Due to the insufficient understanding of the pathogenesis of Alzheimer disease(AD),investigating the early pathophysiological mechanisms underlying AD is particularly essential for advancing subsequent drug therapies. Abnormal protein accumulation is a hallmark characteristic of neurodegenerative diseases such as AD and a sign of proteostasis imbalance. The proteasome plays a remarkable role in maintaining proteostasis mainly by degrading abnormal proteins or polypeptides through ubiquitin-proteasome system (UPS). proteasomes interact with amyloid β-protein (Aβ) and Tau protein in β as both cause and effect which in turn affect neuronal function,glial homeostasis and neural circuit regulation. It has been found that proteasome interacts with Aβ and Tau proteins as both cause and effect,which in turn impacts neuronal function,glial homeostasis and neural circuit regulation. A thorough understanding of the relationship between the proteasome and AD not only provides new clues for exploring the pathogenesis of AD but also holds promise as a major therapeutic target in the future.
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