could alzheimer’s disease be caused by a brain infection?


Infectious Alzheimer's

“Alzheimer’s disease accounts for 60 to 70% of cases of dementia, with an estimated 5 million cases in the US currently. The number of cases in the US is expected to exceed 13 million by 2050, with over 105 million cases worldwide in the next 40 years. Efforts to develop effective pharmaceutical treatments have been futile.  In addition to the hallmark pathological findings in Alzheimer’s, including amyloid plaques, neurofibrillary tangles, tau proteins, and neuronal degeneration, evidence of inflammation is often found. The DNA of herpes simplex virus 1 has also been found to co-localize with amyloid plaques. This possibly spurious finding does not stand in isolation. Indeed, a recent research article documenting microbial infections in animal models of Alzheimer’s disease published in Science Translational Medicine and an editorial published in the Journal of Alzheimer’s Disease by an international consensus group of 33 physicians and scientists presents extensive research evidence from over 100 studies and calls upon the neurological and medical communities to re-examine the bias against an infectious etiology for AD.”   Dr. Theodore Henderson (MD / Ph.D) from a 2016 issue of Neurology Advisor (Could Alzheimer’s Disease be Caused by Infections?)

“The things creeping around in the brain will scare the heebie-jeebies out of you.”  Dr. Robert Moir of the Brain Microbiome Project, in an article discussed at the end of today’s post from the Harvard Gazette

Even though many people are hearing about it for the first time thanks to Bret Stetka’s article from Sunday’s edition of NPR (Infectious Theory Of Alzheimer’s Disease Draws Fresh Interest), it’s not really news that growing numbers of prominent physicians and scientists believe ALZHEIMER’S DISEASE is caused by an infection of the brain.  Stetka states….

“This “germ theory” of Alzheimer’s… has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.  If the germ theory gets traction, even in some Alzheimer’s patients, it could trigger a seismic shift in how doctors understand and treat the disease.”

Two of the studies used as “proofs” for Alzheimer’s as an infectious disease are downright creepy when you start thinking about them.  Both studies were published in 2010, the first in the Journal of the American Geriatric Society (Greater Risk of Dementia when Spouse has Dementia? The Cache County Study), and the second in the Journal of Neruosurgery (Cause-Specific Mortality Among Neurosurgeons)

In the first study, out of almost 2,500 couples looked at that developed DEMENTIA while living in a rural county in Utah…   “Husbands’ baseline ages averaged 75.7 years, while wives’ age averaged 73.1 years.  Duration of marriage at baseline averaged 49 years, with only 3.8% of couples married for less than 10 years, and only 5% married for less than 20 years.  Subjects were followed for up to 12.6 years.  Our results are consistent with other studies demonstrating cognitive deficits in spouses of persons with dementia. We found a clear increased risk of incident dementia among older adults whose spouses have dementia.  A subject whose spouse experienced incident dementia onset had a six-fold increase in the hazard for incident dementia compared to subjects whose spouses were dementia free.”  Did you catch that? Six-fold or 600%.  But as scary as that is, it’s not as jaw-dropping as the study on neurosurgeons.

The single most complex of all the medical specialties is neurology.  And within neurology, neurosurgery is the toughest.  In other words, these are individuals whose cognitive ability, decision making skills, and physical coordination is the pinnacle of their profession.  For this study, cause of death was determined for 94% of the neurosurgeons that died between 1979 and 2005.  “A total of 7562 neurosurgeons practiced in the US during the period from 1979 through 2005. Of these, 755 died during the study period.”  The authors then looked at the number of deaths due to specific causes (Alzheimer’s, PARKINSION’S, CANCER, heart attacks, plane crashes, murder, etc, etc) in the neurosurgeons to the number of deaths caused by the same entity within the general population.  In the case of Alzheimer’s, it was seven times greater in neurosurgeons.  Listen to their explanation.  “With regard to Alzheimer disease and other degenerative neurological disease, it is difficult to associate the increased incidence with any known environmental exposure.”  In other words, there was none, other than the fact that as you’ll see in today’s post, we are increasingly seeing that exposure to germ-infected nervous tissue itself is a risk factor.

