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CALHM1 P86L polymorphism does not alter amyloid-beta or tau in cerebrospinal fluid
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
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2010 (English)In: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 469, no 2, 265-267 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2010. Vol. 469, no 2, 265-267 p.
Keyword [en]
Alzheimer's disease, Amyloid-β, Biomarker, Calcium homeostasis modulator-1, CALHM1, Cerebrospinal fluid, Genotyping SNP, Phospho-tau, Total tau
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-122992DOI: 10.1016/j.neulet.2009.12.011ISI: 000274508700019PubMedID: 20005921OAI: oai:DiVA.org:uu-122992DiVA: diva2:311578
Available from: 2010-04-22 Created: 2010-04-22 Last updated: 2017-12-12Bibliographically approved

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