Consistency in gene-Alzheimer’s disease association studies

Throughout the past decade, a great number of studies have been published searching for a gene-disease association. Ioannidis et al , studying a variety of diseases, pointed out that the first time such a relation is shown it correlates moderately with later results.1 Sporadic Alzheimer’s disease (AD) has been extensively studied searching for gene causation.2 Apart from the well established relation with ApoE e-4 genotype, other gene candidates have weaker associations with AD and their role remains controversial. In fact, results from case-control studies are frequently contradictory and meta-analyses have been conducted to clarify whether a gene-AD association exists.3 The goal of this paper is to describe how the odds ratio between a gene and AD changes as new studies are published. We included case-control studies published before July 2003 on AD and the following polymorphisms: myeloperoxidase 7 (6 studies),4–8 low density lipoprotein receptor related protein gene (LRP) exon 3 polymorphism (10 studies),9–18 Glu298Asp polymorphism in the endothelial nitric oxide synthetase (NOS-3) (10 studies),8,16,19–26 and cathepsin D (14 studies).8,16,27–37 A

Alzheimer's disease · Apolipoprotein E · Bioinformatics · Biology · Disease · Gene · Genetic association · Genotype · Odds ratio · Single-nucleotide polymorphism · Alzheimer's disease research and treatments · Folate and B Vitamins Research · Genetics · Internal Medicine · Medicine · S100 Proteins and Annexins