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Metabolism-centric overview of the pathogenesis of Alzheimer’s disease.

Authors
 Somang Kang  ;  Yong-ho Lee  ;  Jong Eun Lee 
Citation
 Yonsei Medical Journal, Vol.58(3) : 479-488, 2017 
Journal Title
 Yonsei Medical Journal 
ISSN
 0513-5796 
Issue Date
2017
MeSH
Adiponectin/blood ; Adiponectin/metabolism ; Aging*/physiology ; Aging*/psychology ; Alzheimer Disease/metabolism* ; Alzheimer Disease/pathology* ; Amyloid beta-Peptides ; Antioxidants/metabolism ; Biomarkers ; Brain/metabolism* ; Brain/pathology ; Brain/physiopathology ; Brain Chemistry/physiology* ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin/blood ; Insulin/metabolism ; Obesity/metabolism* ; Oxidative Stress/physiology
Keywords
Alzheimer's disease ; adiponectin ; antioxidants ; insulin ; metabolic disease
Abstract
Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia. AD is characterized by the extracellular amyloid beta (Aβ) plaques and intraneuronal deposits of neurofibrillary tangles (NFTs). Recently, as aging has become a familiar phenomenon around the world, patients with AD are increasing in number. Thus, many researchers are working toward finding effective therapeutics for AD focused on Aβ hypothesis, although there has been no success yet. In this review paper, we suggest that AD is a metabolic disease and that we should focus on metabolites that are affected by metabolic alterations to find effective therapeutics for AD. Aging is associated with not only AD but also obesity and type 2 diabetes (T2DM). AD, obesity, and T2DM share demographic profiles, risk factors, and clinical and biochemical features in common. Considering AD as a kind of metabolic disease, we suggest insulin, adiponectin, and antioxidants as mechanistic links among these diseases and targets for AD therapeutics. Patients with AD show reduced insulin signal transductions in the brain, and intranasal injection of insulin has been found to have an effect on AD treatment. In addition, adiponectin is decreased in the patients with obesity and T2DM. This reduction induces metabolic dysfunction both in the body and the brain, leading to AD pathogenesis. Oxidative stress is known to be induced by Aβ and NFTs, and we suggest that oxidative stress caused by metabolic alterations in the body induce brain metabolic alterations, resulting in AD.
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DOI
10.3349/ymj.2017.58.3.479
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
Yonsei Authors
이용호(Lee, Yong Ho) ORCID logo https://orcid.org/0000-0002-6219-4942
이종은(Lee, Jong Eun) ORCID logo https://orcid.org/0000-0001-6203-7413
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/154538
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