It’s Time to Search for the Alzheimer’s Germ

By Leslie C. Norins, MD, PhD | August, 2017

Alzheimer’s disease (AD) is an expanding health problem.  Deaths from it increased 55 percent in 15 years, according to the Centers for Disease Control and Prevention. The affliction breaks hearts of loved ones, and the finances of family, insurance companies, and government. Most everyone knows of a victim.

Despite huge research expenditures, we do not yet know the cause. The “Big Two” suspects seen in patient brains, amyloid plaques and protein tangles, have been studied extensively for years, but so far have not led to many useful answers.

It’s time to make an exhaustive search for the “Alzheimer’s germ” (AG). Singular.  Yes, I believe it’s possible that solely one germ, not yet identified, could be totally responsible for this growing epidemic. We won’t find it without effort. But nobody’s looking yet.

When it’s found, we would reclassify AD as an infection.  Then we could add simple blood tests as a diagnostic tool.  Possibly a vaccine awaits, to keep an invading organism from taking hold.  No new cases would then occur.

But what about current patients with obvious AD, still deteriorating?  Could treatment arrest their decline, or even reverse damage?  Maybe.  It depends on whether an antibiotic or other substance can be found that kills or stalls the invading organism.   And whether the body can repair harm already done.  (Thus far, the brain and nervous system haven’t been able to accomplish much rebuilding after they are disrupted).

Benefits of success are easy to imagine.  But first the germ must be vigorously sought.  In the following paragraphs, I explain how our concept of AD must change, and some research challenges that must be overcome.

Silent infections are common in many infectious diseases

In the simplest picture of an infectious disease, only the obviously infected patients develop antibodies to the invading germ.  Therefore, only those who “look sick” or who “were sick” will have positive blood tests or skin tests.  Their normal-looking fellow citizens will have negative results.

But the situation in nature is often more complicated.  When early epidemiologists investigated polio outbreaks, they found that, as expected, paralyzed patients had antibodies to the polio virus.  But to their surprise, so did thousands of apparently normal people who did not recollect having any illness at all.  In fact, blood tests revealed that most people infected with the polio virus developed no symptoms or only minor ones.  But their positive blood tests showed that the virus had entered their bodies, and stimulated an immune response.  Here’s an important point:  less than one-half percent of polio virus infections resulted in visible paralysis.

Most recently, Zika infection has been of great concern.  Here again, blood tests for antibodies to the Zika virus revealed that 80-90 percent of infections produced no symptoms that the patient could recall.  Even some of the mothers giving birth to microcephalic babies could remember no symptoms.

This condition of “asymptomatic infection” or “asymptomatic carrier” is true for many infectious diseases.  Many outwardly unaffected people, with no specific symptoms, are or were infected by the germ of interest. Examples include tuberculosis, leprosy, typhoid, staphylococci, meningococci, streptococci, HIV, chlamydia, gonorrhea, Epstein-Barr virus, human papilloma virus, and human polyomaviruses.

What if many “normal people” have antibodies to the Alzheimer’s germ?

Be prepared for some surprises when a new blood test is evaluated for detecting a person’s immunological response to infection by the AG.

Yes, it should be positive in 80 to 90 percent of patients having advanced disease and residing in Alzheimer care facilities. (I do not say 100 percent, because some serious dementias diagnosed as Alzheimer’s may actually be caused by some other process that produces similar effects.  The blood test will help clarify that).

But, what if positive results, indicating previous or current germ presence, are also found in blood samples from thousands of normal-appearing siblings, relatives, friends, caregivers, and in some members of the general population?

Oops.  Our understanding of Alzheimer’s disease will have to change.  Right now, the outward signs of progressive dementia arouse suspicion, and then diagnosis, of Alzheimer’s. Most researchers and nonprofit groups seeking a cure view the affliction as something that for as-yet unknown reasons, visibly befalls a significant fraction of people as they age.  The rest of the population is believed not to be affected at all.

