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Neuronal aging: learning from C. elegans.

Chun-Hao ChenYen-Chih ChenHao-Ching JiangChung-Kuan ChenChun-Liang Pan
Published in: Journal of molecular signaling (2013)
The heterogeneity and multigenetic nature of nervous system aging make modeling of it a formidable task in mammalian species. The powerful genetics, simple anatomy and short life span of the nematode Caenorhabditis elegans offer unique advantages in unraveling the molecular genetic network that regulates the integrity of neuronal structures and functions during aging. In this review, we first summarize recent breakthroughs in the morphological and functional characterization of C. elegans neuronal aging. Age-associated morphological changes include age-dependent neurite branching, axon beading or swelling, axon defasciculation, progressive distortion of the neuronal soma, and early decline in presynaptic release function. We then discuss genetic pathways that modulate the speed of neuronal aging concordant with alteration in life span, such as insulin signaling, as well as cell-autonomous factors that promote neuronal integrity during senescence, including membrane activity and JNK/MAPK signaling. As a robust genetic model for aging, insights from C. elegans neuronal aging studies will contribute to our mechanistic understanding of human brain aging.
Keyphrases
  • cerebral ischemia
  • type diabetes
  • signaling pathway
  • genome wide
  • endothelial cells
  • dna methylation
  • metabolic syndrome
  • adipose tissue
  • copy number
  • cell proliferation
  • skeletal muscle
  • cell therapy
  • brain injury