Background: Progressive supranuclear palsy (PSP) is a devastating primary tauopathy with rapid progression to death. Although several therapies currently in the development pipeline show promising safety profiles and robust target engagement, few demonstrated significant efficacy in patients, underscoring the need to interrogate additional targets with novel therapeutic modalities to expand the potential therapeutic arsenal. To diversify the therapeutic avenues for PSP and related tauopathies (e.
View Article and Find Full Text PDFBackground: A complex, multicellular disease with genetic and immunological elements, Alzheimer's disease (AD) affects millions worldwide. There has been previous research linking AD to the missense variants ABI3-rs616338-T and PLCG2-rs72824905-G, and the altered expression of these genes has been shown to disrupt microglial function. In our understanding of AD risk and resilience, limited research has been conducted on how these variants affect microglial subtypes and states in AD.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is neuropathologically characterized by amyloid-β (Aβ) plaques and tau neurofibrillary tangles often quantified by Thal phase and Braak stage, respectively. Aβ also frequently deposits in the cerebrovasculature with severity categorized by a cerebral amyloid angiopathy (CAA) score. These and related measures often show high variability within AD suggesting distinct underlying mechanisms.
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