Impact of α‐synuclein RNA interference on Neuropathological and Clinical Phenotypes in a mouse model of Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the pathologic accumulation of beta amyloid (Aβ), Tau and α‐synuclein (α‐syn). The role of α‐synuclein has been extensively studied in Parkinson’s disease, but less so in AD. Recent studies have shown that α‐syn may also play a role in AD and its downregulation could be protective against the toxic effects of Aβ accumulation. First, we hypothesized that selectively knocking down α‐syn improves the neuropathological, biochemical, and cognitive findings in AD. Second, we tested whether α‐syn ablation could enhance AD treatments with donepezil (pro‐cholinergic) and memantine (glutamate antagonist), which are currently ineffective at slowing progression of disease.