The Alzheimer’s germ may invade many, but only a few develop brain disease

In the case of many other germs, apparently normal populations also show immunological evidence of infection—such as positive blood tests (Zika) or skin tests (TB).  If the AG behaves similarly, it would mean that it infects many people, but only a few develop the devastating brain deterioration we now call “Alzheimer’s Disease”.

Whether a positive blood test, as a person’s only sign of infection by the AG, will ever lead to loss of brain function will have to be determined by longitudinal studies.  If the findings with many other microorganisms prove applicable, the answer is nothing further will happen to most individuals whose blood test is reactive.

So, if many people, or even most, are infected by the theorized AG, why do only some develop what we now label as “Alzheimer’s disease”, with concomitant disastrous loss of mental function? It comes down to variations in human susceptibility to the AG germ.

Genes influence whose Alzheimer infection progresses to brain damage

The role of genetics in susceptibility to germs and development of damage has been made quite clear by research on other diseases.  For example, of all people exposed to the tuberculosis germ only a small fraction develop clinical tuberculosis. Several genes have been spotlighted as responsible for this resistance.

Gene influence on susceptibility has also been flagged in leprosy, fungal infections, Lyme disease, leishmaniasis, syphilis, HIV, malaria, influenza, and other infections. Even kuru, a prion infection as some believe AD to be, has been reported to be blocked by a particular gene mutation.

Thus, for genetic and other reasons, most people infected by many other germs keep those under control and do not develop clinically-evident damage.

Alzheimer gene research actually revealing susceptibility, not cause

Many Alzheimer’s research projects are directed at genetics in one way or another.  Virtually all these hope to shed light on, or even pin down, precisely how certain genes contribute to a supposed “cause” of Alzheimer’s, such as amyloid plaques or protein tangles.

The weakness in ascribing Alzheimer’s completely to genetics was demonstrated in the largest study of identical twins, 12,000 pairs.  In the cases of male twins where one or both developed AD, 55 percent of the time one of the pair had not developed it—despite sharing identical genes with the sibling. (Please note nobody is claiming genetics plays no role at all).

However, in this “new germ” theory of Alzheimer’s, the genetic findings take on a completely different meaning.  They are not illuminating any “cause” of Alzheimer’s; instead, they are revealing which genetic patterns and mutations increase susceptibility to the AG.  This hypothesized germ, in susceptible people, causes brain damage and byproducts, such as amyloid and tangles.

Conversely, when humans do not develop Alzheimer’s disease, which is most people, we may assume their genetics enables them to control AGs which enter their bodies, and thus they resist progression to brain damage.  But those who have been exposed to the AG, but remain asymptomatic, will have a positive blood test for antibodies, and maybe even for antigens of the organism. The AG’s antigens may also be detected in the urine.

Recall that evidence of asymptomatic infection, or even an asymptomatic carrier state, is also seen in many other infectious diseases.

No research looks for the “Alzheimer’s germ”

Huge sums of money are being poured into Alzheimer ‘s research grants.  For FY 2016, an NIH compilation indicated $1.2 billion was allocated.  The amount for FY 2017 is projected at $1.6 billion. Additional financial support is provided by nonprofit organizations and foundation.

Of this torrent of research money, how much is going toward searching for one single, probably undiscovered, germ as the cause of Alzheimer’s?   The candid, but brutal answer is “none”.  (I recognize this frank assessment will evoke rejoinders from some funders and researchers that certain existing projects could, may, might, will, include, relate, contain, touch on, or discuss it.)

I surveyed a master compilation of Alzheimer’s research topics, known as CADRO (Common Alzheimer Disease Research Ontology).

Appendix 2 covers basic research, and its first section is pathogenesis, i.e. causation. It provides 11 categories, which are subdivided into a total of 59 research topics into which scientists can classify their project.   There is no classification mentioning any possibly causative “germ” invaders such as bacteria, viruses, fungi, parasites, or prions.

