ArticleNeuroscience letters2010
CALHM1 P86L polymorphism does not alter amyloid-beta or tau in cerebrospinal fluid.
Article in Neuroscience letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Genome-wide association study of CSF levels of 59 alzheimer's disease candidate proteins: significant associations with proteins involved in amyloid processing and inflammation.PLoS genetics · 2014Pooled it
- CALHM1 deficiency impairs cerebral neuron activity and memory flexibility in mice.Scientific reports · 2016Article
- CALHM1 ion channel elicits amyloid-β clearance by insulin-degrading enzyme in cell lines and in vivo in the mouse brain.Journal of cell science · 2015Article
- Effect of the CALHM1 G330D and R154H human variants on the control of cytosolic Ca2+ and Aβ levels.PloS one · 2014Article
- CALHM1 controls the Ca²⁺-dependent MEK, ERK, RSK and MSK signaling cascade in neurons.Journal of cell science · 2013Article
- Generation of Calhm1 knockout mouse and characterization of calhm1 gene expression.Protein & cell · 2012Article
- Validating predicted biological effects of Alzheimer's disease associated SNPs using CSF biomarker levels.Journal of Alzheimer's disease : JAD · 2010Article
- CALHM1 P86L polymorphism modulates CSF Aβ levels in cognitively healthy individuals at risk for Alzheimer's disease.Molecular medicine (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 4 countries.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.