Stop Microbes to Stop Alzheimer’s?
by Leslie C. Norins, MD, PhD
CEO, Alzheimer’s Germ Quest, Inc.
June 27, 2018
Two new reports: one detecting copious amounts of herpes virus 6a and 7 in the brain (1), and the other finding herpes triggered amyloid seeding (2) have stirred worldwide recognition of the need for more intensive study of—and funding for–the role of microorganisms in the causation of Alzheimer’s disease.
Richard Lathe and Jürgen Haas, of Edinburgh, have declared that these reports create a new paradigm for Alzheimer’s (3). The old idea that amyloid buildup is the cause is being replaced by an understanding that amyloid is a response to a stimulus, likely infectious agents. So, it’s time for expanded and accelerated attention to microorganisms.
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An offered objection isn’t valid
However, several experts were quoted as believing the presence of these newly spotlighted herpes viruses in large numbers of non-Alzheimer’s people or their brain samples precludes the possibility that these organisms, or other widespread ones, could be causing Alzheimer’s.
Their reasoning? Many adults carry the virus, yet only some of them develop Alzheimer’s. So they theorize the virus couldn’t be the trigger—or every carrier would get the disease.
But nature and medicine have already proven such reasoning is incorrect. There are many infectious disease scenarios which exactly comport with the pattern seen with herpes in Alzheimer’s patients. Here are three:
Chickenpox – This varicella-zoster virus infects most normal, unvaccinated children. And though the youngsters usually recover, that virus then “hides” silently in their nerves for decades. When these infected people become seniors, a proportion of them—but by no means all—develop “shingles”, a very painful affliction, from an eruption of that latent virus.
This pattern provided two opportunities for attacking this virus. The first is was in childhood. The chickenpox vaccine has thus almost eliminated the viral outbreaks so common in children of earlier generations. The virus was prevented from getting a toehold in the first place.
And for the senior adults who may still be harboring the virus within their nerves from childhood, there is a varicella-zoster vaccine to reduce the likelihood of shingles erupting in this later period of life.
Human papilloma virus (HPV) – This agent infects many young adults. As infected females grow older, a certain proportion–but by no means all–will develop cervical cancer from the virus. (That is the reason the vaccine Gardasil was introduced–to render the younger recipient immune so that the dangerous virus could not establish residence.)
Syphilis – The causative bacteria invade young adults. A Scandinavian study many decades ago showed that if early syphilis is left untreated, in later life that initial infection causes brain damage, sometimes fatal, in up to 30 percent–note this is not all–of the infected, aging adults. (A prominent example of this late, fatal brain damage is Winston Churchill’s father.)
In the case of syphilis, early treatment with penicillin will cure the infection, and prevent it progressing to the damaging late stage. Even treatment delayed to the late stage may stop further damage.
Reality: Pattern well-proven
So, we can see that the pattern of a dangerous germ’s infecting many people early on, and yet only harming a proportion of those people in later years, is fully proven and accepted in medicine.
Hence, even though some carriers of herpes do not develop Alzheimer’s, herpes virus cannot be excluded as a possible cause of Alzheimer’s in later life. (Nor can we exclude any other infectious organism that fits this pattern.)
Factors tipping carrier into disease
Why do some of the carriers of a virus or bacteria go on to develop the damaging infection the germ can cause, yet other carriers never experience any problems? Factors like genes, lifestyle and environment undoubtedly play a role.
But here’s the vital point: If it is correct that microbes play a necessary trigger role, no matter how many of your genetic or other risk factors, or lifestyle behaviors, are unfavorable, you will not get Alzheimer’s unless the germ enters you and survives in the first place.
Drug and vaccine could prevent Alzheimer’s
Now to emphasize the big implication for ending Alzheimer’s disease. If herpes, or any other infectious organism, can be shown to play a triggering role, counterattack is possible.
An antibiotic can kill bacteria, and an antiviral compound can kill a virus. Many such compounds already exist and more can be developed. By destroying the bacterial or viral participant in the dementia process the brain damage will never develop.
A recent study by Tzeng et al (4) favors this possibility. It reported that of Taiwanese patients with a herpes type 1 or 2 infection, who were checked after 10 years, those who had been treated with antiviral therapy originally had developed significantly less dementia than those who had not received antiviral drugs for their initial herpes infection. Based on this and other Taiwanese findings, a causal role for herpes in dementia seems clear to some experts (5).
Alternatively, a vaccine will prevent the dangerous organism from taking up residence in a person in the first place. Or, if the agent has already invaded, a vaccine could prevent a later eruption which could cause brain damage at a later age.
Summing up: “No germ trigger, no Alzheimer’s bomb explosion.”
1. Readhead B, Haure-Mirande JV, Funk CC, Richards MA, Shannon P, Haroutunian V, Sano M, Liang WS, Beckmann ND, Price ND, Reiman EM, Schadt EE, Ehrlich ME, Gandy S, Dudley JT. Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus. Neuron 99, 1–19 July 11, 2018
2. Eimer, William A. and Vijaya Kumar, Deepak Kumar and Shanmugam, Nanda Kumar N. and Washicosky, Kevin J. and Rodriguez, Alex S. and György, Bence and Breakefield, Xandra O. and Tanzi, Rudolph E. and Moir, Robert D., Alzheimer’s Disease-Associated β-amyloid Is Rapidly Seeded by herpesviridae to Protect Against Brain Infection (2018).
4. Tzeng N-S. et al. (2018) Antiherpetic medications and reduced risk of dementia in patients with herpes simplex virus infections – a nationwide population-based cohort study in Taiwan. Neurotherapeutics, doi: 10.1007/s13311-337018-0611-x.
5. Itzhaki RF and Lathe R. (2018) Herpes viruses and senile dementia: first population evidence for a causal link. J Alzheimers Dis. 64, 363-366
What should you do?
About $2 billion of research dollars are available in the U.S. annually for Alzheimer’s research. A stupendous sum for medical research, by any measure. However, only a paltry amount of this goes to identifying and investigating infectious diseases and microbes in this disease.
Why? Because the big funders, and their grant review committees, are committed to defending and prolonging their past and current expenditures for research on amyloid and tau proteins. Certainly, these were initially logical targets. Unfortunately, these vast investments of billions of dollars have not brought a cure for Alzheimer’s, or even identified the cause of the disease. How likely is it that digging the same well even deeper will yet strike oil?
Hopefully, these influential groups will take a fresh look, and shortly themselves begin providing significant encouragement and financial support for clarifying the role of microorganisms.
But if these leaders are not responsive with significant research monies (i.e. beyond lip service), scientists and all families concerned with Alzheimer’s must take action themselves.
The surest path for them to results will be to influence national and state legislators, and local advocacy chapters, to insist on activating and prioritizing Alzheimer’s germ research. This subject area is too important and plausible to be left starved of research funding.
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