2026-06-14T03:35:59Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/70742025-05-07T09:57:15Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19609

00925njm 22002777a 4500 dc Vázquez-Higuera, José L author Mateo, Ignacio author Sánchez-Juan, Pascual author Rodriguez-Rodriguez, Eloy author Pozueta, Ana author Calero, Miguel author Dobato, José Luis author Frank-García, Ana author Valdivieso, Fernando author Berciano, Jose Miguel author Bullido, María Jesús author Combarros, Onofre author 2011-09-07 BACKGROUND: 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. BMC Res Notes. 2011 Sep 7;4:327. 10.1186/1756-0500-4-327 1756-0500 1756-0500 BMC research notes 21899770 http://hdl.handle.net/20.500.12105/7074 Genetic variation in the tau protein phosphatase-2A pathway is not associated with Alzheimer's disease risk