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From JAMA |

Clusterin as an Alzheimer Biomarker

John Hardy, PhD; Rita Guerreiro, MS, PhD; Simon Lovestone, PhD, MRCPsych
Arch Neurol. 2011;68(11):1459-1460. doi:10.1001/archneurol.2011.1000.
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In a remarkable series of little-noticed studies, May et al1 and Poirier et a12 carried out entorhinal lesions in adult rats to see which genes were acutely upregulated. Their reasoning was that such response genes would be candidate genes for Alzheimer disease. Remarkably, they picked out just 2 genes: apolipoprotein E (ApoE) and clusterin (Clu ; apolipoprotein J). While APOE was shown to be a locus for Alzheimer disease within a couple years,3 the realization that CLU was a locus for the disease was made only with the advent of genome-wide association studies4 clearly documenting that genetic variability at the locus contributed to risk. Unlike APOE, where the major (but not the only) risk is encoded by protein coding change,5 in CLU there is not a common coding variant in European populations even though there are a lot of rare variants.6 Rather, it seems that genetic variability in expression is the underlying reason the CLU locus appears as a risk locus for disease. This genetic variability in expression does not relate to the resting expression of this reactive protein (which is not different based on genotype), but rather most likely relates to genetic variability in damage response expression.6

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