Wisconsin resident and certified dementia communication specialist is creating the dialogue with input from care partners, family members, medical staff, and, most importantly, the individuals living with dementia.

The letters, she says, “can be (written) to dementia, to their future self who they fear might have dementia, or to a loved one with dementia. It can be expressing those fears, sharing their story of dementia, or sharing the gifts of dementia.”

Dementia is, according to, the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to an extent that it interferes with a person’s daily life and activities.

“Dementia is an umbrella term that includes several different types of dementia with their own unique characteristics,” she says. “While dementia can take much away from one’s life, it does not take away their own experiences, joy, or spirit.”

Kathryne’s service to those affected by dementia started on a volunteer basis through middle-school service projects. She focused on aging.

“I was drawn into helping those with dementia first by finding that I connected well with individuals with dementia,” she says. By seeing the great misunderstanding her classmates had about the disease, she felt an even greater pull to work with those living with dementia.

Then in 2005 her grandmother was diagnosed with vascular dementia.

“Around that time not only was I experiencing dementia personally, but I was seeing how professionally it might evolve and become a professional vocation,” Kathryne says.

There is great healing through storytelling, and letter writing is a beautiful and easy form of storytelling.  Kathryne Fassbender

She earned her undergraduate degree in art therapy at Edgewood College in Wisconsin and interned at an adult day program that focused on dementia. From there she has gone on to work as a life-enrichment specialist and now leads dementia training workshops, works as a family consultant, speaks at conferences, and, in 2017, formed the Dementia Letters Project. Besides earning her CDCS last year, she also has earned a certificate in arts and health therapy.

Kathryne attributes the start of the Dementia Letters Project to “a couple of things colliding.”

She says she was beginning to discover people with dementia like Brian LeBlanc and Kate Swaffer who write blogs and are “calling out for people to recognize them and recognize their story and that their story is not what all medical professionals are telling us.”

“It’s not all doom and gloom, it’s not all memory loss and becoming medicalized,” Kathryne says.

She also noted family members and staff at a care community saying that they had fears about dementia but were afraid to share them and needed a platform where they could do that.

The Dementia Letters Project encourages others to share their story of dementia by writing letters for submission to or for sharing within their family.

“These letters can be written to dementia itself, to the individual’s future self, or to a loved one with dementia,” she says. “It can express fears and joys about their personal story of dementia.”

Kathryne emphasizes that these letters are not all about fears, such as worry about when a loved one might the name of their children. It is also about those moments spent together that might not have happened without dementia. The goal of the Dementia Letters Project is to build a community that is “wealthy in hope and connection” for someone with dementia as well as friends, family, and care partners. The website also includes links to resources and Kathryne’s blog.

“My hope with the Dementia Letters Project is to allow those who may not want to be a visible voice via platforms like a blog, book, or speaking engagements to still be able to share their voice,” she says. “I also want families and community members to help us deepen the reality of dementia, to share their fears, their joys, their experiences. There is great healing through storytelling, and letter writing is a beautiful and easy form of storytelling.”

Kathryne says that dementia is more than what we’re reading in news articles or seeing on TV specials. It’s not only despondency; there is also joy, hope, and light—and conveying that to families and care communities has been Kathryne’s mission over the past two years.

“We need to be visionaries and servants of the Lord to individuals with dementia, despite our own fears and misunderstandings,” Kathryne says. “We have a duty to grow in knowledge about dementia and aging so that we can better minister to others.”

At the same time, Kathryne says we must not “medicalize” someone with dementia; we cannot forget to include their faith with the sudden checklist that appears with the diagnosis—making sure they eat, sleep, are dressed, and take prescribed medication. She encourages family members, friends, and care partners to ask themselves how they can make sure that their loved ones are still practicing their faith. Encouraging someone with dementia in their faith can be as simple as singing hymns with them or saying the Lord’s Prayer together—things that are ingrained in them, firmly rooted in their emotional memory.

To someone who is struggling with dementia, Kathryne says, “Your value never decreases in God’s eyes, and your ability to grow in faith never ceases.”

