A variety of epidemiological data argues for a role for persistent viral infection in the development of Alzheimer's disease. This is disputed, however. Some conflicting data shows no signs of a relationship, which suggests that the situation is complicated. Mechanistically, persistent viral infections such as herpesviruses might accelerate the onset of neurodegenerative conditions by provoking greater inflammation, greater numbers of dysfunctional microglia in the brain, and greater amounts of the antimicrobial peptide amyloid-β. Here, however, researchers find evidence for a herpesvirus to promote tau protein aggregation, characteristic of later, more damaging stages of Alzheimer's disease. This adds another interesting wrinkle to the present state of data on mechanisms and epidemiology.
Researchers identified forms of HSV-1-related proteins in Alzheimer's brain samples, with greater amounts of viral proteins co-localized with tangles of phosphorylated tau - one of the hallmarks of Alzheimer's disease pathology - in brain regions especially vulnerable to Alzheimer's across disease stages. Further studies on miniature models of human brains in a Petri dish suggested that HSV-1 infection could modulate levels of brain tau protein and regulate its function, a protective mechanism that seemed to decrease post-infection death of human neurons.
While the precise mechanisms by which HSV-1 influences tau protein and contributes to Alzheimer's disease are still unknown, researchers plan to explore those questions in future research. They aim to test potential therapeutic strategies that target viral proteins or fine-tune the brain's immune response and investigate whether similar mechanisms are involved in other neurodegenerative diseases, such as Parkinson's disease and ALS.
Link: https://www.eurekalert.org/news-releases/1069259
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