Article Text

Download PDFPDF

TGF-β1 gene shows no link with Alzheimer's

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

A study of variation in the gene for transforming growth factor β1 (TGF-β1), has failed to confirm a role for this cytokine in the development of Alzheimer's disease. The case-control study looked for association between the disease and three variants in the coding region of the TGF-β1 gene—one at codon +25 and two in the promoter region at codons −800 and −509.

These variants occurred in a Hardy-Weinberg distribution in the controls. None showed any difference in frequency between the cases and controls, nor were there any allelic differences. Additionally, brain tissue from other patients with Alzheimer's disease showed no differences in amyloid β (Aβ) content according to TGF-β1 genotype. These variants also did not affect age of onset of the disease—for the cases or the brain samples.

The study included 678 cases of sporadic Alzheimer's disease and 667 controls, all of European origin, from France. The gene variants were identified by PCR amplification and restriction fragment analysis. Brains from 81 confirmed cases of Alzheimer's disease from Manchester, UK, underwent DNA extraction and genotyping. The proportion of the tissue taken up with Aβ was estimated from immunohistochemical staining of thin sections.

Research has suggested that cytokines may have a role in Alzheimer's disease, supporting an inflammatory model of pathogenesis. TGF-β1 in particular looked a promising candidate, possibly triggering the accumulation of Aβ in the brain, according to molecular and animal studies.