Autophagy: Novel Insights from Molecular and Chemical Biology

Dear Colleagues,

Chronic neurodegenerative brain disorders, such as Alzheimer’s disease (AD), are the most common form of dementia in the elderly. Dysfunctional protein homeostasis (proteostasis), characterized by the accumulation of protein aggregates such as β-amyloid (Aβ) in AD, is a hallmark of many neurodegenerative diseases. The main proteostasis mechanisms in cells include the autophagy–lysosomal pathway (ALP), the ubiquitin–proteasome system (UPS), and molecular chaperones. These pathways are impaired in AD and other neurodegenerative disorders, contributing to protein aggregation and neuronal death.

Emerging evidence suggests that treatment strategies targeting proteostasis can restore cellular homeostasis and help prevent neurodegeneration. This Special Issue seeks contributions that explore the modulation of cellular clearance pathways, such as autophagy and proteasome, to eliminate toxic aggregates in degenerative dementia and other degenerative disorders. The handling of toxic protein aggregates remains a key therapeutic target in the search for novel remedies.

We particularly encourage studies on small molecules and other innovative approaches that act as modulators of the proteasome, macroautophagy, or chaperone-mediated autophagy. By highlighting novel therapeutic strategies, this Special Issue also aims to provide deeper insights into the molecular mechanisms of cellular clearance systems and their toxic protein aggregates in neurodegeneration.

Dr. Prashant R Bharadwaj
Guest Editor

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