Serum levels and genetic variation of TGF-β1 are not associated with Alzheimer’s disease

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Rodríguez-Rodríguez E, Sánchez-Juan P, Mateo I, Llorca J, Infante J, García-Gorostiaga I, Berciano J, Combarros O. Serum levels and genetic variation of TGF-β1 are not associated with Alzheimer’s disease.

Acta Neurol Scand 2007: 116: 409–412.

© 2007 The Authors Journal compilation © 2007 Blackwell Munksgaard. 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.

Keywords: Alzheimer’s disease; TGF-β1; risk factor; serum

Document Type: Research Article


Affiliations: 1: Neurology Service, ‘Marqués de Valdecilla’ University Hospital, University of Cantabria, Santander, Spain 2: Fundación ‘Marqués de Valdecilla’, IFIMAV, Santander, Spain 3: Division of Preventive Medicine, University of Cantabria School of Medicine, Santander, Spain

Publication date: December 1, 2007



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