New roles for insulin-like hormones in neuronal signalling and protection: new hopes for novel treatments of Alzheimer's disease?

Neurobiol Aging. 2010 Sep;31(9):1495-502. doi: 10.1016/j.neurobiolaging.2008.08.023. Epub 2008 Oct 18.

Abstract

Type 2 diabetes has been identified as a risk factor for Alzheimer's disease (AD). This is most likely due to the desensitisation of insulin receptors in the brain. Insulin acts as a growth factor and supports neuronal repair, dendritic sprouting, and differentiation. This review discusses the potential role that insulin-like hormones could play in ameliorating the reduced growth factor signalling in the brains of people with AD. The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have very similar properties in protecting neurons from toxic effects, and are capable of reversing the detrimental effects that beta-amyloid fragments have on synaptic plasticity. Therefore, incretins show great promise as a novel treatment for reducing degenerative processes in AD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism*
  • Animals
  • Brain / drug effects
  • Brain / metabolism*
  • Humans
  • Incretins / administration & dosage*
  • Incretins / metabolism*
  • Insulin / metabolism*
  • Neuroprotective Agents / metabolism
  • Neuroprotective Agents / therapeutic use
  • Signal Transduction / drug effects*

Substances

  • Incretins
  • Insulin
  • Neuroprotective Agents