Premium
Serum levels and genetic variation of TGF‐β1 are not associated with Alzheimer’s disease
Author(s) -
RodríguezRodríguez E.,
SánchezJuan P.,
Mateo I.,
Llorca J.,
Infante J.,
GarcíaGorostiaga I.,
Berciano J.,
Combarros O.
Publication year - 2007
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2007.00892.x
Subject(s) - transforming growth factor , allele , genotype , alzheimer's disease , medicine , polymorphism (computer science) , endocrinology , genetic variation , biomarker , biology , disease , immunology , genetics , gene
Objective – As transforming growth factor‐β1 (TGF‐β1) determines important neurotrophic and neuroprotective actions, we postulated serum TGF‐β1 levels could be low in Alzheimer’s disease (AD), and TGF‐β1 genetic variation could be associated with AD risk through modulating serum TGF‐β1 levels. Methods – TGF‐β1 (−800) (rs 1800468), (−509) (rs 1800469) and (+869) (rs 1982073) polymorphisms were genotyped in 412 AD patients and 406 controls. We measured serum TGF‐β1 levels (by ELISA) in 63 AD patients and compared them with 77 age‐ and gender‐matched non‐demented controls. Results – Serum TGF‐β1 levels were not different in AD patients than in controls. Distribution of the allele and genotype frequencies of TGF‐β1 polymorphisms did not differ between AD patients and controls. There was no significant correlation between serum TGF‐β1 levels and TGF‐β1 polymorphisms. Conclusion – Serum TGF‐β1 concentration is not a potential biomarker for AD, and TGF‐β1 genetic variants (−800, −509, and +869) are not risk factors for AD.