Inflammation and insulin resistance in Alzheimer’s disease: Partners in crime

Yuval Nash, Dan Frenkel

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Alzheimer’s disease (AD) is the most common brain degenerative disease leading to dementia. Currently, there is no cure or efficient therapy to slow disease progression. While AD has specific disease features including beta amyloid accumulation and tau pathology, other pathological features are also affiliated with the disease and are shared with several other neurodegenerative diseases, including inflammation and impairments in brain insulin signaling. Activation of different known inflammatory factors such as the complement system and cytokines were linked to disease progression. Impairment in brain insulin signaling was found both in AD patients and disease animal models. Furthermore, it was suggested that metabolic disorders and diabetes are among the risk factors in developing AD. Approaches to modulating inflammation or the administration of insulin are currently in AD clinical trials. The current review aims to describe elements of inflammation and impairments in insulin signaling in the disease. Specific emphasis will be given to the potential link between those risk factors and their potential role in the progression of the disease.

Original languageEnglish
Title of host publicationGenetics, Neurology, Behavior, and Diet in Dementia
Subtitle of host publicationThe Neuroscience of Dementia, Volume 2
PublisherElsevier
Pages389-405
Number of pages17
ISBN (Electronic)9780128158685
DOIs
StatePublished - 1 Jan 2020

Keywords

  • AKT
  • Alzheimer’s
  • Beta amyloid
  • Complement system
  • Cytokines
  • Inflammation
  • Insulin
  • Insulin resistance
  • Insulin signaling
  • Risk factors

All Science Journal Classification (ASJC) codes

  • General Neuroscience
  • General Medicine

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