What makes this last study all the more interesting is that it essentially flies in the face of a study published just days ago in JAMA Open (Adolescent Cognitive Aptitudes and Later-in-Life Alzheimer Disease and Related Disorders) showing that individuals who have lower aptitude and cognition in early life tend to end up with Alzheimer’s later in life — something that’s been seen in studies since the early 1920’s.  However, in neurosurgeons who spend significant amounts of time exposed to neurological tissues of those with Alzheimer’s, we see that this doesn’t hold true.  The question now becomes, what is the mechanism for infectious Alzheimer’s?  Listen to this totally CHERRY-PICKED paragraph from the website of the Alzheimer’s Society (Infections & Dementia)……..

“Some of the infections that are thought to be linked to Alzheimer’s include oral herpes,  pneumonia and infection with spirochete bacteria  (the type which cause Lyme disease and some types of gum disease).  There have also been links between Alzheimer’s disease and other infections that cause a long-term activation of the immune system, a process known as chronic inflammation.  The blood-brain barrier protects the brain by controlling what substances can pass from the blood into brain tissue. In Alzheimer’s disease, the blood-brain barrier is damaged, particularly in the brain region affected by Alzheimer’s.  Evidence  suggests that inflammation, the Alzheimer’s hallmark amyloid protein and the ApoE4 gene, which are all linked to Alzheimer’s disease, can contribute to the breakdown of the blood-brain barrier. Once it has been weakened, bacteria, viruses, and other harmful substances can get through into the brain more easily.  If infectious bacteria, viruses or fungi reach the brain they can activate special immune cells in the brain called microglia. When microglia are activated, they can cause inflammation in the brain. This type of inflammation is thought to be involved in the progression of dementia by causing nerve cell death. There is also some evidence that inflammation in the body caused by chronic infections like gum disease can cause inflammation in the brain. Because the blood-brain barrier of people with Alzheimer’s is leakier than normal, one theory is that active immune cells and the substances involved in the body’s inflammatory response can get through into the brain.  This causes the brain’s own immune cells to activate, leading to inflammation and possibly death of brain cells. Brain inflammation can also make the blood-brain barrier even leakier, allowing more of the body’s immune cells through and starting a vicious cycle of damage.” 

Allow me to break this down for you.  Under certain EPIGENETIC conditions we’ll talk more about momentarily, infections of various sorts can attack the vessels around the brain that make up the blood/brain barrier, causing something I refer to as “THE LEAKIES” (in this specific case, ‘Leaky Brain Syndrome’).  The microbes then attack the brain itself, where they activate MICROGLIA, causing nerve cells in the brain to both degenerate and even die.  Left unchecked, the process feeds itself causing even more inflammation, which turns the vicious cycle even faster.  The end result is a degradation of motor skills, cognition, emotions, language, etc, etc, etc, that will eventually lead to death.  It’s yet another example of inflammation leading to fibrosis, and fibrosis being the number one cause of death in America (HERE), responsible for almost half our our national mortality.

Naples, Florida is not only home to the famous neurologist and author of Grain Brain, DR. DAVID PERLMUTTER, it’s also where Dr. Leslie Norins lives.  Dr. Norins got his BS from Johns Hopkins in 1958, his M.D. from Duke four years later, and his Ph.D. from the University of Melbourne where he studied immunology with the Nobel Laureate, Sir MacFarlane Burne.  In January of this year, he offered a one million dollar prize to whoever can “provide persuasive evidence” that virus, bacteria, fungi, or other infectious agents are behind our national explosion of Alzheimer’s Disease. Since Dr, Norins is the unquestioned leader in this line of research, you may want to read his article that contains the “Top Ten” reasons he believes Alzheimer’s is an infectious disease (It’s Time to Find the “Alzhiemer’s Germ”).  Be assured, however, that Norins is far from alone in his assertions.  Let me take you through just a tiny bit of what we’ve seen over the past decade.

