کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4337349 | 1614751 | 2016 | 8 صفحه PDF | دانلود رایگان |
• Future studies should consider the interaction of vascular, genetic risk factors in the development of cognitive impairment in AD.
• Molecular basis of AD isn’t understood, genetic factors are anticipated to participate in the development and progression of AD.
• AD in patients should be assessed by combining risk factors, cognitive and genetic tests, and management must be provided.
• The risk genes point to the potential for biomarkers for AD, to possible new targets for future disease modifying therapies.
Alzheimer’s Disease is the leading neurodegenerative cause of dementia. The pathogenesis is not clearly understood yet, is believed to be the complex interaction between genetic and environmental factors. Consequently vascular risk factors and Apolipoprotein E genotyping are increasingly gaining importance.This study aimed at assessing the relationships between Alzheimer’s Disease and Apolipoprotein E phenotype and vascular risk factors. Patients diagnosed with “possible Alzheimer’s Disease” in the Gazi University, Department of Neurology, were included in the study and age-matched volunteer patients who attended the polyclinic were included as a control group. In this study, the risk factors including low education level, smoking, hyperlipidemia, higher serum total cholesterol levels, and hyperhomocysteinemia were found to be statistically significantly more common in the Alzheimer’s Disease group in comparison to the Control Group, while all Apolipoprotein E ε4/ε4 genotypes were found in the Alzheimer’s Disease group.The presence of the Apolipoprotein E ε4 allele is believed to increase vascular risk factors as well as to affect Alzheimer’s Disease directly. The biological indicators which are used in identifying the patients’ genes will be probably used in the treatment plan of the patients in the future.
Journal: Neuroscience - Volume 325, 14 June 2016, Pages 124–131