| pubmed-article:12736093 | pubmed:abstractText | There is evidence that indicates the involvement of environmental and genetic factors in the pathogenesis of post-stroke dementia (PSD). In the present work, we examined different polygenic influences on the risk of PSD in a series of stroke patients. We studied 150 consecutive patients evaluated 3 months after suffering acute strokes. All patients were evaluated with a prospective standard protocol and genotyped for vascular disease-associated polymorphisms in the genes coding for apolipoprotein E (including apoE coding and apoE promoter polymorphisms), angiotensin-converting enzyme (ACE) and alpha-1-antichymotrypsin (ACT). Thirty-two cases (21.3%) resulted in dementia 3 months after the stroke. In patients with PSD, the frequency of apoE epsilon 4 (0.08), ACE-D (0.64), ACT-A (0.62) alleles and apoE gene promoter polymorphisms (-491/A, 0.88; -427/C, 0.02) was similar to that of patients without PSD (apoE epsilon 4: 0.10, p=0.79; ACE-D: 0.56, p=0.36; ACT-A: 0.51, p=0.21; -491/A: 0.86, p=1.00; -427/C: 0.08, p=0.29). Our data indicate that PSD is not associated with the genetic risk factors of vascular dementia (VD) that were studied, and that additional factors may contribute to the pathogenesis of PSD. | lld:pubmed |