In 2009 a team of Canadian researchers published a study titled Alzheimer’s Disease and Infection: Do Infectious Agents Contribute to Progression of Alzheimer’s Disease? in the journal, Alzheimer’s & Dementia.  They concluded that, “Infection with several important pathogens could constitute risk factors for cognitive impairment, dementia, and Alzheimer’s disease (AD) in particular. This review summarizes the data related to infectious agents that appear to have a relationship with AD. Infections with herpes simplex virus type 1, picornavirus, Borna disease virus, Chlamydia pneumoniae, Helicobacter pylori, and spirochete were reported to contribute to the pathophysiology of AD or to cognitive changes. Based on these reports, it may be hypothesized that central nervous system or systemic infections may contribute to the pathogenesis or pathophysiology of AD, and chronic infection with several pathogens should be considered a risk factor for sporadic AD.”  Interesting; particularly the part about H. PYLORI.  By the way, Herpes Type I is the virus responsible for cold sores.

In 2011, a group of five physicians working at Philadelphia’s Center for Chronic Disorders of Aging published a scientific paper in Intech Open (Evidence for an Infectious Etiology in Alzheimer’s Disease) that discussed the discovery of the disease by German psychiatrist / neurologist, Aloysius Alzheimer, (1864-1915).  “The possibility of an infectious etiology of several chronic diseases, including Alzheimer′s Disease, has long been debated. More than a century ago Alois Alzheimer studied neurological infection with Treponema pallidum, the causative agent of syphilis, a spirochete later associated with dementia in 1913. There are many chronic diseases for which there is strong evidence of an infectious etiology, and numerous chronic diseases for which there is suspicion of infection as the etiologic agent for that disease.”  As you can see, the infectious theory of Alzheimer’s is nothing new.  BTW, the tables that show the diseases known to be and thought to be caused by chronic infection are shocking.

Dr. Emily Deans of Evolutionary Psychiatry, writing for Psychology Today (Could Alzheimer’s Dementia Be Caused by a Virus?) stated, “The whole theory is based on the following premise: there’s a continuous, chronic infection supplying persistent live microorganisms, and their toxic products stimulate the host’s (that’s you) inflammatory response.  The pathogen itself damages the neurons, and the brain’s inflammatory response also damages the neurons.” Some of the pathogens she specifically mentioned that I have not already mentioned include CMV / EBV, Herpes Simplex 6 (the cause of Roseola, not to be confused with ROSACEA) and HIV.  The chief inflammatory mediators?  They are some of the biggest of the big-hitters in their class; IL-6, TNF-ALPHA, and iNOS.  So, regardless of Alzheimer’s cause (many scientists now refer to it as Type III Diabetes), inflammation is always a player.  Also compare what she says about the occult (hidden) nature of these infections to the chronic infections associated with ROOT CANALS, remembering that herpes virus’ (for instance, chickenpox) can hide in nerve roots for decades, reemerging later as SHINGLES if immunity is compromised by stress.

“The ability of a host (you, or me) to handle an infection depends on genetic, dietary, and other environmental factors such as age, stress, and immune status.  Viruses, parasites, and bacteria are sneaky – I daresay sneakier even than Homo sapiens, and the closeted nerve cells are a perfect place for an unnoticed infection to simmer for decades.  Microorganisms can continuously release toxins, leading to chronic inflammation and damage.  Treating a chronic infection and boosting a healthy immune system could possibly be a useful way to fight a number of neurodegenerative diseases, even Alzheimer’s.”

I mentioned CMV (Cytomegalo Virus) earlier (it’s strongly associated with EBV or Epstein Barr Virus), both of which cause mononucleosis.  In 2014 the Journal of Infectious Diseases (Cytomegalovirus Infection and Risk of Alzheimer Disease in Older Black and White Individuals) made some interesting correlations to CMV and several diseases, Alzheimer’s included.  “Human cytomegalovirus (CMV) is prevalent in older adults and has been implicated in many chronic diseases of aging.  These results suggest that CMV infection is associated with an increased risk of Alzheimer’s Disease and a faster rate of cognitive decline in older diverse populations.

