CALHM1 P86L polymorphism does not alter amyloid-β or tau in cerebrospinal fluid

NEUROSCIENCE LETTERS

卷:469

Article

Giedraitis, Vilmantas²  Glaser, Anna²  Sarajarvi, Timo³  Brundin, RoseMarie²  Gunnarsson, Malin Degerman²  Schjeide, Brit-Maren^4,5  Tanzi, Rudolph E.⁵  Helisalmi, Seppo³  Pirttila, Tuula³  Kilander, Lena²  Lannfelt, Lars²  Soininen, Hilkka³  Bertram, Lars^4,5  Ingelsson, Martin²  Hiltunen, Mikko^1,3 

[1] Univ Kuopio, Dept Neurol, FIN-70211 Kuopio, Finland

[2] Uppsala Univ, Dept Publ Hlth Geriatr, Rudbeck Lab, Uppsala, Sweden

[3] Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland

[4] Max Planck Inst Mol Genet, Dept Vertebrate Genom, Neuropsychiat Genet Grp, Berlin, Germany

[5] Harvard Univ, Sch Med, Massachusetts Gen Hosp, MIND,Genet & Aging Res Unit,Dept Neurol, Charlestown, MA USA

关键词: CALHM1;    Calcium homeostasis modulator-1;    Amyloid-beta;    Alzheimer's disease;    Cerebrospinal fluid;    Biomarker;    Total tau;    Phospho-tau;    Genotyping SNP;   

DOI  :  10.1016/j.neulet.2009.12.011

来源: Elsevier

【 摘 要 】

Recently, the P86L alteration in CALHM1 (calcium homeostasis modulator-1) was reported to be associated with Alzheimer's disease (AD). Moreover, the risk allele increased amyloid-beta (A beta) levels in conditioned media from cultured cells. Therefore, we hypothesized that CALHM1 P86L may modulate A beta or tau levels in cerebrospinal fluid (CSF). Nearly 200 individuals with AD or other cognitive disorders were included for CSF analysis and CALHM1 genotyping. No significant differences in CSF levels of A beta 42, tau or phospho-tau were found across the various CALHM1 genotypes. In conclusion, we found no evidence that CALHM1 P86L is associated with altered CSF levels of the investigated AD biomarkers. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

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