Germ hunters missing at 2017 Alzheimer’s research conference

In July 2017, the Alzheimer’s Association convened an international conference in London at which researchers “from 70 countries” could share progress. The program reflected the current research areas of most emphasis worldwide. The keyword index of the numerous presentations showed, not surprisingly, the largest number of entries for amyloid/APP, 110.  The next most common item was tau, the tangled protein; 85.  Inflammation, the body’s reaction to something, had 45 mentions.

In contrast, presentations of possible germ importance had only single digit presence: prion proteins 8, infectious disease 4, bacteria 1.  Virus was not even listed as a keyword.

No Alzheimer research interest group on “germs”

One of the most prominent associations of researchers interested in Alzheimer’s is the International Society for Advancing Alzheimer’s Research and Treatment, commonly known as ISTAART.  (Disclosure: I am a recent member).  I viewed its online membership information as a reasonable representation of current research interests.

There are about 2400 members.  Those interested in a particular subject can create a PIA (Professional Interest Area).  Currently there are 18 such groups.

There is not a group listed for an extrinsic cause of AD, or an even narrower one interested in finding a new bacterium, virus, prion or other infectious agent.  (Therefore, I joined a subgroup interested in immunity and one interested in biofluid markers, as conceivably these could become home to researchers who find a specific germ, or who develop a blood, urine, or spinal fluid diagnostic test for it.)

Infections emphasized in 2016

In April 2016, a group of 33 prominent Alzheimer’s researchers authored an editorial urging more research on infection as a possible cause of AD.  They mentioned several known infections that seemed relevant:  herpes simplex virus, chlamydia, HIV, syphilis, and fungus.

Their plea has not yet been reflected in any major shifts in research funding.  The “big two” money recipients are still amyloid plaques and tau protein tangles.

Also in 2016, a research team at Harvard postulated that the beta-amyloid plaques characteristic of Alzheimer’s pathology are a kind of immune response to invasion, perhaps repeated ones, by already-known organisms. Other scientists have flagged herpes and fungi as possible culprits.

Inflammations resulting from infections by various known pathogens were also posited to cause leaky blood vessels, thus allowing intravascular substances to leak out and damage nerve cells in the brain, i.e. inflammation.

Thus, after many years of “infections” being dismissed out of hand and largely ignored by funders, the research climate for investigating them may be getting better.  Although the wedge opening the door to funding has been organisms already recognized, there is no reason the new paradigm cannot be extended to searching for an as-yet-undiscovered germ.

Why hasn’t the Alzheimer’s germ been found in 110 years?

Alois Alzheimer published the account of his first patient in 1907.  By then, a few diseases had been proven to be caused by bacteria, e.g. anthrax, tuberculosis and cholera.  In the years that followed, numerous other afflictions supposedly due to other factors were determined to be infectious in origin.  For example, malaria had been attributed to bad air from swamps, and polio to filth.

Even in recent decades, an infectious cause has been identified for diseases afflicting the population.   The Legionnaires disease bacterium was not identified until 1977 (the year following the epidemic which named the disease), but then retrospective studies revealed earlier “mystery” epidemics had actually been caused by it.

The worldwide influenza epidemic of 1917 killed millions, but the causative virus was not isolated until 1933.

Kuru, a mysterious, supposedly hereditary affliction of the nervous system, was investigated in 1957, but only in 1966 was proven to come from a transmissible agent.

More recently, reflect on the headlines about SARS, Zika, HIV/AIDS, “flesh -eating bacteria”, and other infections, to realize not all disease-causing germs had been recognized by the time you were born.  Therefore, it is logical to expect discoveries of such previously unappreciated agents to continue.  The AG can be among these.

Thus, the fact that no germ has yet been discovered for a disease of unknown cause, like AD, does not exclude an infectious agent being later pinpointed.  And when that happens, suddenly all the strange features of the disease previously ascribed to other incitements and reasonings start aligning with the revealed agent.

The Alzheimer germ may already be appearing in labs

There’s a slim chance the AG could be “hiding in plain sight”.  By this I mean it readily grows on one or more of the growth foods used routinely to encourage the growth of bacteria or viruses. And, when blood, sputum, or spinal fluid from an Alzheimer’s patient who happens to become acutely ill and feverish is being tested for the presence of a known infectious agent, the AG may also be present in the sample and grow.