Kathryne spreads awareness and builds bridges by speaking at conferences. She realized there was a need for people who aren’t medical professionals but who are working with someone living with dementia to “enter the public speaking round.” She describes the medical community as being very “siloed,” especially when it comes to aging and dementia. Doctors and nurses will be in one silo and think they’re right, while academic researchers will be in their separate silo, and then those who take a more creative approach to dementia care will be in their silo.

“We need more bridges,” Kathryne says, “because we’re not really going to break the barrier of where we are right now with knowledge of dementia until we start communicating with each other and learn how to put our language into another person’s language, and then be able to share that with families. That’s where I am—trying to figure out that spot, that in-between spot, that can put medical research and creative aging language into layman’s terms.”



Please remember that both dementia and Alzheimer’s can be caused by Lyme/MSIDS. Deal with the infections and you can often gain cognitive ability back:  Within this article, Dr. Marc Siegel explains on ‘Fox & Friends’ how Kris Kristofferson was diagnosed with Alzheimer’s but actually had Lyme Disease.  (Warning:  the news reporter propagates a myth that “One antibiotic,” prophylactically will cure LD if used early.)

Does Alzheimer’s Disease Stem From Infection? Scientists Debate & One Company Targets Gingivitis Bacterium to Slow Alzheimer’s Progression

Does Alzheimer’s Disease Stem From Infection?

Scientists debate, and one company targets gingivitis bacterium to slow Alzheimer’s progression

LOS ANGELES — Is there an infectious link to Alzheimer’s disease?

That’s a question of debate, and opinion was divided at the 2019 Alzheimer’s Association International Conference (AAIC) now underway here.

“Ideas in this area of research are still evolving; there is now growing evidence that microbes such as bacteria and viruses may play a role in degenerative brain diseases such as Alzheimer’s,” said Maria Carillo, PhD, chief science officer of the Alzheimer’s Association.

New research suggests infectious agents may be triggering immune reactions related to plaques and tangles and that loss of cognitive function in Alzheimer’s disease may stem from several different disease processes in the brain, not just one, she added.

A common virus coupled with a genetic factor — namely herpes simplexvirus 1 (HSV-1) and the APOE4 gene — can create a major risk for Alzheimer’s disease, noted Ruth Itzhaki, PhD, of the University of Manchester in England. The viral concept of Alzheimer’s proposes that HSV-1 in the brain of APOE4 carriers accounts a high percentage of Alzheimer’s cases. It postulates that HSV-1 travels to the brain earlier in life and establishes a latent infection that, when activated, “leads to viral damage in infected cells and viral-induced inflammation,” she said.

Recent studies have found an increased abundance of human herpesvirus6A (HHV-6A), HHV-7, HHV-6B, and HSV-1 in post-mortem Alzheimer’s disease brains, said Ben Readhead, MBBS, of Arizona State University in Tempe.

“These findings indicate that these species are capable of perturbing host cellular networks that are central to the pathogenesis of Alzheimer’s disease and offer testable hypotheses to guide further evaluation of the pathogen hypothesis of Alzheimer’s,” Readhead noted.

But associations seen in laboratory and epidemiological studies do not demonstrate causality, “and in fact, reverse causation must be considered more likely,” said Todd Golde, MD, PhD, of the University of Florida in Gainesville.

While neurodegeneration or other states “may very well enable slight reactivation of latent viruses present in many human brains” and there’s strong evidence that an additional hit from an infection can impair cognition, there’s no evidence for causality, he observed. “Trying to pin an infectious origin of Alzheimer’s disease on a virus or a bacteria may distract the field from more impactful research,” he said.

And open questions still need to be answered, said Michael Heneka, MD, PhD, of University Hospital Bonn in Germany. “The precise time point in the pathogenesis of Alzheimer’s at which bacteria may enter the brain needs to be determined, since these phenomena may present just late-stage events,” he said. “Furthermore, it remains elusive how bacteria would overcome the intrinsic innate immune defense of microglia that usually shield the brain from such invasion.”

One group looking for a causal link is testing whether targeting Porphyromonas gingivalis bacteria can slow or halt the progression of Alzheimer’s disease. In the GAIN trial, researchers from the biotech company Cortexyme are studying COR388 — an oral agent that inhibits gingipain proteases secreted by P. gingivalis, the culprit behind degenerative gum disease — in people with mild to moderate Alzheimer’s disease.

