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However, little was known about the possible effect of <jats:italic>CLU<\/jats:italic> genetic variants on AD pathology in brain. Here, we evaluated the interaction between 7 <jats:italic>CLU<\/jats:italic> SNPs (covering 95% of genetic variations) and the role of <jats:italic>CLU<\/jats:italic> in \u03b2-amyloid (A\u03b2) deposition, AD-related structure atrophy, abnormal glucose metabolism on neuroimaging and CSF markers to clarify the possible approach by that <jats:italic>CLU<\/jats:italic> impacts AD. Finally, four loci (rs11136000, rs1532278, rs2279590, rs7982) showed significant associations with the A\u03b2 deposition at the baseline level while genotypes of rs9331888 (P\u2009=\u20090.042) increased A\u03b2 deposition. Besides, rs9331888 was significantly associated with baseline volume of left hippocampus (P\u2009=\u20090.014). We then further validated the association with A\u03b2 deposition in the AD, mild cognitive impairment (MCI), normal control (NC) sub-groups. The results in sub-groups confirmed the association between <jats:italic>CLU<\/jats:italic> genotypes and A\u03b2 deposition further. Our findings revealed that <jats:italic>CLU<\/jats:italic> genotypes could probably modulate the cerebral the A\u03b2 loads on imaging and volume of hippocampus. These findings raise the possibility that the biological effects of <jats:italic>CLU<\/jats:italic> may be relatively confined to neuroimaging trait and hence may offer clues to AD.<\/jats:p>","DOI":"10.1038\/srep26027","type":"journal-article","created":{"date-parts":[[2016,5,27]],"date-time":"2016-05-27T09:38:19Z","timestamp":1464341899000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["Effect of CLU genetic variants on cerebrospinal fluid and neuroimaging markers in healthy, mild cognitive impairment and Alzheimer\u2019s disease 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