β-amyloid deposition-based research on neurodegenerative disease and their relationship in elucidate the clear molecular mechanism

Abstract

Alzheimer's disease (AD) is characterized by the central feature of dysregulated metabolism of β-amyloid peptide (Aβ). BACE1, which is the enzyme responsible for the production of Aβ, has been identified as a promising therapeutic target. Recent research has uncovered a regulatory correlation between BACE1 and Clusterin, a glycoprotein that plays a role in the clearance of Aβ. Research has demonstrated that the inhibition or downregulation of BACE1 results in elevated expression of Clusterin in astrocytes, which subsequently promotes the effective removal of Aβ. Clusterin functions as a molecular chaperone, facilitating the internalization and degradation of amyloid-beta (Aβ) by astrocytes. The aforementioned regulatory pathway exhibits a compelling avenue for therapeutic interventions in Alzheimer's disease. The modulation of BACE1 activity with the aim of promoting Clusterin expression and subsequent clearance of Aβ has the potential to mitigate the burden of Aβ and ameliorate the pathology associated with Alzheimer's disease. Additional investigation is required to clarify the fundamental molecular mechanisms and assess the therapeutic viability of directing attention towards BACE1 and Clusterin in relation to Aβ elimination. Comprehending this regulatory pathway has the potential to provide novel perspectives on the pathogenesis of Alzheimer's disease and direct the advancement of inventive therapeutic approaches.