Earlier research identified the bacterium in brains and cerebrospinal fluid of people with Alzheimer’s disease, said Michael Detke, MD, PhD, Cortexyme’s chief medical officer, who reviewed the science behind the study at AAIC. Moreover, levels of gingipain proteases correlate with tau and ubiquitin pathology, Detke told MedPage Today.

Studies of wild type mice showed that oral infection with P. gingivalis invaded the brain and led to plaques, inflammation, and the loss of hippocampal neurons — effects which were blocked when the animals received COR388.

The drug was rapidly absorbed and well-tolerated in a phase I study of 24 older healthy volunteers. A smaller study of nine people with Alzheimer’s disease — six taking COR388 and three taking placebo – showed patients treated with the drug trended toward better memory scores and exhibited improvements in verbal skills, using more prepositions in their speech patterns over 28 days.

People taking COR388 also had reduced protein fragmentation and roughly 30% lower levels of inflammation, Detke said. The phase II/III GAIN trial in 570 Alzheimer’s patients in the U.S. and Europe is underway, with ADAS-Cog11 change at 48 weeks as the primary endpoint. Top-line results are expected late in 2021.

Itzhaki and Readhead reported no disclosures. Heneka reported relationships with IFM Therapeutics, Alector, Schering, Pfizer, Novartis, Roche, Abbvie, and Biogen, and is a co-inventor on patents and patent applications relating to Alzheimer’s diagnostics and therapeutics. Golde reported relationships with ProMIS Neuroscience, Eli Lilly, Novartis, Bristol Myers Squib, Abbvie, Lundbeck, Biogen, and Pfizer; he is a co-inventor on multiple patents and patent applications relating to Alzheimer’s therapeutics. Detke is an employee of Cortexyme.


For more: researchers/

Lyme, Alzheimer’s, Enbrel – New Potential Treatment

Thursday, June 6, 2019

By Dr. Jaller

Lyme, Alzheimer’s, Enbrel — New Potential Treatment


I have learned that most people want a simple sound bite answer or conclusion. The edges of medicine always operate in the grey and nuanced.

It has long been dogma in Lyme circles that immune suppressing drugs, e.g. Enbrel are very dangerous and should not be used.  The same is true with prednisone.

I have patients who get the occasional injection by their rheumatologist; joint pain gets better and they are no worse for the wear.

The drug is used for psoriasis amongst other many other conditions. The drug has serious side effects: its use should not be taken lightly.

A study suppressed by Pfizer, brought to light by the Washington Post, was based on insurance company data considering outcomes of  hundreds of thousands of patients and found those taking Enbrel had a 64% decrease in the incidence of Alzheimer’s disease. 

Enbrel impairs the function of TNF alpha, a master cytokine responsible for trafficking immune cells.

Pfizer did not make the disclosure because: a generic version will be  available.  A shiny new, me-too drug promoted heavily by pharm reps costing obscene amounts of money will take its place. Doctors will be given shiny data, along with lunch, proving equivalency? with the old drug.

The myth that generics are poor (dangerous) and lack quality control may be resurrected.

Watch out for first year generic prices: cute trick. For the first year a single company is given a monopoly and only required to reduce the price by 20%.  “See, the generic is almost as cheap as the brand,” the rep will inform a doctor. This is a bad pro big-pharma rule passed by Congress decades ago I’m sure) by the way. Cheap is a relative term.

The pharmaceutical giant, Pizer has excuses, reasons why it withheld the data, for example, they  claimed the data is wrong because of biological plausibility: the molecule is too large to cross the blood brain barrier.

Really? I care if the molecule gets into the brain; maybe it’s an advantage.  The brain has its own immune system which needs to be tweaked lightly. Ask anyone who has had a brain Herxheimer reaction knows. The Cytokine storm which may make you crazy results from peripheral cytokine reactions/overproduction primarily.  And there is no data the molecule cannot get into the brain. Cytokines get in the brain.

Alzheimer’s is in part motivated by inflammation. Other major factors are: production of amyloid beta protein (AB) (plaques and tangles), genetic factors and multiple external factors.

