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Microbial links to Alzheimer’s disease

Summary

Researchers are investigating whether common infections from bacteria, viruses, and fungi might trigger or worsen Alzheimer’s disease. Studies show that pathogens like the bacteria that causes gum disease and certain herpes viruses can reach the brain and trigger inflammation and amyloid-beta accumulation, key features of Alzheimer’s. While the evidence is promising, scientists haven’t yet proven whether these infections cause Alzheimer’s or simply make existing disease worse.

Background

Alzheimer’s disease (AD) is the most common cause of dementia in the United States, affecting approximately 10.8% of individuals aged 65 and above. Despite extensive research, the underlying cause of AD remains incompletely understood. Evidence suggests that infectious pathogens, including bacteria, viruses, and fungi, may trigger or contribute to AD pathology.

Objective

This mini review examines the current evidence demonstrating the potential role of bacterial, fungal, and viral pathogens in the onset and progression of Alzheimer’s disease. The authors evaluate mechanisms by which microbial infections may contribute to AD pathology and neuroinflammation.

Results

The review identifies multiple pathogens associated with AD pathology: bacteria including Porphyromonas gingivalis, Chlamydia pneumoniae, and Borrelia burgdorferi; fungi such as Candida albicans and Malassezia; and viruses including herpes simplex virus-1, cytomegalovirus, and others. Evidence suggests these pathogens may activate neuroinflammatory pathways and contribute to amyloid-β plaque formation and tau phosphorylation.

Conclusion

While correlative evidence linking microbial infections to AD is mounting, causative relationships remain largely unproven. Future research should clarify whether pathogens initiate AD or exacerbate existing pathology, explore polymicrobial causality, and investigate how microbiome dysbiosis contributes to disease progression.
  • Published in:PLoS Pathogens,
  • Study Type:Review,
  • Source: 10.1371/journal.ppat.1013599, PMID: 41129511
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