In 2015, Australian researchers analyzed 25 high quality studies on the subject of Alzheimer’s as an infectious disease, coming to some conclusions of their own, which were later published in the Journal of Alzheimer’s Disease (Bacterial Infection and Alzheimer’s Disease: A Meta-Analysis).  Here are some scary excerpts from the study’s abstract.

“The possibility of an infectious etiology for Alzheimer’s disease (AD) has been repeatedly postulated over the past three decades.  We found over a ten-fold increased occurrence of AD when there is detectable evidence of spirochetal infection and over a four-fold increased occurrence of AD in a conservative risk estimate. We found over a five-fold increased occurrence of AD with Chlamydophila pneumoniae infection. This study shows a strongly positive association between bacterial infection and AD.”

2016 saw a group of 31 scientists and physicians from some of the world’s most elite universities and research facilities publish a study in IOS Medicine (Microbes and Alzheimer’s Disease) concluding, “AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic.

ARS Technica published an article by Dr. Beth Moles (Brain Infections May Spark Alzheimer’s, New Study Suggests) that broke down a study from Science Translational Medicine titled Amyloid-β Peptide Protects Against Microbial Infection in Mouse and Worm Models of Alzheimer’s Disease, in which she referred to the beta amyloid plaques (Aβ) as “microbial booby traps” as opposed to something that’s historically been seen as an abnormal or pathological finding.   From the abstract…..  “Aβ and its propensity for aggregation are widely viewed as intrinsically abnormal. However, in new work, Kumar et al. show that Aβ is a natural antibiotic that protects the brain from infection. Most surprisingly, Aβ aggregates trap and imprison bacterial pathogens. It remains unclear whether Aβ is fighting a real or falsely perceived infection in AD. However, in any case, these findings identify inflammatory pathways.”  In other words, whether the brain is actually fighting an infection or simply thinks it is, these plaques grow as they trap bacteria, virus, and fungus in the brain.

Another freaky study was published in 2016, in the July issue of Clinical Infectious Diseases (Seroprevalence of Toxoplasma Gondii Infection in Patients with Alzheimer’s Disease).  Although the average person has never heard of TG (A PARASITE), listen to these conclusions.  “Toxoplasmosis is one of the most important diseases in humans and animals. Almost one-third of the human population around the world is infected with toxoplasmosis. The agent of this parasitic disease is a protozoan called Toxoplasma gondii (T. gondii) that causes encephalitis in people with suppressed immune systems and abortion, mental retardation and chorioretinitis in the fetus. Alzheimer’s disease (AD) is the most important neurodegenerative disease. Higher prevalence of T. gondii in patients with AD compared to controls showed the possible impact of this parasite in AD, which may exacerbate symptoms, and this requires special attention of specialists and patient families.

Remember when I hinted earlier that Alzheimer’s might not only be infectious, but may be far more transmissible between humans than ever dreamed?  The oldest scientific publication in America, Scientific American, published a piece by Dr. Alison Abbot titled The Red Hot Debate About Transmissible Alzheimer’s, based on an article she had written for Nature, called More Evidence Emerges for ‘Transmissible Alzheimer’s’ Theory.  In her article she desceibed Dr. John Collinge as studying the brains of four deceased individuals who had received injections of HGH from cadavers that had been infected with the virus that causes Creutzfeldt–Jakob Disease, which is a deadly neurological disease somewhat related to “Mad Cow” (about 1 in a million people die of CJD in the US each year).  Listen to what Mole said….

“For Collinge, the reason that these brains looked extraordinary was not the damage wrought by prion disease; it was that they were scarred in another way. ‘It was very clear that something was there beyond what you’d expect,’ he says. The brains were spotted with the whitish plaques typical of people with Alzheimer’s disease. They looked, in other words, like young people with an old person’s disease.  If true, that could have far-reaching implications: the possibility that ‘seeds’ of the amyloid-β protein involved in Alzheimer’s could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures.”