It is thought that AB protein is a naturally occurring antibiotic which responds to inflammation. Discussed elsewhere. Lyme resides in the brain along with many  bacteria, viruses, protozoans. It is true that spirochetes have been reported to aid in the transportation of AB into the brain.  Infection (or colonization) may be omnipresent and therefore not the whole story — or the most critical piece.

The vast majority of my patients present with cognitive complaints. Many or most Lyme patients, at one time or another fit the criteria for a disorder call MCI, minimal cognitive impairment. The mainstream medical community considers this a pre-Alzheimer’s condition, often.

What’s a Lyme patient to do?

First off, if symptoms completely resolve with usual therapy do nothing.

If you are a patient who has had very aggressive therapy, e.g. months of IV antibiotics and cognitive symptoms persist, look up MCI and consider the following:

Get an AB PET. The tests measures metabolic activity in the brain and the presence of early AB protein deposition. IF the test is positive you are at very high risk for developing Alzheimer’s.

Prednisone and Enbrel have largely been seen as dangerous because patients are misdiagnosed and not also treated for Lyme. Enbrel is likely tolerably safe, in many cases, considering benefit to risk ratio.

A lot of money has been spent searching for an Alzheimer’s cure. To no avail. Nothing very promising in the literature.

I for one am very angry with Pfizer. I suppose it is typical behavior in the industry. We still need big pharma. Don’t throw out the baby with bathwater. Hold them accountable. But, do not  conclude big pharma is corrupt therefore all drugs developed through the system are fruit of a poisoned tree and are therefore inherently untrustworthy and dangerous — in addition to being immorally overpriced.

It’s a bad syllogism. Drug companies are a very necessary evil.

Getting back to Enbrel.  Is this a silver bullet?.  More comment, biostatistics and analysis are required as well as prospective RCT medical studies. Since the drug will be generic soon big pharma will not finance the research. Fortunately, Alzheimer’s, a burgeoning epidemic as our population ages, is well funded through private sources.

Ideal prospective studies, which will likely be done make observations moving forward starting with a baseline current population. The process is slow.

Retrospective, population studies, primarily manipulation of data already there will not take long. These studies are never as good as prospective studies but perhaps good enough.

If you want my  bottom line: don’t run out and get Enbrel– YET.

I am not endorsing the use of the drug for any medical condition, including Alzheimer’s. This site is for informational purposes only. Medical care can only be delivered by a certified medical practioner who properly evaluates your particular issues. Please don’t diagnose or treat yourself Dr. Jaller’s practice is in Maryland
Regarding immune suppressants, many LLMD’s use them IF the patient is also on antimicrobial therapy at the same time. This tandem usage will protect the patient from a worsening infection(s), be it Lyme or any of the coinfections or even a latent infection.
Talk with your doctor about all treatments.

Response From Dr. Paul Auwaerter Regarding the IDSA Grant (Part 2)

Response from Dr. Paul Auwaerter regarding the IDSA grant (Part 2)

JUL 5, 2019 — 

Please see today’s letter to the TBDWG…….

———- Original Message ———-
Cc: (98 Undisclosed recipients)
Date: July 5, 2019 at 9:07 AM
Subject: NEW: Response from Dr. Paul Auwaerter regarding the IDSA grant to search for an infectious cause of Alzheimer’s disease.

July 5, 2019

The IDSA Foundation
1300 Wilson Boulevard Suite 300
Arlington, VA 22209
Attn:  Paul Auwaerter, vice chair of the IDSA Foundation

Dear Dr. Auwaerter,

Lyme disease is recognized as the fastest growing vector-borne infectious disease in the United States with an estimate of over 300,000 new cases yearly. [i] It is imperative that at least one (or more) of those $100,000 IDSA Foundation grants is earmarked for research related to Borrelia infections and possible connection to Alzheimer’s disease.

Rheumatic fever as you know is a consequence of untreated strep throat leading to irreversible heart disease. We have evidence that untreated Lyme is just as destructive as Dr. Neil Spector’s untreated Lyme infection required a heart transplant.[ii]  Kris Kristofferson’s untreated Lyme led to a misdiagnosis of Alzheimer’s disease [iii] and Dr. Vincent M. Tedone has identified Lyme in his daughter’s neurodegenerative ALS diagnosis. [iv]

Personal Health; When Lyme invades the brain and spinal system.

