The Peripheral Amyloid-β Nexus: Connecting Alzheimer's Disease with Atherosclerosis through Shared Pathophysiological Mechanisms

被引:0
作者
Khowdiary, Manal M. [1 ]
Al-kuraishy, Hayder M. [2 ]
Al-Gareeb, Ali I. [3 ]
Albuhadily, Ali K. [2 ]
Elhenawy, Ahmed A. [4 ,5 ]
Rashwan, Eman K. [6 ]
Alexiou, Athanasios [7 ,8 ]
Papadakis, Marios [9 ]
Abo-El Fetoh, Mohammed E. [10 ]
Batiha, Gaber El-Saber [11 ]
机构
[1] Umm Al Qura Univ, Fac Sci Appl, Dept Chem, Lieth Coll, Mecca, Saudi Arabia
[2] Mustansiriyah Univ, Coll Med, Dept Clin Pharmacol & Med, Baghdad, Iraq
[3] Jabir ibn Hayyan Med Univ, POB 13, Kufa, Kufa, Iraq
[4] Al Azhar Univ, Fac Sci, Chem Dept, Cairo 11884, Egypt
[5] AlBaha Univ, Fac Sci, Chem Dept, Al Bahah 65731, Saudi Arabia
[6] Jouf Univ, Coll Med, Dept Physiol, Akaka, Saudi Arabia
[7] Funogen, Dept Res & Dev, Athens 11741, Greece
[8] Chandigarh Univ, Univ Ctr Res & Dev, Chandigarh Ludhiana Highway, Mohali, Punjab, India
[9] Univ Witten Herdecke, Univ Hosp, Heusnerstre 40, D-42283 Wuppertal, Germany
[10] Egyptian Russian Univ, Fac Pharm, Pharmacol & Toxicol Dept, Badr City 11829, Cairo, Egypt
[11] Damanhour Univ, Fac Vet Med, Dept Pharmacol & Therapeut, Damanhour 22511, AlBeheira, Egypt
关键词
Alzheimer's disease; Atherosclerosis; Amyloid-beta (A beta); Vascular dysfunction; Neuroinflammation; Oxidative stress; Insulin resistance; A beta clearance pathways; PRECURSOR PROTEIN; BACE1; ACTIVITY; A-BETA; RISK; INFLAMMATION; DYSFUNCTION; DEMENTIA; TAU; NEUROPATHOLOGY; ABNORMALITIES;
D O I
10.1007/s12017-025-08836-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer's disease (AD) and atherosclerosis (AS) are two chronic diseases with seemingly distinct pathologies. However, emerging research points to a bidirectional relationship driven by common mechanisms, such as inflammation, oxidative stress, and dysregulation of Amyloid-Beta (A beta). This review focuses on the role of A beta as a critical molecular link between AD and AS, emphasizing its contribution to neuronal impairment and vascular damage. Specifically, peripheral A beta produced in the pancreas and skeletal muscle tissues exacerbates AS by promoting endothelial dysfunction and insulin resistance (IR). Furthermore, AS accelerates AD progression by impairing cerebral blood flow and inducing chronic hypoxia, causing A beta accumulation. This review critically evaluates recent findings, highlighting inconsistencies in clinical studies and suggesting future research directions. Understanding the bidirectional influence of AD and AS could pave the way for novel therapeutic approaches targeting shared molecular pathways, particularly emphasizing A beta clearance and inflammation.
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页数:13
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