Is sporadic Alzheimer disease the brain type of non-insulin dependent diabetes mellitus? A challenging hypothesis

J Neural Transm (Vienna). 1998;105(4-5):415-22. doi: 10.1007/s007020050067.

Abstract

The hypothesis is forwarded that sporadic late-onset Alzheimer disease is caused by non-insulin dependent diabetes mellitus which is confined to the brain. This hypothesis is based on the findings of Frölich and coworkers (this volume) who clearly demonstrate a perturbation of the neuronal insulin/ insulin receptor signal transduction pathway which is considered to be the pathobiochemical basis for the drastic reduction in glucose/energy metabolism in Alzheimer brain. As a consequence of this abnormality, advanced glycation end products are formed. Münch et al. (this volume) evaluate the impacts of the latter related to oxidative stress and the formation of beta-amyloid and neurofibrillary tangles.

MeSH terms

  • Age of Onset
  • Alzheimer Disease / etiology
  • Alzheimer Disease / physiopathology*
  • Brain / metabolism*
  • Brain / physiopathology
  • Diabetes Mellitus, Type 2 / complications
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Energy Metabolism
  • Glucose / metabolism
  • Glycation End Products, Advanced
  • Humans
  • Insulin / physiology
  • Models, Neurological
  • Neurons / physiology*
  • Receptor, Insulin / physiology
  • Signal Transduction

Substances

  • Glycation End Products, Advanced
  • Insulin
  • Receptor, Insulin
  • Glucose