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dc.contributor.authorVázquez Higuera, José Luis
dc.contributor.authorMateo Fernández, José Ignacio
dc.contributor.authorSánchez Juan, Pascual 
dc.contributor.authorRodríguez Rodríguez, Eloy
dc.contributor.authorPozueta, Ana
dc.contributor.authorCalero Lara, Miguel
dc.contributor.authorDobato Ayuso, José Luis
dc.contributor.authorFrank García, Ana
dc.contributor.authorValdivieso Amate, Fernando
dc.contributor.authorBerciano Blanco, José Ángel 
dc.contributor.authorBullido, María Jesús
dc.contributor.authorCombarros Pascual, Onofre 
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.description.abstractBACKGROUND: Tau abnormal hyperphosphorylation and the formation of neurofibrillary tangles in AD brain is the result of upregulation of tau kinases and downregulation of tau phosphatases. METHODS: In a group of 729 Spanish late-onset Alzheimer's disease (AD) patients and 670 healthy controls, we examined variations into a set of candidate genes (PPP2CA, PPP2R2A, ANP32A, LCMT1, PPME1 and PIN1) in the tau protein phosphatase-2A (PP2A) pathway, to address hypotheses of genetic variation that might influence AD risk. RESULTS: There were no differences in the genotypic, allelic or haplotypic distributions between cases and controls in the overall analysis or after stratification by age, gender or APOE ε4 allele. CONCLUSION: Our negative findings in the Spanish population argue against the hypothesis that genetic variation in the tau protein phosphatase-2A (PP2A) pathway is causally related to AD risk.es_ES
dc.format.extent5 p.es_ES
dc.publisherBioMed Centrales_ES
dc.rightsAtribución 3.0 Españaes_ES
dc.sourceBMC Research Notes. 2011 Sep 7;4:327es_ES
dc.titleGenetic variation in the tau protein phosphatase-2A pathway is not associated with Alzheimer's disease riskes_ES

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Atribución 3.0 EspañaExcept where otherwise noted, this item's license is described as Atribución 3.0 España