Article Text
Abstract
Background: There is evidence that inflammatory processes may contribute to the development of Alzheimer's disease through production of cytokines and free radicals that damage neurones. A recent study has shown that transforming growth factor β1 (TGF-β1) signalling in astrocytes promotes Aβ production and could play a critical role in the formation of amyloid plaques in the brain.
Objectives: To explore the impact of the −800 and −509 TGF-β1 promoter polymorphisms and the +25 polymorphism on the risk of occurrence of Alzheimer's disease in a large population of sporadic cases and controls, and on the amyloid β (Aβ) load in the brains of Alzheimer patients.
Methods: The TGF-β1 genotypes of the three polymorphisms were determined in 678 sporadic Alzheimer's disease patients and 667 controls. They were also characterised, along with Aβ load, in the brains of 81 necropsy confirmed Alzheimer patients.
Results: No significant variations in the distribution of the genotypes and haplotypes were observed between Alzheimer patients and controls, or in the amount of Aβ deposition.
Conclusions: These results do not suggest an influence of genetic variability at the TGF-β1 gene locus on the occurrence of Alzheimer's disease.
- Alzheimer's disease
- TGF-β1
- amyloid β protein
- polymorphism