Molecules, Vol. 24, Pages 3372: Autophagy Modulation as a Treatment of Amyloid Diseases

Molecules, Vol. 24, Pages 3372: Autophagy Modulation as a Treatment of Amyloid Diseases Molecules doi: 10.3390/molecules24183372 Authors: Zoe Mputhia Eugene Hone Timir Tripathi Tim Sargeant Ralph Martins Prashant Bharadwaj Amyloids are fibrous proteins aggregated into toxic forms that are implicated in several chronic disorders. More than 30 diseases show deposition of fibrous amyloid proteins associated with cell loss and degeneration in the affected tissues. Evidence demonstrates that amyloid diseases result from protein aggregation or impaired amyloid clearance, but the connection between amyloid accumulation and tissue degeneration is not clear. Common examples of amyloid diseases are Alzheimer’s disease (AD), Parkinson’s disease (PD) and tauopathies, which are the most common forms of neurodegenerative diseases, as well as polyglutamine disorders and certain peripheral metabolic diseases. In these diseases, increased accumulation of toxic amyloid proteins is suspected to be one of the main causative factors in the disease pathogenesis. It is therefore important to more clearly understand how these toxic amyloid proteins accumulate as this will aide in the development of more effective preventive and therapeutic strategies. Protein homeostasis, or proteostasis, is maintained by multiple cellular pathways—including protein synthesis, quality control, and clearance—which are collectively responsible f...
Source: Molecules - Category: Chemistry Authors: Tags: Review Source Type: research