However, because nobody is looking for any germ other than a known one, the AG will be called a “contaminant”, and disregarded.

Microbiologists must search for the Alzheimer’s germ 

Nobody know in advance what kind of nutrients the AG might require to grow in the lab.  Some germs have peculiar requirements; they are picky eaters. Therefore, patient samples that might contain the AG will have to be placed onto or into each of the wide array of lab “foods” available, hoping that at least one of them will encourage it to multiply so it becomes more apparent. Eggs and tissue cultures of various cells may also have to be inoculated if the AG is a type of virus or rickettsia.

The right nutrients can be crucial.  For example, the Legionnaires bacterium grew on only one of 17 common bacterial media (food blends) tested. These germs were initially found only because a scientist had inoculated patient samples into eggs, looking for rickettsia; luckily, the Legionnaires bacteria also grew there.

The right lab conditions play a role too.  The Legionnaire’s bacterium needs an atmosphere with augmented carbon dioxide.  So does the gonococcus—which can be asymptomatically infecting women.

And patience may be necessary.  While bacteria like staph and strep multiply quickly enough to be visible in a day or two, mycobacteria (TB) can take weeks.

Routine clinical labs might fail to grow it

Most all clinical labs in the U.S. are highly competent. There are periodic distributions of test samples to tests to confirm their proficiency.  However, some infectious organisms prove a challenge.  For example, the College of American Pathologists was said to find that “as many as two-thirds of clinical microbiology laboratories were unable to grow a pure and heavy culture” of the Legionnaires bacteria. Thus, it might take a highly experienced lab focusing on finding the AG to detect it.

Will the Alzheimer’s germ produce effects in research animals?

Mice and rats.  These are the laboratory animals most often inoculated with germs that cause human disease. But what happens?  Sometimes the bacteria or virus will indicate its presence by killing the animal.  Other times it may cause symptoms, like accumulation of fluid in the abdomen.  Whatever occurs, it rarely is an exact replication of the human disease caused by the germ.

So, what should scientists look for in lab animals after injecting them with samples from Alzheimer’s patients? How would one test a lab animal for mental deterioration?  Damage to brain anatomy could be assessed by post-mortem examination.

But in animal species, the AG might behave quite differently than it does in humans.  For example, it might favor organs other than the brain.

Ofttimes the inoculated germ multiplies, and even spreads throughout the animal, but no ill effects are seen.  And in other cases, the germ seems to disappear; the animal was somehow inhospitable, or even resistant, to it.

Animal species might be crucial

Which species of lab animal would be optimal to inoculate with the possible AG?  It’s hard to guess in advance.  If one goes by popularity, which includes cost and convenience aspects, here are percentages of species used in research, as compiled by the European Union: mice 59, rats 18, fish 9, birds 6, rabbits 3, other rodents 2, and reptiles 1.  A National Library of Medicine compilation from published research found 50,000 studies used mice and 36,000 employed rats.  Just 1300 used actual guinea pigs, despite the appropriation of that name to indicate all research subjects.  Thus, you can see that mice are the candidates in first place.  So they should at least be tried.

But a number of germs take hold only in less common animal hosts.  Ferrets are great for influenza virus research (but measles virus won’t take hold in them.)  Some can be infected with the agent of SARS (severe acute respiratory syndrome), but they resist MERS (Middle East respiratory syndrome).

Leprosy bacillus? The armadillo is the go-to. Chimpanzees were essential to show kuru was caused by a transmissible agent.  Macaques were important for HIV and Ebola.

So, to “cover all bases”, it may be necessary to inject many animal species with patient samples that might contain the AG.  Just because mice are the most convenient and least costly lab animals, it does not mean that the AG will grow in them, let alone cause recognizable ill effects or pathological changes.

Would we recognize Alzheimer’s in a lab animal?

