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Genetic evidence for protective effects of angiotensin converting enzyme against Alzheimer's disease but not other neurodegenerative diseases
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  • David Ryan,
  • Ville Karhunen,
  • Su Bowen,
  • Matthew Traylor,
  • Tom Richardson,
  • Stephen Burgess,
  • I Tzoulaki,
  • Dipender Gill
David Ryan
St George's University Hospitals NHS Foundation Trust

Corresponding Author:davidkdryan@gmail.com

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Ville Karhunen
Imperial College London
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Su Bowen
Imperial College London
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Matthew Traylor
Queen Mary University of London
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Tom Richardson
University of Bristol
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Stephen Burgess
University of Cambridge Institute of Public Health
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I Tzoulaki
Imperial College London
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Dipender Gill
St George's University Hospitals NHS Foundation Trust
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Abstract

Genetic evidence has supported a protective effect of cerebral angiotensin converting enzyme (ACE) against Alzheimer’s disease (AD). However, it is unclear whether this is mediated through blood pressure and extends to other neurodegenerative diseases. We performed genetic colocalization investigating an effect of cortical ACE expression on AD risk. We further investigated whether any effect of ACE expression is mediated through changes in blood pressure, and whether effects extend to Parkinson’s disease, small vessel disease or cognitive function. There was genetic evidence supporting a protective effect of cortical ACE expression on AD risk. Although higher cortical ACE expression was associated with higher blood pressure, there was no strong evidence to support that its association with AD was mediated through blood pressure, nor that ACE expression affected risk of other neurodegenerative traits. Genetic evidence supports protective effects of cerebral ACE expression on AD, but not other neurodegenerative outcomes.