Background <p>Atherosclerosis (AS) and Alzheimer's disease (AD) are both multifactorial in nature and share many risk factors. Vascular dementia and AD may occur together, and a substantial proportion of AD cases also have signs of cardiovascular disease, a relationship well-established by cohort studies. The risk factors could contribute to persistent smoldering inflammation, including activation of complement at sites of endothelial injury and/or by accumulation of molecular aggregates.</p> Methods <p>To examine the possible bridging points between AD and AS, we constructed a comprehensive narrative review.</p> Results <p>A connecting point between AD and AS is inflammation. Contrary to prior assumptions, a significant linkage exists between systemic inflammation and neuroinflammation. Activities of complement, a key effector of innate immunity, are of special interest in the pathogenesis of both diseases.</p> Conclusion <p>AS and AD share a partially overlapping array of pathophysiological mechanisms.</p>

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Exploring the intersection of atherosclerosis and Alzheimer’s disease: the role of inflammation and complement activation

  • Emilia Vataja,
  • Giorgio Ratti,
  • Adrian Safa,
  • Marta Pagano,
  • Luigia Ferrante,
  • Seppo Meri,
  • Karita Haapasalo

摘要

Background

Atherosclerosis (AS) and Alzheimer's disease (AD) are both multifactorial in nature and share many risk factors. Vascular dementia and AD may occur together, and a substantial proportion of AD cases also have signs of cardiovascular disease, a relationship well-established by cohort studies. The risk factors could contribute to persistent smoldering inflammation, including activation of complement at sites of endothelial injury and/or by accumulation of molecular aggregates.

Methods

To examine the possible bridging points between AD and AS, we constructed a comprehensive narrative review.

Results

A connecting point between AD and AS is inflammation. Contrary to prior assumptions, a significant linkage exists between systemic inflammation and neuroinflammation. Activities of complement, a key effector of innate immunity, are of special interest in the pathogenesis of both diseases.

Conclusion

AS and AD share a partially overlapping array of pathophysiological mechanisms.