The landslide continued right on into 2017.  Listen to the words of a group of Polish researchers, writing in Current Neuropharmacology (The Infectious Etiology of Alzheimer’s Disease).  “Inflammation is a part of the first line of defense of the body against invasive pathogens, and plays a crucial role in tissue regeneration and repair. A proper inflammatory response ensures the suitable resolution of inflammation and elimination of harmful stimuli, but when the inflammatory reactions are inappropriate it can lead to damage of the surrounding normal cells.”  Above and beyond the microorganisms we’ve already talked about, they mentioned Herpes Simplex 2 (most commonly associated with genital herpes), Hepatitis C, and a couple of types of bacteria found in chronic oral infections such as gingivitis and periodontal disease (HERE).

What have we seen this year — 2018? First, in June, a group of 15 researchers published a study in Neuron titled Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus, that showed not only several strains of the herpes virus in Alzheimer’s brains, but that their DNA had actually been incorporated into the neuronal DNA of affected parts of the brain, causing a myriad of downstream consequences, including increased amyloid plaques in “epigenetically” susceptible individuals.

Then in July, a groundbreaking study was published in Frontiers in Aging Neuroscience (16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain) that used some extremely complicated technology to show how neuroinflammation responsible for neuronal degeneration and death is coming from microorganisms that manage to make their way into the brain.  Providing yet another example of “Leaky Brain Syndrome” (see earlier link), Science Daily (Bacteria Found in Alzheimer’s Brains) said of this study…..  “The brain is normally sealed behind specialized blood vessels that make it very difficult for things like bacteria in the blood to enter. However, at least one of the genetic risk-factors for Alzheimer’s disease may cause these blood vessels to lose some of their integrity, which could allow bacteria to enter and colonize the brain.”  What bacteria did they find that we have not mentioned already?  Shigella, E. Coli, and Salmonella, along with the tell-tale sign of gram negative bacteria; the portion of the outer membrane known as lipopolysaccharides / endotoxins (HERE).

Finally, there was an astounding study from Frontiers in Aging Neuroscience titled It’s Never Too Early or Too Late—End the Epidemic of Alzheimer’s by Preventing or Reversing Causation From Pre-birth to Death.  The gist of the study?  Infections, both viral and bacterial, are picked up by the fetus because mom became infected.  These organisms remain dormant or hidden (occult) for decades, until individuals start going through something known as IMMUNOSENESCENCE” — age-related decline of the immune system that also happens to be associated with increased inflammation.  Once these bacteria or virus are acted upon by EPIGENETIC FACTORS, the diseases begin to manifest themselves visibly.  Check out the summary of this amazing study that was done by a couple of researchers with degrees from Harvard / MIT.

“Sub-optimal health and chronic inflammation predisposes individuals to opportunistic infections and a myriad of diseases throughout the continuum of life provide information about risk and susceptibility to future Alzheimer’s disease. Poor health status, periodontal diseases, congenital infections, depression, diabetes, eye diseases, to name a few, provide a roadmap of progression towards neurodegenerative disorders. Fundamental to the onset and propagation of all these diseases is immune system immaturity, dysfunction and senescence that facilitate proliferation of opportunistic infection. Clinically, medicine must change its paradigm of managing disease symptoms and adopt a proactive approach of testing for immune health status, by way of biomarkers of inflammation, to identify those at risk of future Alzheimer’s and other chronic diseases.”

The authors, like the folks who recently declared war on heart attacks (HERE), went on to claim that “PREVENTION” could cut Alzheimer’s incidence by half.  The problem is, as we’ve seen over and over again, prevention, in the way that the medical community thinks of it, doesn’t work.  At all (HERE).  Honestly thought, forget about expensive “testing” for INFLAMMATION because I’ve already provided my patients and readers the world’s simplest DIY home test for determining whether you are likely inflamed (HERE). 

