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Published on: January 4, 2018
Insulin/IGF-like signalling, the central nervous system and aging
Susan Broughton1, Linda Partridge
1UCL Institute of Healthy Aging, GEE (Genetics, Evolution and Environment), University College London, Gower St., London WC1E 6BT, UK.
Manipulating insulin/IGF-like signalling (IIS) in the nervous system can extend lifespan. Understanding IIS
Area of Science:
- Genetics and Molecular Biology
- Neuroscience
- Aging Research
Background:
- Genetic mutations in model organisms reveal conserved pathways influencing lifespan.
- Insulin/IGF-like signalling (IIS) is a key evolutionarily conserved pathway affecting lifespan and organismal functions.
- IIS mutations impact growth, metabolism, reproduction, stress resistance, and longevity.
Purpose of the Study:
- To review the current understanding of the nervous system's role in IIS-mediated lifespan extension.
- To explore how IIS influences neuronal function throughout the aging process.
- To discuss the interplay between IIS, neuronal function, and overall lifespan.
Main Methods:
- Review of existing scientific literature on IIS, aging, and the nervous system.
- Analysis of studies involving genetic manipulations of IIS in model organisms.
- Examination of research on tissue-specific effects of IIS on lifespan and neuronal health.
Main Results:
- Lowered IIS in the central nervous system (CNS) can extend lifespan.
- IIS plays a crucial neuroprotective role, supporting neuronal growth and survival.
- The nervous system influences lifespan extension through both endocrine and cell-autonomous mechanisms.
Conclusions:
- Altered IIS in the nervous system is a significant factor in lifespan extension.
- IIS's effects on lifespan and neuronal function can be partially dissociated.
- Tissue-specific IIS modulation and understanding cellular defense mechanisms are key to defining IIS's role in aging.
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