The link between metabolic syndrome and Alzheimer disease: A mutual relationship and long rigorous investigation

被引：41

作者：

Al-kuraishy, Haydar M. ^{[1
]}

Jabir, Majid S. ^{[2
]}

Albuhadily, Ali K. ^{[1
]}

Al-Gareeb, Ali I. ^{[1
]}

Rafeeq, Mayyadah F. ^{[2
]}

机构：

[1] Mustansiriyah Univ, Coll Med, Dept Clin pharmacol & Med, Baghdad, Iraq

[2] Technol Univ, Dept Appl Sci, Baghdad, Iraq

来源：

AGEING RESEARCH REVIEWS | 2023年 / 91卷

关键词：

Metabolic syndrome; Alzheimer disease; Amyloid beta; Insulin resistance; Obesity; Hypertension; BRAIN INSULIN-RESISTANCE; AMYLOID-BETA-PROTEIN; NF-KAPPA-B; DIABETES-MELLITUS; OXIDATIVE STRESS; A-BETA; RISK-FACTOR; INFLAMMATION; ACID; PATHOGENESIS;

D O I：

10.1016/j.arr.2023.102084

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

It has been illustrated that metabolic syndrome (MetS) is associated with Alzheimer disease (AD) neuropathology. Components of MetS including central obesity, hypertension, insulin resistance (IR), and dyslipidemia adversely affect the pathogenesis of AD by different mechanisms including activation of renin-angiotensin system (RAS), inflammatory signaling pathways, neuroinflammation, brain IR, mitochondrial dysfunction, and oxidative stress. MetS exacerbates AD neuropathology, and targeting of molecular pathways in MetS by pharmacological approach could a novel therapeutic strategy in the management of AD in high risk group. However, the underlying mechanisms of these pathways in AD neuropathology are not completely clarified. Therefore, this review aims to elucidate the association between MetS and AD regarding the oxidative and inflammatory mechanistic pathways.

引用

页数：10

共 180 条

[71] Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease [J].

Guo, Tiantian ;

Zhang, Denghong ;

Zeng, Yuzhe ;

Huang, Timothy Y. ;

Xu, Huaxi ;

Zhao, Yingjun .

MOLECULAR NEURODEGENERATION, 2020, 15 (01)

[72] Deletion of Cardiomyocyte Glycogen Synthase Kinase-3 Beta (GSK-3β) Improves Systemic Glucose Tolerance with Maintained Heart Function in Established Obesity [J].

Gupte, Manisha ;

Umbarkar, Prachi ;

Singh, Anand Prakash ;

Zhang, Qinkun ;

Tousif, Sultan ;

Lal, Hind .

CELLS, 2020, 9 (05)

[73] The NALP3 inflammasome is involved in the innate immune response to amyloid-β [J].

Halle, Annett ;

Hornung, Veit ;

Petzold, Gabor C. ;

Stewart, Cameron R. ;

Monks, Brian G. ;

Reinheckel, Thomas ;

Fitzgerald, Katherine A. ;

Latz, Eicke ;

Moore, Kathryn J. ;

Golenbock, Douglas T. .

NATURE IMMUNOLOGY, 2008, 9 (08) :857-865

[74] The Amyloid-β Pathway in Alzheimer's Disease [J].

Hampel, Harald ;

Hardy, John ;

Blennow, Kaj ;

Chen, Christopher ;

Perry, George ;

Kim, Seung Hyun ;

Villemagne, Victor L. ;

Aisen, Paul ;

Vendruscolo, Michele ;

Iwatsubo, Takeshi ;

Masters, Colin L. ;

Cho, Min ;

Lannfelt, Lars ;

Cummings, Jeffrey L. ;

Vergallo, Andrea .

MOLECULAR PSYCHIATRY, 2021, 26 (10) :5481-5503

[75] Maternal immune activation and neuroinflammation in human neurodevelopmental disorders [J].

Han, Velda X. ;

Patel, Shrujna ;

Jones, Hannah F. ;

Dale, Russell C. .

NATURE REVIEWS NEUROLOGY, 2021, 17 (09) :564-579

[76] The Role of Microglia and the Nlrp3 Inflammasome in Alzheimer's Disease [J].

Hanslik, Kendra L. ;

Ulland, Tyler K. .

FRONTIERS IN NEUROLOGY, 2020, 11

[77] Regional differences in cortical benzodiazepine receptors of Alzheimer, vascular, and mixed dementia patients [J].

Hanyu, Haruo ;

Kume, Kazumasa ;

Sato, Tomohiko ;

Hirao, Kentaro ;

Kanetaka, Hidekazu ;

Sakurai, Hirofumi ;

Iwamoto, Toshihiko .

JOURNAL OF THE NEUROLOGICAL SCIENCES, 2012, 323 (1-2) :71-76

[78] Protective effects of luteolin against amyloid beta-induced oxidative stress and mitochondrial impairments through peroxisome proliferator-activated receptor ?-dependent mechanism in Alzheimer's disease [J].

He, Zhijun ;

Li, Xiaoqian ;

Wang, Zi ;

Cao, Yingqi ;

Han, Shuangxue ;

Li, Nan ;

Cai, Jie ;

Cheng, Shuiyuan ;

Liu, Qiong .

REDOX BIOLOGY, 2023, 66

[79] Amyloid β-protein is degraded by cellular angiotensin-converting enzyme (ACE) and elevated by an ACE inhibitor [J].

Hemming, ML ;

Selkoe, DJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (45) :37644-37650

[80] Plasma Free Fatty Acid Concentration as a Modifiable Risk Factor for Metabolic Disease [J].

Henderson, Gregory C. .

NUTRIENTS, 2021, 13 (08)

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