Vázquez-Higuera, José LMateo, IgnacioSánchez-Juan, PascualRodriguez-Rodriguez, EloyPozueta, AnaCalero, MiguelDobato, José LuisFrank-García, AnaValdivieso, FernandoBerciano, Jose MiguelBullido, María JesúsCombarros, Onofre2019-02-012019-02-012011-09-07BMC Res Notes. 2011 Sep 7;4:327.1756-0500http://hdl.handle.net/20.500.12105/7074BACKGROUND: 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.engVoRhttp://creativecommons.org/licenses/by/4.0/Atribución 4.0 Internacional218997704132710.1186/1756-0500-4-3271756-0500BMC research notesopen access