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Microbial links to Alzheimer’s disease

Summary

This review examines whether germs like bacteria, fungi, and viruses might play a role in causing Alzheimer’s disease. Scientists have found that certain bacteria from the mouth and gut, fungal infections, and cold sores (herpes viruses) appear more frequently in Alzheimer’s patients and may trigger the brain changes that damage memory and thinking. While the evidence is promising, researchers still need to determine whether these infections actually cause Alzheimer’s or simply make it worse once it develops.

Background

Alzheimer’s disease is a common neurodegenerative disorder characterized by amyloid-β plaques, tau protein hyperphosphorylation, neuronal death, and memory deficits. Despite extensive research, the underlying cause remains unclear. Evidence suggests infectious pathogens including bacteria, viruses, and fungi may trigger or contribute to AD pathology.

Objective

This mini review examines the current evidence for pathogens’ role in AD etiology, focusing on bacterial, fungal, and viral contributions to disease onset and progression. The review presents correlations between microbes and AD pathologies while discussing whether pathogens are causative agents or contributing factors.

Results

Multiple bacterial pathogens including Porphyromonas gingivalis, Chlamydia pneumoniae, and Borrelia burgdorferi show correlations with AD pathology. Fungal species like Candida albicans and Malassezia have been detected in AD brains. Herpesviruses, particularly HSV-1 and HHV-6, demonstrate associations with AD, especially in APOE ε4 carriers.

Conclusion

Growing evidence supports associations between microbial infections and Alzheimer’s disease through multiple mechanisms including neuroinflammation, amyloid-β accumulation, and tau phosphorylation. However, evidence remains largely correlative rather than definitively causative, and further comprehensive studies are needed to establish causality and explore polymicrobial contributions.
  • Published in:PLoS Pathogens,
  • Study Type:Review,
  • Source: PMID: 41129511, DOI: 10.1371/journal.ppat.1013599
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