Abstract

van Exel and colleagues present an elegant study testing relationships between vascular and inflammatory traits and the risk of Alzheimer's disease (AD) development. They compared middle-aged offspring of AD cases with similar offspring of nondemented parents and observed greater inflammatory response to challenge and increased hypertension in those at high genetic risk. These observations join a growing body of evidence implicating inflammation/innate immunity as a crucial component in disease development. Recent discoveries of new risk genes for Alzheimer's disease also implicate innate immunity and to some extent vascular health as potentially important in pathogenesis. Further identification and refinement of putative disease mechanisms is likely as the genetic architecture of AD is uncovered through current large-scale association and sequencing studies.

Highlights

  • Abstract van Exel and colleagues present an elegant study testing relationships between vascular and inflammatory traits and the risk of Alzheimer’s disease (AD) development

  • The reason most of us in the field of complex genetics search for genes that contribute to disease development is that these genes will pinpoint mechanisms of primary importance to pathogenesis

  • Using a variation on this theme, van Exel and colleagues sought to identify traits associated with genetic risk before the development of Alzheimer’s disease (AD) [1]

Read more

Summary

Introduction

Abstract van Exel and colleagues present an elegant study testing relationships between vascular and inflammatory traits and the risk of Alzheimer’s disease (AD) development. The reason most of us in the field of complex genetics search for genes that contribute to disease development is that these genes will pinpoint mechanisms of primary importance to pathogenesis. Using a variation on this theme, van Exel and colleagues sought to identify traits associated with genetic risk before the development of Alzheimer’s disease (AD) [1]. The study used an elegant design to identify primary events related to disease susceptibility in those at high genetic risk.

Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call