If you don’t know what to look for, how will you recognize it?  OK, inoculate many lab animals with samples from AD patients.  But what to consider “positive”?  Amyloid plaques in the brain could be exciting, but they don’t guarantee dementias even in humans.  Protein tangles?  Hmm, maybe. Deterioration of cognition?  Could be difficult to detect in animals.

But now it could get exciting.  Animal studies of the new AG might reveal it spreads, early-on, throughout the animal’s body, like syphilis and tuberculosis.  It only “acts up” preferentially in certain organs later.  In a different species, it’s not guaranteed that it will attack the brain; maybe it will be the spinal cord, or even the kidney, or lung. We may even find that AD is a systemic infection, in both lab animals and humans.  But we have been focusing only on the brain because, in autopsies and imaging of terminal-stage disease, that was the organ where damage was detected.

Will additional money stimulate searching for the Alzheimer’s germ?

There’s already a billion dollars in American research funding in the pipeline, plus hundreds of millions more around the world.  I can’t with a straight face argue that more money is needed, though of course it will always be welcomed.

The short answer is that more interest and money must be diverted from yet further refinement of “safe” topics to “long shots” and risky possibilities. This should include arranging multiple searches for the AG.

However, the existing peer review committees that rank research proposals may not be the best arbiters for this new research.  After all, most of these scientists are already heavily invested in what has drawn the big bucks so far.  So it may be against human nature to expect them, and the granting agencies and foundations, to say they might have backed the wrong horses.  (Of course, if and when evidence of an AG is presented, they will all be gracious and professional enough to acknowledge it).

Infectious disease experts need to get activated

A Catch-22 situation exists with attention to human infections.  Until the cause is first suspected to be infectious, no infectious disease experts are interested.  Once the germ is discovered, they pile in, and many aspects of the pathogenesis are rapidly illuminated.   Drugs for treatment, and even vaccines, usually follow.

Before the causative germ is discovered, many other specialties carry on the principal research searching for a cause and attempting a cure: biochemists, geneticists, pathologists, toxicologists, pharmacologists, etc. All are reputable scientists doing what they do best.  All stay busy characterizing what is present or absent in patients or lab animals, and how it gets that way.  Except not one specifically seeks, let alone discovers, the germ actually causing the problem.

For example, H. pylori, the causative bactrerium of gastric ulcers, was discovered by the unusual persistence of an Australian researcher, who even swallowed some of the germs to show they produced a stomach ulcer. His findings overturned decades of medical beliefs in other causes.

The Legionnaire’s bacterium was discovered, months after everybody else had given up, by the chance persistence of a CDC scientist, whose specialty was actually rickettsia. That overturned all sorts of strange theories as to what had caused the namesake epidemic, and enabled decades of earlier mysterious outbreaks to be accurately classified in retrospect.

What would trigger action by the infectious disease community?

The guaranteed hot buttons today are fevers and body counts.  Think Ebola, SARS, AIDS, Zika, swine flu, and superbugs.

In other words, show the infectious disease professionals a dangerous and fast-acting scourge fitting the classic picture of an infectious disease, and they’re on it full force, no holds barred. Government labs snap to attention, and research grants appear like magic. Usually world-class success is obtained, and the threat is eliminated or contained.

But if a mystery condition is not considered to be typically infectious, few if any infectious disease clinicians or microbiologists try to reveal an as-yet-undetected causative bacterium, virus, prion, or parasite.  Grant committees would not assign much priority to such long- shot searches, and infection detectives like the CDC are preoccupied with “obvious infections” and various crises.

How different from the earliest decades of infectious disease, when almost every sickness that could be examined was tested to possibly reveal germs. Low budget.  And it paid off.  TB bacilli showed the disease wasn’t caused by inheritance.  Identifying the organisms of cholera and typhoid replaced strange theories about those diseases. Malaria turned out not to be caused by swamp air, and polio wasn’t caused by filth.

Why hasn’t Alzheimer’s attracted the infectious disease crowd?

Here’s the peculiar situation.  In 2016, 33 of the top Alzheimer’s researchers pleaded—in an editorial—for more research on an infectious cause of the disease. But they themselves are not especially known for their expertise in niches of infectious disease, though they have great talents in diverse other areas.

