Can Viral Infections Lead to Alzheimer’s Disease?
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Can Viral Infections Lead to Alzheimer’s Disease?
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Can Viral Infections Lead to Alzheimer’s Disease?
This week, nearly 8,000 researchers have gathered in Philadelphia, USA, for the world’s largest Alzheimer’s disease (AD) conference .
Meanwhile, just a few kilometers away, another 80 researchers are discussing a groundbreaking idea:
Infections might cause Alzheimer’s disease .
A Paradigm Shift: Could Alzheimer’s Disease Be Infection-Driven?
In a report by Science, Harvard neuroscientist William Eimer stated, “The mere fact of holding this conference is a major turning point in the field of Alzheimer’s disease.”
For a long time, Alzheimer’s disease (AD), commonly referred to as “senile dementia,” was considered a degenerative disease. Despite its prevalence and familiarity, its pathogenesis remains hypothetical.
AD is currently defined by progressive cognitive and behavioral impairments, characterized by amyloid-beta (Aβ) deposition and tau protein hyperphosphorylation in the brain. The prevailing hypothesis suggests that an imbalance in the production and clearance of Aβ initiates neuronal degeneration and dementia, which then triggers a series of pathological processes, including tau protein hyperphosphorylation, inflammatory responses, and neuronal death .
In 1960, researchers discovered Aβ protein plaques (commonly known as “senile plaques”) in the brains of elderly patients. By 1991, the process of Aβ production was elucidated, leading to the hypothesis that excessive Aβ deposition with age might cause AD.
Subsequent research has broadened the factors influencing AD beyond its previous classification as a purely degenerative disease, now considering lifestyle, comorbidities, and educational factors.
However, the evidence presented by these 80 scholars suggests another possibility: Alzheimer’s disease may also be linked to past infections.
William Eimer’s team reported their groundbreaking research showing that infections are not only related to Aβ but also activate tau proteins (research results yet unpublished, shared only at the conference).
In 2016, William and his mentor Robert Moir discovered a crucial clue in their preliminary studies on mice and worm models, revealing that Aβ actually has a role in resisting infections .
Two years later, they provided more direct evidence, showing that Aβ aggregates in response to herpes simplex virus 1 (HSV-1) infection, suggesting that this protein might be a protective response to infections .
Could Various Pathogens Cause Alzheimer’s Disease?
At the conference, numerous researchers shared their findings, potentially revolutionizing our understanding that many pathogens might be associated with AD.
Firstly, bacteria. For example, Porphyromonas gingivalis, an anaerobic bacterium known for causing chronic periodontitis, was found to trigger AD-like pathological changes, including excessive Aβ deposition, when repeatedly affecting the gums of mice .
Then, viruses. One year later, another team discovered that HSV-1 could induce AD-like changes in 3D stem cell-derived human brain tissue models .
William’s team also confirmed that when human neurons are exposed to HSV-1, tau proteins aggregate to combat the infection. HSV-1 is the virus responsible for oral herpes, affecting an estimated 67% of people under 50 worldwide .
Additionally, fungi have not been excluded. Immunologist David Corry and his team at Baylor College of Medicine found that mice infected with Candida albicans developed typical AD symptoms such as anxiety, memory impairment, and brain atrophy six months post-infection . They are also studying how Candida albicans invades and affects human brain tissue.
Other pathogens frequently found in AD patients’ brains include Chlamydia pneumoniae, suggesting even a bout of pneumonia might be related to AD.
Furthermore, AD has shown signs of being transmissible. A Nature Medicine paper published earlier this year found that Aβ might pose a transmission risk .
The UK’s National Prion Clinic identified eight patients with early-onset AD who had neither familial nor sporadic AD but had received contaminated cadaver-derived human growth hormone (c-hGH) treatment in their youth, which might have transmitted Aβ to these patients, leading to AD.
Although the study emphasized that symptoms arose after repeated exposure to contaminated c-hGH, and no evidence suggests that Aβ can spread under other circumstances, the potential public health impact and the need for primary prevention of iatrogenic AD must be considered.
Treating AD with Anti-Infectives and Vaccines?
Based on these findings, many teams are exploring the use of anti-infective drugs to treat AD. Columbia University is conducting a clinical trial of the antiviral drug valacyclovir for herpesvirus treatment in AD patients. A clinical study targeting P. gingivalis is also in preparation, involving 300 patients. Although previous trials with this drug in mild to moderate AD patients were unsuccessful, researchers believe it may still be effective for those carrying the bacterium .
Vaccines are also being considered. Last week, a study published in Nature Medicine analyzed the health records of over 200,000 people and found that those vaccinated with the shingles vaccine Shingrix had a 17% lower risk of developing AD within six years . Another study published in May showed that early vaccination reduced dementia risk by 20% .
For decades, biomarkers have been crucial for diagnosis, and new drugs targeting Aβ have entered clinical use. However, our understanding of AD continues to evolve rapidly.
Despite these advances, if damage has already occurred, antimicrobial treatments may be ineffective, and preventing all infections early in life is challenging. Whether infection prevention and control are truly new directions for AD research remains to be seen, indicating a long road ahead.
Our understanding of Alzheimer’s disease may still undergo many more paradigm shifts as new theories and research emerge.
Can Viral Infections Lead to Alzheimer’s Disease?
(source:internet, reference only)
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