Metabolic triad in brain aging: Mitochondria, insulin/IGF-1 signalling and JNK signalling

Fei Yin, Tianyi Jiang, Enrique Cadenas

Research output: Contribution to journalArticlepeer-review

46 Scopus citations

Abstract

Mitochondria generate second messengers, such as H2O 2, that are involved in the redox regulation of cell signalling and their function is regulated by several cytosolic signalling pathways. IIS [insulin/IGF1 (insulin-like growth factor 1) signalling] in the brain proceeds mainly through the PI3K (phosphatidylinositol 3-kinase)-Akt (protein kinase B) pathway, which is involved in the regulation of synaptic plasticity and neuronal survival via the maintenance of the bioenergetic and metabolic capacities of mitochondria. Conversely, the JNK (c-Jun N-terminal kinase) pathway is induced by increased oxidative stress and JNK translocation to the mitochondrion results in impairment of energy metabolism. Moreover, IIS and JNK signalling interact with and antagonize each other. This review focuses on functional outcomes of a metabolic triad that entails the co-ordination of mitochondrial function (energy transducing and redox regulation), IIS and JNK signalling, in the aging brain and in neurodegenerative disorders, such as Alzheimer's disease.

Original languageEnglish (US)
Pages (from-to)101-105
Number of pages5
JournalBiochemical Society transactions
Volume41
Issue number1
DOIs
StatePublished - Feb 2013
Externally publishedYes

Keywords

  • Brain aging
  • C-Jun N-terminal kinase (JNK)
  • Energy metabolism
  • Insulin/insulin-like growth factor-1 signalling
  • Mitochondrion
  • Neurodegeneration

ASJC Scopus subject areas

  • Biochemistry

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