By  JANE E. BRODY FEB. 15, 1995


Focusing on the acute stage of Lyme disease after early treatment misses the horribly disabled who have gone months, years or decades before diagnosis and it’s time to recognize this fault in the science.

Subjective symptoms after treatment of early Lyme disease.
Gary Wormser, New York Medical College Jan 2010

It is common knowledge that Dr. Allen Steere has had a career long fixation on the swollen arthritic knee presentation of Lyme disease.

“Charting the scope of Lyme disease”
Marisa Venegas, New York Times 1988 Accession number 30957138

Quote from Dr. Raymond Dattwyler:

“This disease can involve virtually every organ system of the body, Dr. Dattwyler said. It makes sense to look at this as a whole-body disease, rather than narrowly. In syphilis, which is a similar spirochetal illness in some ways, there is also arthritis. If I concentrated on that aspect of syphilis, it would be ludicrous….”

And then there is this paper from Dr. Robert Bransfield…..

Aggressiveness, violence, homicidality, homicide, and Lyme disease  Oct 2017


Dr. Auwaerter,

It is imperative that research continues in the area of Borrelia infections and possible connection to Alzheimer’s disease and I must insist that funding be restricted from the researchers who are identified as defendants in the racketeering lawsuit as these individuals clearly have a conflict of interest.

The following list of additional references was recently brought to my attention:

Alzheimer’s disease, dementia, Parkinson’s disease, brain atrophy caused by spirochetes and other pathogens of infectious diseases

Respectfully submitted,

Carl Tuttle

Lyme Endemic Hudson, NH

Cc: Tick-Borne Disease Working Group


[i] Data and Surveillance
[ii] Doctor Hopes His Medical Journey Inspires Others
[iii] “A Slow Slipping Away”— Kris Kristofferson’s Long-Undiagnosed Battle with Lyme Disease
[iv] A Revolutionary Idea: Bacteria Causes Neurodegenerative Conditions–nerve-disease.html


On July 3, 2019 at 8:12 AM Paul Auwaerter <> wrote:

Dear Mr. Tuttle,

The grants for research are evaluated by an independent scientific review board. I do not sit on this board, and I cannot speak for them. The IDSA Foundation encourages applications, and we do not exclude any pathogen.  I expect the grant awards to be highly competitive.


Paul G. Auwaerter, MD

Vice Chair, IDSA Foundation
Sherrilyn and Ken Fisher Professor of Medicine
Clinical Director, Division of Infectious Diseases
Johns Hopkins University School of Medicine
Baltimore, Maryland USA

Assistant: Stephanie Knight


T: 443-287-4800

F: 410-502-7029

Personal Health; When Lyme invades the brain and spinal system.
Meanwhile, within weeks of entering the body, the spirochete, a bacterium that resembles the organism that causes syphilis, can…

Pathology Lecture On Lyme Disease in Human Brains – Microbiologist Tom Grier  (Sign up here)

Pathology Lecture Lyme disease in Human Brains

Tue, May 21, 6:00 PM – 8:00 PM

Event details

Tuesday May 21st, 6 PM Superior Library all are welcome FREE! This is a lecture on human brain research looking for the Lyme bacteria in Alzheimer’s brains. Several local cases will be discussed. (This is not a Lyme prevention lecture.) The family of bacteria that causes Lyme disease has been known for 100+ years to enter the human brain. Yet no tax dollars have ever been spent to study the effects of Lyme disease in the human brain. We have images of both Borrelia miyamotoi and Borrelia burgdorferi forming biofilms inside amyloid plaques in Alzheimer’s brains.

Please bring your friends for coffee and cookies and a medical discussion on cutting edge research. Lyme disease is not the easily diagnosed and easily treated disease that we have been told about, it is found inside human cells including neurons, and behind the blood brain barrier where blood tests cannot detect it, and the new species of Borrelia are not detected by any tests. For more photos email me at Not recommended for young kids to attend. Nothing is being sold or promoted accept new research. Tom Grier



If you are able to attend this lecture, I highly recommend it.  Tom has done amazing work and has uncovered many important aspects of this disease(s) that mainstream medicine is frankly ignoring.

For more: