RT Journal Article SR Electronic T1 Association study of three polymorphisms of TGF-β1 gene with Alzheimer's disease JF Journal of Neurology, Neurosurgery & Psychiatry JO J Neurol Neurosurg Psychiatry FD BMJ Publishing Group Ltd SP 62 OP 64 DO 10.1136/jnnp.73.1.62 VO 73 IS 1 A1 L Araria-Goumidi A1 J C Lambert A1 D M A Mann A1 C Lendon A1 B Frigard A1 T Iwatsubo A1 D Cottel A1 P Amouyel A1 M C Chartier-Harlin YR 2002 UL http://jnnp.bmj.com/content/73/1/62.abstract AB 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.