A Single Pathway Targets Several Health Challenges of the Elderly

UNCP Author/Contributor (non-UNCP co-authors, if there are any, appear on document)
Dr . Ben Bahr, William C. Friday Chair and Professor of Molecular Biology and Biochemistry (Creator)
The University of North Carolina at Pembroke (UNCP )
Web Site: http://www.uncp.edu/academics/library

Abstract: New avenues to modulate the autophagy–lysosomal route of protein clearance have the potential to help treat several disease states to which the elderly are particularly vulnerable. Two recent papers identi?ed distinct ways to tap into the lysosomal degradation pathway of autophagy to reduce age-related protein accumulation events. Shoji-Kawata et al. (Nature 2013;494:201–206) describe a new autophagy-inducing peptide, Tat-Beclin 1, that enhances the clearance of polyglutamine aggregates related to Huntington’s disease and, interestingly, suppresses viral and bacterial infections. Savolainen et al. (Neurobiol Dis 2014;68:1–15) describe a prolyl oligopeptidase inhibitor that reduces a-synuclein species related to Parkinson’s disease and other a-synucleinopathies, and this inhibitor caused a concomitant increase in autophagic activation markers. Previous studies have also linked the autophagy–lysosomal pathway to the protective clearing of the A ß peptides of Alzheimer’s disease and tau species of tauopathies. Enhancing autophagy–lysosomal ef?ciency may provide a therapeutic avenue for diverse types of proteinopathies, including the most common neurodegenerative disorders of the elderly.

Additional Information

Rejuvenation Research 17.4 (2014)
Language: English
Date: 2014
Autophagy-Lysosomal, Protein Clearance, Peptide, Prolyl Oligopeptidase Inhibitor, Proteinopathies, Eldery, Neurodegenerative Disorders

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