ReviewPLoS pathogens2022
Infectious origin of Alzheimer's disease: Amyloid beta as a component of brain antimicrobial immunity.
Review in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed.
- Cytomegalovirus-induced T cell responses accelerate Alzheimer's disease progression in mice.Brain : a journal of neurology · 2026Article
- Glymphatic system dysfunction: a link between sleep disorders and neurodegeneration.Psychopharmacology · 2026Review
- Pathological or preventative? Amyloid-β as an effector of innate immunity.Infection and immunity · 2026Review
- Chemokines in Alzheimer's Disease: Early Defence, Late Damage and the Impact of Sex and Infection.Basic & clinical pharmacology & toxicology · 2026Review
- iPSC-Derived 3D Brain Organoids as Next-generation Platforms to Study Viral and Toxicant-associated Neurodegeneration.Stem cell reviews and reports · 2026Review
- Convergence of neuroinflammation across major neurotropic viral exposomes in AD and ADRD.Journal of neuroinflammation · 2026Review
- Role of Microbial Toxins in Neurodegenerative Diseases: Insights and Future Perspectives.Biomolecules · 2026Review
- Protein Modifications and Quality Control System: Target for Alzheimer's Disease Therapy.International journal of molecular sciences · 2026Review
- Viral Mimicry of Alzheimer's Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence.Journal of molecular neuroscience : MN · 2026Review
- Is Alzheimer's an Autoimmune Disease?Molecular neurobiology · 2026Review
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- The triple-hit hypothesis of Alzheimer's disease: blood-brain barrier breakdown, infection, and neuroimmune activation as a unified etiological framework.Frontiers in neuroscience · 2026Article
- Pathogens Association with Alzheimer Disease: Emerging Concepts and New Perspectives.Current gene therapy · 2026Review
- Marine-Derived Natural Substances with Anticholinesterase Activity.Marine drugs · 2025Review
- Longitudinal Association of Inflammatory Diets on Cognition in Older Adults: Insights from the Oral-Gut-Brain Axis.Journal of the American Geriatrics Society · 2025Article
- Microglial Drivers of Alzheimer's Disease Pathology: An Evolution of Diverse Participating States.Proteins · 2025Review
- What would it take to prove that a chronic infection is a causal agent in Alzheimer's disease?Trends in neurosciences · 2025Review
- Bacteria in the brain: do they have a role in the pathogenesis of Alzheimer's disease?Current opinion in psychiatry · 2025Review
- Biofilm-Associated Amyloid Proteins Linked with the Progression of Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Differential Transcriptional Programs Reveal Modular Network Rearrangements Associated with Late-Onset Alzheimer's Disease.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The amyloid cascade hypothesis, focusing on pathological proteins aggregation, has so far failed to uncover the root cause of Alzheimer's disease (AD), or to provide an effective therapy. This traditional paradigm essentially explains a mechanism involved in the development of sporadic AD rather than its cause. The failure of an overwhelming majority of clinical studies (99.6%) demonstrates that a breakthrough in therapy would be difficult if not impossible without understanding the etiology of AD. It becomes more and more apparent that the AD pathology might originate from brain infection. In this review, we discuss a potential role of bacteria, viruses, fungi, and eukaryotic parasites as triggers of AD pathology. We show evidence from the current literature that amyloid beta, traditionally viewed as pathological, actually acts as an antimicrobial peptide, protecting the brain against pathogens. However, in case of a prolonged or excessive activation of a senescent immune system, amyloid beta accumulation and aggregation becomes damaging and supports runaway neurodegenerative processes in AD. This is paralleled by the recent study by Alam and colleagues (2022) who showed that alpha-synuclein, the protein accumulating in synucleinopathies, also plays a critical physiological role in immune reactions and inflammation, showing an unforeseen link between the 2 unrelated classes of neurodegenerative disorders. The multiplication of the amyloid precursor protein gene, recently described by Lee and collegues (2018), and possible reactivation of human endogenous retroviruses by pathogens fits well into the same picture. We discuss these new findings from the viewpoint of the infection hypothesis of AD and offer suggestions for future research.
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