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Publications

Journal Article Review Epublish

PubMed: 40032716 DOI: 10.1007/s12017-025-08836-2

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

Neuromolecular Med 27(1):20

Authors: Manal M Khowdiary, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Albuhadily, Ahmed A Elhenawy, Eman K Rashwan, Athanasios Alexiou, Marios Papadakis, Mohammed E Abo-El Fetoh, Gaber El-Saber Batiha

Affiliations

  • Department of Chemistry, Faculty of Applied Science, Lieth Collage, Umm Al-Qura University, 24382, Makkah, Saudi Arabia.
  • Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
  • Jabir Ibn Hayyan Medical University, Al-Ameer Qu./Najaf-Iraq, PO. Box13, Kufa, Iraq.
  • Chemistry Department, Faculty of Science, Al-Azhar University, Nasr City, Cairo, 11884, Egypt.
  • Chemistry Department, Faculty of Science, AlBaha University, 65731, Al Bahah, Saudi Arabia.
  • Department of Physiology, College of Medicine, Jouf University, Akaka, Saudi Arabia.
  • Department of Research & Development, Funogen, 11741, Athens, Attiki, Greece.
  • University Centre for Research & Development, Chandigarh University, Chandigarh-Ludhiana Highway, Mohali, Punjab, India.
  • University Hospital, University of Witten-Herdecke, Heusnerstrasse 40, 42283, Wuppertal, Germany.
  • Department of Pharmacology and Toxicology, Faculty of Pharmacy, Egyptian Russian University, Badr City, 11829, Cairo, Egypt.
  • Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, AlBeheira, Egypt.

Abstract

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 (Aβ). This review focuses on the role of Aβ as a critical molecular link between AD and AS, emphasizing its contribution to neuronal impairment and vascular damage. Specifically, peripheral Aβ 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 Aβ 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 Aβ clearance and inflammation.

MeSH

Muscles, Alzheimer Disease, Research, Atherosclerosis, Amyloid, Nervous System Diseases