Conversely, the infectious disease community is preoccupied with its own favorite subjects, which do not include a non-febrile chronic disease with years-long decline of brain function as the main symptom. Thus, few if any infectious disease specialists or microbiologists. have taken an interest in AD so far.

Obviously, there needs to be cross-pollination, and cooperative projects, between the two camps of experts. Some national government or non-profit group, preferably with research funds to dole out, must take the lead.  The national societies of relevant professionals also should lend their weight to alliances and mutual efforts.

Brain samples are not sufficient

Because brain deterioration is the definitive characteristic of AD at autopsy and in imaging, it seemed logical to early scientists to assume that its cause, or answer, would be found in brain specimens.  That’s the reason generous donors have provided brains post-mortem to the several brain banks which exist.

The formalin-preserved bits are perfect for the study of tissue architecture.  Perhaps some dead, preserved AGs are still within these specimens, and can be visualized if they attract one of the many chemical stains for microorganisms.

The fresh-frozen samples can be used in all sorts of biochemical and genome studies. Maybe the AG, in suspended animation, is within these fresh-frozen brain samples, and can be coaxed to grow if the right nutrients can be found for it. Certainly, it would be worth trying an array of microbiological foods.

But nobody knows if the AG, dead or alive, is in the brain samples.  Perhaps the patient’s body disintegrated the germ, or cleared it away, before fatal damage set in.

Serum samples must be studied

If the usual samples saved are post-mortem brain tissues, and not much else, one can guess the organizers of the collections were pathologists or neurologists. They focus on the end-state organ of the disease. It can provide reliable proof of a diagnosis, and may even shed light on the pathologic damage which produced the damage.

However, infectious disease explorers have broader needs.  They want to understand how and when a germ entered the body, what resistance the patient offered, and when this arose.

The body’s production of antibodies against the invader can provide vital information on all these items.  Because theses immune molecules are contained within the clear part of the blood, the serum, it is necessary to collect samples of it from the patient.  This is accomplished conveniently and easily by a simple venipuncture, often as part of blood tests being obtained for other determinations. A sample can also be obtained post-mortem.

Detecting the body’s specific response to the germ being investigated effectively proves that organism is, or was, present, and thus is likely playing a role in the ailment.

Further, by collecting serum samples from the same patient over time, one can trace the rise and subsequent decline of the antibody response. It may also be possible to infer when the germ invaded.

Imperative to obtain and bank serum samples

As far as I can determine, there is no national program, or well-known regional one, to collect serum samples from Alzheimer patients, either serially during life, or at post-mortem.  I enquired of several brain banks if they also bank serum samples from the brain donors, and they responded they do not. (Donor serum is usually tested for presence of hazardous infectious agents, such as hepatitis virus and HIV, but this is done to forewarn staff to be extra-cautious in handling the specimen; that serum sample is not forwarded to, or kept at, the brain bank.)

Henceforth, a post-mortem serum specimen for freezing and banking should, whenever possible, accompany every brain sample donated to a brain bank.

I did learn that in a few, small Alzheimer’s studies sequential serum samples may be being banked.  These will be valuable to analyze if some of these individuals develop AD.  But I suspect the motivation for collection was probably to analyze for non-immunological molecules. Nevertheless, these longitudinal samples can be put to use as part of examining AG suspects.

Overall, however, we need a significant program launched immediately to do two things: (a) collect and bank a serum sample from every patient who dies from AD, and (b) sequentially collect serum samples over time from several thousand people as they age, and some of them develop AD.  Then, antibodies to the AG, and perhaps even some fragments of the germs themselves, can be detected in these samples.

Additionally, it is possible some already-existing serum collections from large populations could be redeployed to aid the search for AG antibodies.  And, population surveys currently in progress could be administratively modified to make their serum samples available for AG antibody testing.

