title: Deletion/insertion polymorphism of the angiotensin-converting enzyme gene and white matter hyperintensities in dementia: A pilot study.
abstract: OBJECTIVE
  To examine the association between the angiotensin-converting enzyme (ACE) deletion/insertion (D/I) polymorphism and white matter hyperintensities (WMHs) in patients with dementia.
  
  
  METHODS
  Observational pilot study with adjustment for potential confounders using analysis of covariance.
  
  
  METHODS
  Secondary care old-age psychiatry services in greater Manchester, United Kingdom.
  
  
  METHODS
  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).
  
  
  METHODS
  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 epsilon4 allele.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Psychiatry, Education and Research Center, South Manchester University Hospital, Manchester, United Kingdom. nitin.purandare@manchester.ac.uk
authors.forename: Nitin
authors.initials: N
authors.lastname: Purandare
authors.forename: Richard C
authors.initials: RC
authors.lastname: Oude Voshaar
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Davidson
authors.forename: Linda
authors.initials: L
authors.lastname: Gibbons
authors.forename: Jayne
authors.initials: J
authors.lastname: Hardicre
authors.forename: Jane
authors.initials: J
authors.lastname: Byrne
authors.forename: Charles
authors.initials: C
authors.lastname: McCollum
authors.forename: Alan
authors.initials: A
authors.lastname: Jackson
authors.forename: Alistair
authors.initials: A
authors.lastname: Burns
authors.forename: David M A
authors.initials: DM
authors.lastname: Mann
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000235:genetics* / Q000473:pathology; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics; D001921:Brain / Q000473:pathology*; D015140:Dementia, Vascular / Q000235:genetics* / Q000473:pathology; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010865:Pilot Projects; D011110:Polymorphism, Genetic / Q000235:genetics*
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D007703:Peptidyl-Dipeptidase A