Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer’s disease –conformist, nonconformist, and realistic prospects for AD pathogenesis
Open accessAbstract
BACKGROUND: Alzheimer's disease (AD) is a fatal disease that threatens the quality of life of an aging population at a global scale. Various hypotheses on the etiology of AD have been developed over the years to guide efforts in search of therapeutic strategies. MAIN BODY: In this review, we focus on four AD hypotheses currently relevant to AD onset: the prevailing amyloid cascade hypothesis, the well-recognized tau hypothesis, the increasingly popular pathogen (viral infection) hypothesis, and the infection-related antimicrobial protection hypothesis. In briefly reviewing the main evidence supporting each hypothesis and discussing the questions that need to be addressed, we hope to gain a better understanding of the complicated multi-layered interactions in potential causal and/or risk factors in AD pathogenesis. As a defining feature of AD, the existence of amyloid deposits is likely fundamental to AD onset but is insufficient to wholly reproduce many complexities of the disorder. A similar belief is currently also applied to hyperphosphorylated tau aggregates within neurons, where tau has been postulated to drive neurodegeneration in the presence of pre-existing Aβ plaques in the brain. Although infection of the central nerve system by pathogens such as viruses may increase AD risk, it is yet to be determined whether this phenomenon is applicable to all cases of sporadic AD and whether it is a primary trigger for AD onset. Lastly, the antimicrobial protection hypothesis provides insight into a potential physiological role for Aβ peptides, but how Aβ/microbial interactions affect AD pathogenesis during aging awaits further validation. Nevertheless, this hypothesis cautions potential adverse effects in Aβ-targeting therapies by hindering potential roles for Aβ in anti-viral protection. CONCLUSION: AD is a multi-factor complex disorder, which likely requires a combinatorial therapeutic approach to successfully slow or reduce symptomatic memory decline. A better understanding of how various causal and/or risk factors affecting disease onset and progression will enhance the likelihood of conceiving effective treatment paradigms, which may involve personalized treatment strategies for individual patients at varying stages of disease progression.
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Pathogens including Helicobacter pylori, various bacteria of liver, gut, lungs and mouth, and viruses including EBV, CMV, HIV, HSV-1, HSV-2, HHV-6A/HHV-7 can infiltrate the CNS and dysregulate AD-associated neurological function.
“Related pathogens include Helicobacter pylori, various bacteria of the liver, gut, lungs (pneumonia) and mouth, as well as viruses to include Epstein Barr virus, CMV, HIV, oral herpes HSV-1, genital herpes HSV-2, human herpesvirus (HHV)-6A/HHV-7 (recently reviewed in [530]). These pathogens can infiltrate the CNS and dysregulate AD-associated neurological function.”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [530]
Many studies have linked AD to a diverse variety of bacterial and viral pathogens.
“Many studies have linked AD to a diverse variety of bacterial and viral pathogens [529–531].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [530]
Significant overlap exists between expression of AD-associated genes and genomic viral load in the CNS; viral abundance may determine AD progression through regulation of genes associated with APP processing.
“Significant overlap exists between the expression of AD-associated genes and genomic viral load in the CNS; for example, viral abundance may determine AD progression through the regulation of genes associated with APP processing [529–531].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [530]
A recent multi-omic study identified enrichment of HHV-6A and HHV-7 in AD patients compared to controls.
“A recent multi-omic study identified an enrichment of HHV-6A and HHV-7 in AD patients compared to controls [529–531].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [530]
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- Authors
- Li, H., Liu, C.-C., Zheng, H., & Huang, T. Y.
- Affiliations
- Mayo Clinic in Florida (US)
- Baylor College of Medicine (US)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Li, Hongmei
- Huang, Timothy Y.
- Venue
- Translational Neurodegeneration
- Published
- 2018-12
- Volume
- 7
- Issue
- 1
- Pages
- 34-34
- ISSN
- 2047-9158 (ISSN-L)
- PMC
- PMC6306008
- OpenAlex
- W2906630689
- Cited by
- 103
- References
- 321
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 12 · 2023: 16 · 2022: 13 · 2021: 16 · 2020: 25 · 2019: 8
- FWCI
- 1.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Translational Neurodegeneration (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (AG059217, AG061875, AG062257, AG057509, AG054111, AG020670, AG057981)
- BrightFocus Foundation (A2016346F)
- Alzheimer Association (AARG-17-500335)
- Florida Department of Health (8AZ07)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, amyloid hypothesis, tau hypothesis, viral infection hypothesis, amyloid-beta, tau hyperphosphorylation, neurodegeneration, AD pathogenesis, risk factors, personalized treatment
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