Consistency in gene-Alzheimer’s disease association studies
- 1Division of Preventive Medicine and Public Health, University of Cantabria School of Medicine, Spain
- 2Service of Neurology, University Hospital Marqués de Valdecilla, Santander, Spain
- Correspondence to: Dr J Llorca Medicina Preventiva y Salud Pública, Avda Cardenal Herrera Oria s/n, 39011 Santander, Spain; llorcajunican.es
- Accepted 4 May 2004
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 ε-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.
METHOD
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 …
