Cited by 103Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer’s disease –conformist, nonconformist, and realistic prospects for AD pathogenesis

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Li, Hongmei, Liu, Chia-Chen, Zheng, Hui, Huang, Timothy Y.·2018·Translational Neurodegeneration

DOI 10.1186/s40035-018-0139-3PMC PMC6306008

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Abstract

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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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.
ORCID: Li, Hongmei
Liu, Chia-Chen
Zheng, Hui
Huang, Timothy Y.
Venue: Translational Neurodegeneration
Publisher: Springer Science and Business Media LLC
Published: 2018-12
Volume: 7
Issue: 1
Pages: 34-34
ISSN: 2047-9158 (ISSN-L)
DOI: 10.1186/s40035-018-0139-3
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: cc-by
creativecommons.org/licenses/by/4.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 23 d)
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: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer’s disease –conformist, nonconformist, and realistic prospects for AD pathogenesis

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