Molecular Mechanism of Autophagy: Its Role in the Therapy of Alzheimer's Disease

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder of progressive dementia that is characterized by the accumulation of beta-amyloid (Aβ)-containing neuritic plaques and intracellular Tau protein tangles. This distinctive pathology indicates that the protein quality control is compromised in AD. Autophagy functions as a "neuronal housekeeper" that eliminates aberrant protein aggregates by wrapping then into autophagosomes and delivering them to lysosomes for degradation. Several studies have suggested that autophagy deficits in autophagy participate in the accumulation and propagation of misfolded proteins (including Aβ and Tau). In this review, we summarize current knowledge of autophagy in the pathogenesis of AD, as well as some pathways targeting the restoration of autophagy. Moreover, we discuss how these aspects can contribute to the development of disease-modifying therapies in AD.

Keywords: Alzheimer`s disease; amyloid beta; autophagy; autophagy-related interventions; mTOR-dependent pathway; mTOR-independent pathway; propagation of amyloid beta and tau; tau.