Mechanisms of aging-related proteinopathies in Caenorhabditis elegans.

Abstract

Aging is the most important risk factor for human neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. Pathologically, these diseases are characterized by the deposition of specific protein aggregates in neurons and glia, representing the impairment of neuronal proteostasis. However, the mechanism by which aging affects the proteostasis system and promotes protein aggregation remains largely unknown. The short lifespan and ample genetic resources of Caenorhabditis elegans (C. elegans) have made this species a favorite model organism for aging research, and the development of proteinopathy models in this organism has helped us to understand how aging processes affect protein aggregation and neurodegeneration. Here, we review the recent literature on proteinopathies in C. elegans models and discuss the insights we have gained into the mechanisms of how aging processes are integrated into the pathogenesis of various neurodegenerative diseases.

• Authors: Dong-Kyu Kim, Tae Ho Kim, Seung-Jae Lee
• Journal: Experimental & molecular medicine (Exp Mol Med) Vol. 48 Issue 10 Pg. e263 (10 07 2016) ISSN: 2092-6413 [Electronic] United States
• PMID: 27713398 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)

Chemical References

• Protein Aggregates

Topics

• Aging
• Animals
• Autophagy
• Caenorhabditis elegans (metabolism, physiology)
• Disease Models, Animal
• Humans
• Neurodegenerative Diseases (metabolism, pathology)
• Neurons (metabolism, pathology)
• Protein Aggregates
• Protein Aggregation, Pathological (metabolism, pathology)
• Signal Transduction