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We devised a unique strategy that combines distinct mouse strains that vary naturally in amyloid-\u03b2 production with transcriptomics to identify kinesin light chain-1\n                    <jats:italic>(Klc1<\/jats:italic>\n                    ) splice variant E as a modifier of amyloid-\u03b2 accumulation, a causative factor of AD. In AD patients, the expression levels of\n                    <jats:italic>KLC1<\/jats:italic>\n                    variant E in brain were significantly higher compared with levels in unaffected individuals. The identification of\n                    <jats:italic>KLC1<\/jats:italic>\n                    variant E suggests that dysfunction of intracellular trafficking is causative in AD.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1307345111","type":"journal-article","created":{"date-parts":[[2014,2,5]],"date-time":"2014-02-05T00:08:01Z","timestamp":1391558881000},"page":"2638-2643","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":43,"title":["Transcriptome analysis of distinct mouse strains reveals kinesin light chain-1 splicing as an amyloid-\u03b2 accumulation modifier"],"prefix":"10.1073","volume":"111","author":[{"given":"Takashi","family":"Morihara","sequence":"first","affiliation":[{"name":"Department of Psychiatry, Graduate School of Medicine, Osaka University, Osaka 565-0871, 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