Metabolic derangements mediate cognitive impairment and Alzheimer's disease: role of peripheral insulin-resistance diseases

Panminerva Med. 2012 Sep;54(3):171-8.

Abstract

Herein, we review evidence that systemic insulin-resistance diseases linked to obesity, type 2 diabetes, and non-alcoholic steatohepatitis promote neurodegeneration. Insulin-resistance dysregulates lipid metabolism, which promotes ceramide accumulation with attendant inflammation and endoplasmic reticulum (ER) stress. Mechanistically, we propose that toxic ceramides generated in extra-CNS tissues, e.g. liver, get released into peripheral blood, and subsequently transit across the blood-brain barrier into the brain where they induce brain insulin-resistance, inflammation, and cell death (extrinsic pathway). These abnormalities establish or help propagate a cascade of neurodegeneration associated with increased ER stress and ceramide generation, which exacerbate brain insulin-resistance, cell death, myelin degeneration, and neuro-inflammation. The data suggest that a mal-signaling network mediated by toxic ceramides, ER stress, and insulin-resistance should be targeted to disrupt positive feedback loops that drive the AD neurodegeneration cascade.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / complications
  • Alzheimer Disease / therapy*
  • Blood-Brain Barrier
  • Brain / pathology
  • Central Nervous System / pathology
  • Ceramides / chemistry
  • Ceramides / metabolism
  • Cognition Disorders / complications
  • Cognition Disorders / pathology
  • Cognition Disorders / therapy*
  • Diabetes Mellitus / pathology
  • Endoplasmic Reticulum / metabolism
  • Humans
  • Inflammation
  • Insulin Resistance
  • Lipid Metabolism
  • Models, Biological
  • Neurodegenerative Diseases / pathology
  • Obesity

Substances

  • Ceramides