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<p>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.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月3日

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  • 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

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 (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.