| Literature DB >> 20674091 |
Mercé Boada1, Carmen Antunez, Jesús López-Arrieta, Antonio Caruz, Concha Moreno-Rey, Reposo Ramírez-Lorca, Francisco Jesús Morón, Isabel Hernández, Ana Mauleón, Maiteé Rosende-Roca, Pablo Martínez-Lage, Juan Marín, Lluis Tárraga, Montserrat Alegret, José Rafael Pedrajas, Nuria Urda, José Luis Royo, María Eugenia Saez, Javier Gayán, Antonio González-Pérez, Luis Miguel Real, Agustín Ruiz, José Jorge Galán.
Abstract
The present research is aimed at assessing the role of 3 estrogen receptor alpha (ESR1) gene variants in late onset Alzheimer's disease (AD) susceptibility. One thousand one hundred thirteen unrelated late onset sporadic AD patients, 1109 healthy controls and 121 neurologically healthy elderly controls were used to carry out case-control genetic association studies with ESR1 rs3844508, rs2234693, and ESR1 noncoding deletion 1 (ESR1-NCD1) polymorphisms. Thirty-five healthy male samples were used for molecular analyses. The rs2234693 polymorphism is associated with AD in our population (odds ratio [OR], 1.29; p = 0.008). The rs3844508 marker confers protection against AD in males (OR, 0.57; p = 0.001) and the deletion ESR1-NCD1 is a risk factor for AD in women (OR, 1.67; p < 0.001). Molecular analyses on ESR1-NCD1 indicate that this deletion confers a higher response to estradiol activity on ESR1 receptor and it is also associated with differential expression of ESR1 isoforms. Our results support the involvement of ESR1 gene in AD and point to the existence of sexual dimorphism for ESR1 markers. In addition, carriers of ESR1-NCD1 deletion could overrespond to estradiol action.Entities:
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Year: 2010 PMID: 20674091 DOI: 10.1016/j.neurobiolaging.2010.06.016
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673