While the abstract notes that HSV-1 can delete mitochondrial DNA and this occurs in AD, the causal relationship remains unclear. Determining whether viral-induced mitochondrial dysfunction directly drives AD pathology versus being a secondary effect is crucial for therapeutic targeting. Gap type: open_question Source paper: Interactions between the products of the Herpes simplex genome and Alzheimer's disease susceptibility genes: relevance to pathological-signalling cascades. (2008, Neurochem Int, PMID:18164103)
Landscape Summary: Does HSV-1-mediated mitochondrial DNA deletion causally contribute to AD pathogenesis? is a 0.77 priority gap in neurodegeneration. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
Does HSV-1-mediated mitochondrial DNA deletion causally contribute to AD pathogenesis? — INVOKE-2 (completed)
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