This work investigated how CTSH is regulated and how it influences early AD pathophysiology, and how it influences early AD pathophysiology.
Abstract
Lysosomal dysfunction contributes to Alzheimer's disease (AD) by impairing protein clearance and promoting neuroinflammation. Cathepsin H (CTSH), a lysosomal protease, recently emerged as a protective AD locus. We investigated how CTSH is regulated and how it influences early AD pathophysiology.
Synaptic dysfunction is an early feature of Alzheimer's disease (AD) and proper localization of proteins involved in pre‐ and post‐synaptic composition is dependent on endosomal recycling and trafficking, cellular processes involving the AD risk gene sortilin‐related receptor 1 (SORL1).
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A variety of evidence now supports two interrelated hypotheses concerning Alzheimer’s disease (AD) neurofibrillary pathology (NFT), its prevention and treatment. The first hypothesis: the receptor type protein tyrosine phosphatase D (PTPRD) plays a key role in AD NFT pathogenesis by modulating activities of neuronal gl...
George R. Uhl, Joungil Choi, B. Kannan et al.· Biomedicines· 0 citations
Genetic studies have increasingly de fi ned two major biological subtypes of Parkinson ’ s disease (PD): lysosomal PD (LysoPD), exempli fi ed by GBA1 , and mitochondrial PD (MitoPD), typi fi ed by PRKN and PINK1 .
Apolipoprotein E (APOE) ε4 is the strongest genetic risk factor for late‐onset Alzheimer's disease (AD), but its contribution to disease pathogenesis remains incompletely understood.
A. Shvetcov, Shannon Thomson, Mark E. Graham et al.· Alzheimer's & Dementia· 0 citations
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