Deletion/Insertion Polymorphism of the Angiotensin-Converting Enzyme Gene and White Matter Hyperintensities in Dementia: A Pilot Study
Article first published online: 18 JUL 2006
Journal of the American Geriatrics Society
Volume 54, Issue 9, pages 1395–1400, September 2006
How to Cite
Purandare, N., Oude Voshaar, R. C., Davidson, Y., Gibbons, L., Hardicre, J., Byrne, J., McCollum, C., Jackson, A., Burns, A. and Mann, D. M. A. (2006), Deletion/Insertion Polymorphism of the Angiotensin-Converting Enzyme Gene and White Matter Hyperintensities in Dementia: A Pilot Study. Journal of the American Geriatrics Society, 54: 1395–1400. doi: 10.1111/j.1532-5415.2006.00841.x
- Issue published online: 7 SEP 2006
- Article first published online: 18 JUL 2006
- ACE polymorphism;
- white matter lesions
OBJECTIVES: To examine the association between the angiotensin-converting enzyme (ACE) deletion/insertion (D/I) polymorphism and white matter hyperintensities (WMHs) in patients with dementia.
DESIGN: Observational pilot study with adjustment for potential confounders using analysis of covariance.
SETTING: Secondary care old-age psychiatry services in greater Manchester, United Kingdom.
PARTICIPANTS: Ninety-seven patients with dementia: 49 with Alzheimer's disease (AD, National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria) and 48 with vascular dementia (VaD, National Institute of Neurological Disorders and Stroke/Association Internationale pour la Recherche et l'Enseignement en Neurosciences criteria).
MEASUREMENTS: The ACE D/I polymorphism, WMHs (deep WMHs (DWMHs) and periventricular hyperintensities (PVHs)) on T2-weighted magnetic resonance imaging, and potential cardiovascular confounders.
RESULTS: The D/D polymorphism of the ACE genotype was associated with severity of DWMH (P=.005) but not PVH (P=.34), corrected for age, cardiovascular risk factors, and type of dementia. Post hoc analyses were limited by statistical power but suggested an interaction with the apolipoprotein E ɛ4 allele.
CONCLUSION: The results support previous observations that genetic factors influence the development of WMHs in dementia. The involvement of the ACE D/I polymorphism in the pathogenesis of DWMHs in dementia (AD and VaD), by a mechanism that is independent of its association with cardiovascular risk factors, should be confirmed in a large population-based sample.