Abstract
The pathogenesis of Alzheimer’s disease (AD) has not been definitely confirmed so far. As a result, a cure for AD is lacking, and current treatments are limited to modest symptomatic relief. Accumulation of damaged proteins and formation of protein aggregates are found in AD brains, suggesting impairment of protein degradation is contained by the pathogenesis of AD. Impairment of ubiquitin-proteasome system has been found in Alzheimer Disease. Here we demonstrate ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) which plays a role in neuronal ubiquitination/de-ubiquitination machinery participates in the pathogenesis of AD.
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