Urine samples, easily obtained, will also provide evidence

Urine samples are among the easiest medical specimens to obtain and preserve.  And immunological progress and nucleic acid techniques have made it possible to identify specific antibodies, and even tiny fragments of infectious agents, in urine.  Therefore, research directors and grantors for Alzheimer’s projects should start making certain that, whenever possible, urine samples are also procured and banked.

Spinal fluid samples: valuable but scarce

Antibodies and antigenic fragments of germs are often found in spinal fluid when germs invade the central nervous system.  It is likely then, that the AG will leave one or another calling card there also.  These samples are not easy to obtain, but by fortunate happenstance they are often sought by clinicians in cases where a central nervous system pathological process is suspected. New micro-techniques permit immunoassay of tiny amounts of precious liquids like these. Thus, wherever possible, portions of spinal fluid samples should also be banked.  Even if many such samples are from non-AD cases, the finding that they are negative for the AG will help assess the specificity of any new assay.

Be ready for surprise revelations about Alzheimer’s.

Quite often in infectious disease, when a way is found to visualize or grow a new germ, or to detect its antigenic fragments or the body’s antibody reaction to it, the understanding of the organism and the spectrum of its invasiveness changes greatly.

A frequent revelation is that in addition to the relatively few patients with obvious disease, many apparently normal people also have been infected by the germ.   An antibody test (e.g. hepatitis C) or skin test (e.g. TB) reveals that the germ previously entered the body. But somehow the person resisted it, or kept it in check.

Sometimes the germ itself is found sitting on the person, not causing any harm, whereas when it is transmitted from them to a more susceptible individual it can cause a deadly infection (examples: staphylococci in the nose and meningococci in the throat).

And a current disease may turn out to be a late variant of an earlier one (example:  shingles eruptions in adults are reactivations of childhood chickenpox that stayed dormant in the patient’s nerves for decades).

Thus, the AG may turn out to infect many people, but in most of those it doesn’t progress to brain damage and AD.  Or. AD damage could stem from late reactivation of some early infection that doesn’t resemble it at all.

Or, surprise.  The AG antibody or antigen test on spinal fluid taken from a supposedly different brain or spinal cord affliction may also be positive—thus revealing a previously unsuspected link between that illness and AD.


Despite the seriousness of Alzheimer’s disease, a rising number of cases, and billions of dollars spent on research, no cause or cure has been found.  Infectious agents, the cause of many other damaging afflictions, have not yet been exhaustively sought, though both classic and newer methods are readily available.  The unfortunate chasm between the current Alzheimer’s research programs and the resources of infectious disease experts and microbiologists has delayed this quest.  It is time to launch a unified drive combining all pertinent professionals and techniques, to detect and characterize the Alzheimer’s germ, if it exists.  To not search guarantees we will never find it▪︎


Dr. Leslie Norins has never participated in research on Alzheimer’s disease.  Instead, he writes from his perspective of 43 years as a leading publisher of newsletters for healthcare professionals.  In his early career, he directed a research laboratory at the Centers for Disease Control and Prevention. He is a graduate of Johns Hopkins University, and received his M.D. from Duke University School of Medicine.  His Ph.D. is from the University of Melbourne, where he studied immunology with Sir Macfarlane Burnet, Nobel Laureate. He has also served on committees of the National institutes of Health and the World Health Organization, and has been a fellow of the Infectious Diseases Society of America.

Further information about Alzheimer’s disease

Alzheimer’s Association.

National Institute on Aging (NIH).


(To me, syphilis seemed a worthy analogy, as back in the 1970’s I had been director of the CDC’s Venereal Disease Research Laboratory. The spirochete which causes the disease eluded detection for centuries.  Syphilis, like leprosy and tuberculosis, was thought to be inherited (sound familiar?).  The germ still—more than 100 years after its discovery– cannot be continually grown on standard bacteria food, and so must be passaged in rabbits.  Human infection can lie asymptomatic for 10-30 years before neurosyphilis may show up—some of its brain signs resemble AD..  Even then only one-third of all those infected years earlier develop this or another late complication.  Blood tests are the necessary tool for diagnosis of both clinically evident problems and asymptomatic “latent syphilis”.)

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