dc.creator | Siokas V., Aslanidou P., Aloizou A.-M., Peristeri E., Stamati P., Liampas I., Arseniou S., Drakoulis N., Aschner M., Tsatsakis A., Mitsias P.D., Bogdanos D.P., Hadjigeorgiou G.M., Dardiotis E. | en |
dc.date.accessioned | 2023-01-31T09:56:48Z | |
dc.date.available | 2023-01-31T09:56:48Z | |
dc.date.issued | 2020 | |
dc.identifier | 10.1007/s12031-020-01507-w | |
dc.identifier.issn | 08958696 | |
dc.identifier.uri | http://hdl.handle.net/11615/79029 | |
dc.description.abstract | Alzheimer’s disease (AD) is a complex genetic disorder. To date, published data have reported conflicting results on the role of CD33 rs3865444 polymorphism in AD. The present study aimed at evaluating the effect of rs3865444 on AD in a large cohort of Greek native patients with AD. We also conducted a meta-analysis by pooling information from different studies on the same topic. Patients with AD (n = 327) and healthy controls (n = 327) were analyzed and genotyped for rs3865444. Single locus analyses were run to explore possible associations between CD33 rs3865444 polymorphism and AD. Our analysis yielded no significant interaction between AD and the CD33 rs3865444 polymorphism. The lack of interaction between the two variables persisted even after a pooled meta-analysis of 8 studies (with 13 datasets), with 4015 AD cases and 7981 controls. The overall results do not support the hypothesis that CD33 rs3865444 polymorphism increases the risk of AD. The results also suggest that the identification of functional variants in CD33 that are indisputably correlated with AD may be an important factor to investigate in future genetic screening studies. © 2020, Springer Science+Business Media, LLC, part of Springer Nature. | en |
dc.language.iso | en | en |
dc.source | Journal of Molecular Neuroscience | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85079793851&doi=10.1007%2fs12031-020-01507-w&partnerID=40&md5=25335e2d1a2219cd55a643917085bb63 | |
dc.subject | CD33 antigen | en |
dc.subject | CD33 antigen | en |
dc.subject | aged | en |
dc.subject | Alzheimer disease | en |
dc.subject | Article | en |
dc.subject | Caucasian | en |
dc.subject | cohort analysis | en |
dc.subject | controlled study | en |
dc.subject | DNA isolation | en |
dc.subject | DNA polymorphism | en |
dc.subject | ethnicity | en |
dc.subject | female | en |
dc.subject | gene frequency | en |
dc.subject | gene interaction | en |
dc.subject | genetic association | en |
dc.subject | genetic model | en |
dc.subject | genetic susceptibility | en |
dc.subject | genotype | en |
dc.subject | human | en |
dc.subject | inheritance | en |
dc.subject | major clinical study | en |
dc.subject | male | en |
dc.subject | Alzheimer disease | en |
dc.subject | genetics | en |
dc.subject | single nucleotide polymorphism | en |
dc.subject | very elderly | en |
dc.subject | Aged | en |
dc.subject | Aged, 80 and over | en |
dc.subject | Alzheimer Disease | en |
dc.subject | Female | en |
dc.subject | Humans | en |
dc.subject | Male | en |
dc.subject | Polymorphism, Single Nucleotide | en |
dc.subject | Sialic Acid Binding Ig-like Lectin 3 | en |
dc.subject | Humana Press Inc. | en |
dc.title | Does the CD33 rs3865444 Polymorphism Confer Susceptibility to Alzheimer’s Disease? | en |
dc.type | journalArticle | en |