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In the current study, we examined a large series of neuropathologically confirmed LBD cases (n = 980 in the discovery series, n = 503 in the replication series) and performed genome-wide association studies of 11 different neuropathological outcome measures.<\/jats:p>\n                  <jats:p>The 11 neuropathological outcomes included Braak neurofibrillary tangle (NFT) stage, Thal amyloid phase, LBD subtype, Lewy body (LB) counts in five different brain regions, dorsolateral and ventromedial putaminal tyrosine hydroxylase immunoreactivity and neuronal loss in the ventrolateral part of the substantia nigra. Associations between variants and outcomes were assessed using regression models appropriate for the nature of the given neuropathological outcome and that were adjusted for age at death, sex and top principal components of genetic data.<\/jats:p>\n                  <jats:p>In the discovery series, APOE rs429358 (i.e. APOE \u03b54) was associated with a greater severity of each of Braak NFT stage [odds ratio (OR) = 3.07, P = 2.34 \u00d7 10\u221232], Thal amyloid phase (OR = 3.57, P = 3.28 \u00d7 10\u221229) and LBD subtype (OR = 1.78, P = 9.85 \u00d7 10\u22129), with similar findings observed in the independent replication series (Braak NFT stage, OR = 2.30, P = 2.70 \u00d7 10\u221211; Thal amyloid phase, OR = 3.17, P = 6.39 \u00d7 10\u221218; LBD subtype, OR = 2.68, P = 3.85 \u00d7 10\u221210). In the subgroup of cases with lower levels of Alzheimer's disease pathology (Braak NFT stage \u2264 III and Thal amyloid phase \u22642), there was a strong association between APOE rs429358 and LBD subtype even when adjusting for Braak stage and Thal phase in the discovery series (n = 218, OR = 2.47, P = 0.007) and the replication series (n = 141, OR = 3.60, P = 0.006). Although additional genome-wide significant associations were identified in the discovery series between LINC01581\/MCTP2 rs547411734 and lower middle frontal LB counts, between TLE3 rs3743309 and lower cingulate LB counts, and between GRIN2A\/ATF7IP2 rs1097915 and lower parahippocampal LB counts, these findings were not observed in the replication series.<\/jats:p>\n                  <jats:p>Our results indicate that the APOE \u03b54 allele is the most prominent genetic determinant of severity of neuropathology in LBD. These findings represent a key step forward in our understanding of genetic drivers of neuropathological features in LBD. Future studies utilizing meta-analytical approaches will be important to more precisely assess other associations that were not quite genome-wide significant in the discovery series.<\/jats:p>","DOI":"10.1093\/brain\/awaf105","type":"journal-article","created":{"date-parts":[[2025,3,14]],"date-time":"2025-03-14T16:22:46Z","timestamp":1741969366000},"page":"2785-2796","source":"Crossref","is-referenced-by-count":7,"title":["Genome-wide association study of neuropathological features in Lewy body disease"],"prefix":"10.1093","volume":"148","author":[{"given":"Rebecca R","family":"Valentino","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Jacksonville, FL 32224 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8868-9700","authenticated-orcid":false,"given":"Shunsuke","family":"Koga","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Jacksonville, FL 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