| Literature DB >> 27574384 |
Elizabeth Hitchner1, Doug Morrison2, Phoebe Liao3, Allyson Rosen3, Wei Zhou4.
Abstract
While carotid interventions help decrease the risk of stroke, nearly 40% of patients experience cognitive deterioration. Genetic polymorphism in apolipoprotein E (ApoE) and brain-derived neurotrophic factor (BDNF) have been implicated in cognitive impairment; however, it is unclear whether they may influence cognitive changes in patients undergoing carotid intervention. In this study, we seek to assess the role of genetic polymorphisms in carotid intervention-related cognitive change. Polymorphisms related to cognitive function were chosen for this preliminary analysis. Over 2 years, patients undergoing carotid interventions were prospectively recruited. Patients underwent neuropsychological testing 2 weeks prior to and at 1 month following their procedure. Saliva samples were collected for genetic analysis. Logistic regressions were used to identify associations between polymorphisms and cognitive measures. A total of 91 patients were included; all were male with an average age of 70 years. The majority of patients exhibited hypertension (95%) and a history of smoking (81%). Presence of ApoE 4 allele was associated with depression (p= 0.047). After correcting for age and genetic polymorphisms in BDNF and serotonin transporter (5-HTT), ApoE 4 allele was associated with depression (p= 0.044) and showed a trend with baseline cognitive impairment (p= 0.10). Age ≥ 70 years was associated with baseline cognitive impairment after adjusting for the three genetic polymorphisms (p= 0.03). Patients with ApoE 4 and BDNF A polymorphisms performed less well on the visual and verbal memory measures, respectively. Polymorphisms in ApoE and BDNF may provide insight on cognition in patients undergoing carotid interventions; however, the mechanism of this relationship remains unclear.Entities:
Keywords: carotid endarterectomy; carotid stenosis; carotid stent; cognition; genetic; internal carotid artery; polymorphism
Year: 2016 PMID: 27574384 PMCID: PMC5001867 DOI: 10.1055/s-0036-1580696
Source DB: PubMed Journal: Int J Angiol ISSN: 1061-1711