Lack of association between the brain-derived neurotrophin factor (C-270T) polymorphism and late-onset Alzheimer's disease (LOAD) in Brazilian patients
Authors: Nishimura, Agnes1; Oliveira, João2; Mitne-Neto, Miguel3; Guindalini, Camila3; Nitrini, Richardo4; Bahia, Valéria4; Brito-Marques, Paulo5; Otto, Paulo3; Zatz, Mayana3
Source: Journal of Molecular Neuroscience, Volume 22, Number 3, October 2004 , pp. 257-260(4)
Publisher: Humana Press
Abstract:
After the identification of the apolipoprotein E gene isoform (APOE-ε4) as a risk factor for late-onset Alzheimer's disease (LOAD), the search for other polymorphisms associated with AD has been undertaken by many groups of investigators around the world. These studies have shown controversial results in many populations. More recently, a single nucleotide polymorphism in the promoter region of the brain-derived neurotrophin factor (BDNF) was found to be a risk factor for AD in two independent population studies. Here we report the analysis of this polymorphism in a group of 188 LOAD Brazilian patients compared to matched normal controls. A strong association between the APOE-ε4 polymorphism and LOAD was observed, but there was no significant association between this BNDF polymorphism and affected patients. The possibility that other polymorphisms or mutations in this gene play a role in the development of AD cannot be ruled out. However, the results of the present study suggest that in opposition to the two reported studies, this polymorphism does not seem to be implicated in LOAD Brazilian patients. It also shows the importance of replication studies in different populations, as susceptibility loci might differ in different ethnic groups; this will have important implications in future treatments with pharmacological agents.Keywords: Alzheimer's disease; polymorphism; BDNF; susceptibility locus
Document Type: Research article
DOI: http://dx.doi.org/10.1385/JMN:22:3:257
Affiliations: 1: Human Genome Research Center, Biology Department, Institute of Biosciences, University of São Paulo-IBUSP, São Paulo, Brazil, Email: mayazatz@usp.br 2: Neurology Department of the David Geffen Medical School, UCLA, Los Angeles, CA, 3: Human Genome Research Center, Biology Department, Institute of Biosciences, University of São Paulo-IBUSP, São Paulo, Brazil, 4: Department of Neurology, Faculty of Medicine, University of São Paulo, São Paulo, Brazil, 5: Behavior Neurology Center, Faculty of Medical Sciences, Recife, Brazil,
Publication date: 2004-10-01
- In this: publication
- By this: publisher
- In this Subject: Anatomy & Physiology , Zoology , Neurology & Psychiatry
- By this author: Nishimura, Agnes ; Oliveira, João ; Mitne-Neto, Miguel ; Guindalini, Camila ; Nitrini, Richardo ; Bahia, Valéria ; Brito-Marques, Paulo ; Otto, Paulo ; Zatz, Mayana

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