In a study that examined the effects of influenza virus H1N1 on proteins associated with neurodegenerative diseases, researchers found that H1N1 blocks protein degradation pathways in human neural cell cultures, inducing formation of alpha-synuclein and disrupted-in-schizophrenia 1 (DISC1) protein aggregates; the results were mirrored in murine brains, as increased alpha-synuclein and DISC1 expression levels were detected 4 weeks after intranasal H1N1 infection, raising the possibility that regular anti-influenza vaccination might minimize the risk of Parkinson's disease and related illnesses, according to the authors.
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Article #19-06466: "Disruption of cellular proteostasis by H1N1 influenza A virus causes α-synuclein aggregation," by Rita Marreiros et al.
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