Role of insulin resistance in Alzheimer’s disease

Zhiyou Cai, Ming Xiao, Liying Chang, Liang Jun Yan

Research output: Contribution to journalReview article

16 Citations (Scopus)

Abstract

A critical role of insulin resistance (IR) in Alzheimer’s disease (AD) includes beta-amyloid (Aβ) production and accumulation, the formation of neurofibrillary tangles (NFTs), failure of synaptic transmission and neuronal degeneration. Aβ is sequentially cleavaged from APP by two proteolytic enzymes: β-secretase and γ-secretase. IR could regulate Aβ production via enhancing β- and γ-secretase activity. Meanwhile, IR induces oxidative stress and inflammation in the brain which contributes toAβ and tau pathology. Aβ accumulation can enhance IR through Aβ-mediated inflammation and oxidative stress. IR is a possible linking between amyloid plaques and NFTs pathology via oxidative stress and neuroinflammation. Additionally, IR could disrupt acetylcholine activity, and accelerate axon degeneration and failures in axonal transport, and lead to cognitive impairment in AD. Preclinical and clinical studies have supported that insulin could be useful in the treatment of AD. Thus, an effective measure to inhibit IR may be a novel drug target in AD.

Original languageEnglish
Article numberA001
Pages (from-to)839-851
Number of pages13
JournalMetabolic Brain Disease
Volume30
Issue number4
DOIs
StatePublished - 1 Aug 2015

Fingerprint

Insulin Resistance
Alzheimer Disease
Insulin
Amyloid Precursor Protein Secretases
Oxidative stress
Neurofibrillary Tangles
Oxidative Stress
Pathology
Amyloid
Axonal Transport
Amyloid Plaques
Encephalitis
Synaptic Transmission
Acetylcholine
Axons
Peptide Hydrolases
Brain
Inflammation
Pharmaceutical Preparations

Keywords

  • Alzheimer’s disease
  • Cognitive impairment
  • Insulin resistance
  • Tau hyperphosphorylation

Cite this

Cai, Zhiyou ; Xiao, Ming ; Chang, Liying ; Yan, Liang Jun. / Role of insulin resistance in Alzheimer’s disease. In: Metabolic Brain Disease. 2015 ; Vol. 30, No. 4. pp. 839-851.
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Role of insulin resistance in Alzheimer’s disease. / Cai, Zhiyou; Xiao, Ming; Chang, Liying; Yan, Liang Jun.

In: Metabolic Brain Disease, Vol. 30, No. 4, A001, 01.08.2015, p. 839-851.

Research output: Contribution to journalReview article

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AU - Cai, Zhiyou

AU - Xiao, Ming

AU - Chang, Liying

AU - Yan, Liang Jun

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AB - A critical role of insulin resistance (IR) in Alzheimer’s disease (AD) includes beta-amyloid (Aβ) production and accumulation, the formation of neurofibrillary tangles (NFTs), failure of synaptic transmission and neuronal degeneration. Aβ is sequentially cleavaged from APP by two proteolytic enzymes: β-secretase and γ-secretase. IR could regulate Aβ production via enhancing β- and γ-secretase activity. Meanwhile, IR induces oxidative stress and inflammation in the brain which contributes toAβ and tau pathology. Aβ accumulation can enhance IR through Aβ-mediated inflammation and oxidative stress. IR is a possible linking between amyloid plaques and NFTs pathology via oxidative stress and neuroinflammation. Additionally, IR could disrupt acetylcholine activity, and accelerate axon degeneration and failures in axonal transport, and lead to cognitive impairment in AD. Preclinical and clinical studies have supported that insulin could be useful in the treatment of AD. Thus, an effective measure to inhibit IR may be a novel drug target in AD.

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