The question then becomes, what are you going to do about it, because anti-inflammation drugs have been proven to have more side effects than you can shake a stick at (HERE and HERE).  Furthermore, even though lots of these studies are talking about more immunizations to somehow stop these microbes from taking hold in our bodies, I would argue that VACCINES are a significant factor in the inflammatory process (HERE) as well as a major player in why our collective immune systems are, in the words of these authors, “immature” even in old age.  It’s the result of immune systems that are never allowed to develop normally because we are now vaccinating against everything under the sun (HERE).  Not surprisingly, this leads to immune systems that become “BOOSTED / JACKED / HYPED,” which in turn frequently leads to autoimmunity and neuroinflammatory / neurodegenerative conditions.  Case in point is the undeniable explosion of all neurological diseases, from AUTISM to Alzheimer’s.

The next question that must be answered is how to reconcile the infectious theory of Alzheimer’s with the Type III Diabetes theory of Alzheimer’s (DIABETES OF THE BRAIN) that I left links to earlier?  Alvin Powell, writing in the May 11, 1017 issue of the Harvard Gazette (Probe of Alzheimer’s Follows Paths of Infection: Starting With Microbes, Harvard Researchers Outline a Devastating Chain of Events) attempts to do just that in this short paragraph.

“This explanation would fill a significant blank in our framework for the causes of Alzheimer’s disease, create a new understanding of amyloid beta’s role in the body, and possibly open new fronts for treating or preventing the condition by attacking infection before plaques begin to form.  It also has the potential to lump Alzheimer’s with diabetes and other autoimmune diseases in which a revved-up immune system goes too far and turns on the body. Scientists have already noted enough similarities between Alzheimer’s and diabetes that some have wondered whether Alzheimer’s should be thought of as ‘type 3 diabetes.'”

The gist of his article is as follows.

  • Amyloid isn’t as bad as once thought and is not really the culprit (remember the study showing that it actually acts as a microbial “trap“?).
  • There are numerous indications that Alzheimer’s is yet another of the myriad of AUTOIMMUNE DISEASES that have literally “EXPLODED” across the Westernized world.
  • Alzheimer’s that’s purely “genetic” (“Familial Alzheimer’s“) accounts for about 5% of all cases; the other 95% are known as “Sporadic Alzheimer’s“).
  • Epigenetics are much more important than genetics (HERE), a factor I’ve tried to beat into my reader’s heads for years (“A variant of the gene APOE has been identified as a risk factor in sporadic Alzheimer’s. But having the variant doesn’t make the disease inevitable, and not having it doesn’t rule it out. Which has left scientists wondering what other non-genetic factors are at play.“)
  • The idea that Alzheimer’s disease might be caused by infection isn’t new.
  • When all is said and done it might be that Alzheimer’s is a ‘dysbiosis’ of the brain, a sign that the microbiome is out of whack.

Quite interesting in light of what you’ve seen regarding what I’ve shown you in the past regarding both MICROBIOME and DYSBIOSIS — both of which have the propensity to lead to incredible numbers of problems, including —- “The Leakies” that were mentioned several times in today’s post.  Oh; and lest you forget, all infections, dysbiosis included, are fed by sugar (HERE), which also happens to feed cancer (HERE).  So; how would one go about preventing Alzheimer’s in a manner consistent with health, but not associated with the medical model of “Prevention” discussed earlier? 

The very first step is realizing that you are the one and only person who can really prevent inflammation and neuro-inflammation. You doctor can’t do it for you with a drug or recommendation that’s likely wrong to begin with (HERE).  HERE is a simple, generic protocol that provides a starting point for addressing systemic inflammation.  And if you found today’s post helpful, interesting, and relevant, be sure to like, share or follow on FACEBOOK, because everyone has friends and loved ones who could benefit from this information. 

Share on facebook
Share on twitter
Share on linkedin
Share on pinterest
Share on reddit

Leave a Reply

Your email address will not be published. Required fields are marked *