PhD Scientific Days

Poster Presentation: Neurosciences

P47: No association between ABCA1 promoter polymorphism and Alzheimer’s disease risk

Előadó neve

Giricz, Zsófia

Előadó munkahelye

University of Szeged Faculty of Medicine, Department of Psychatry

Előadó telefonszáma

06203440903

Előadó e-mail címe

giriczzsofia@gmail.com

Az előadás címe

No association between ABCA1 promoter polymorphism and Alzheimer’s disease risk

Szerző(k) neve és munkahelye

Zsófia Giricz, Ágnes Fehér, Anna Juhász, Andrea Koncz, Magdolna Pákáski, Zoltán Janka, János Kálmán
Department of Psychiatry, University of Szeged, Szeged, Hungary

Szekció

Poster Presentation: Neurosciences

Data of the presenter

Doctoral School of Clinical Medicine
Program: Clinical and Experimental Neuroscience
Supervisors: Kálmán János, Fehér Ágnes
email: giriczzsofia@gmail.com

Text of the abstract

Alzheimer's disease (AD) is a genetically complex neurodegenerative disorder. A good positional and functional candidate gene for AD is ABCA1, since it is located near to the linkage peak at locus 9q22 identified by genome-wide AD linkage studies and plays an important role in cellular cholesterol efflux. In the present case-control association study, we examined the possible association of the ABCA1 G-17C promoter polymorphism (rs2740483) with AD risk.

A total of 350 patients with late-onset AD and 257 elderly, cognitively intact, healthy control subjects were involved in the current study. A consensus clinical diagnosis of AD was established according to the NINCDS-ADRDA criteria. The genetic analyses were performed by TaqMan real-time PCR method.

No statistically significant difference was found in the distribution of genders or in mean age between AD and control groups (p>0.05). The investigated genotype frequencies were in Hardy-Weinberg equilibrium for both cases and controls (p>0.05). Comparison of ABCA1 G-17C genotype frequencies between AD and control groups showed no statistically significant difference (χ2=2.353 (2) p=0.308), although the C/C genotype occurred with a slightly higher frequency in the AD than in the control group (AD: 10.0%, control: 7.0%).

Our results do not support the hypothesis that ABCA1 G-17C polymorphism is associated with late-onset AD; however, further confirmations with independent samples are required. The study was supported by a grant from TÁMOP-4.2.2A-11/1/KONV-2012-0052.

Azonosító

P47

Kind

Szabad

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1009

Authors (legacy)