{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T02:52:19Z","timestamp":1793674339702,"version":"4.5.1"},"reference-count":58,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T00:00:00Z","timestamp":1750377600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/100009619","name":"AMED","doi-asserted-by":"crossref","award":["JP18dm0207018, JP19dm0207072, JP18dk0207026, JP19dk0207049"],"award-info":[{"award-number":["JP18dm0207018, JP19dm0207072, JP18dk0207026, JP19dk0207049"]}],"id":[{"id":"10.13039\/100009619","id-type":"DOI","asserted-by":"crossref"}]},{"name":"JSPS KAKENHI","award":["26713031, 18K07543 and 23H02825"],"award-info":[{"award-number":["26713031, 18K07543 and 23H02825"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Lewy body disease (LBD) is a neurodegenerative disease characterized by Lewy bodies, and it clinically presents dementia with Lewy bodies (DLB) and Parkinson's disease (PD). Alzheimer's disease (AD) pathologies frequently coexist with LBD, complicating the clinical manifestation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We evaluated the impact of AD pathologies, including amyloid-\u03b2 and tau depositions, on cognitive dysfunction and glucose metabolism in LBD using multiple positron emission tomography scans.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Our study cohort consisted of 14 patients diagnosed with LBD, including five from the PD spectrum and nine from the DLB spectrum. In addition, 12 amyloid-negative cognitively healthy controls (HCs) and 13 amyloid-positive AD-spectrum patients were included. We subsequently explored the influence of amyloid and tau deposition on cognitive dysfunction and glucose metabolism among the LBD patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In the LBD group, 44.4% of the DLB patients were amyloid-positive, and all PD patients were amyloid-negative. While tau accumulation was lower than in AD and similar to HCs at the group level, tau accumulation in the AD signature region was correlated with cognitive dysfunction. Among the changes in glucose metabolism, the cingulate island sign (CIS) index was elevated compared to AD. However, as cognitive impairment progressed, the CIS index decreased, reflecting reduced metabolism in the posterior cingulate gyrus, which was closely associated with tau accumulation in the same region.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings indicate that AD pathologies, and particularly tau accumulation, significantly impact both cognitive dysfunction and glucose metabolism in LBD. This underscores the importance of addressing AD-related changes in the clinical management of LBD patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251351220","type":"journal-article","created":{"date-parts":[[2025,6,20]],"date-time":"2025-06-20T03:03:19Z","timestamp":1750388599000},"page":"1074-1086","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Concurrent Alzheimer's disease pathologies in Lewy body diseases affect cognition and glucose metabolism in the posterior cingulate gyrus: A multimodal PET study"],"prefix":"10.1177","volume":"106","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-6429-0628","authenticated-orcid":false,"given":"Kosei","family":"Nakamura","sequence":"first","affiliation":[{"name":"Department of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan"},{"name":"Department of Functional Neurology &amp; 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Quantum Science and Technology, Chiba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3001-9605","authenticated-orcid":false,"given":"Ming-Rong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Advanced Neuroimaging Center, Institute for Quantum Medical Science, National Institutes for Quantum Science and Technology, Chiba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6786-678X","authenticated-orcid":false,"given":"Kazunori","family":"Kawamura","sequence":"additional","affiliation":[{"name":"Advanced Neuroimaging Center, Institute for Quantum Medical Science, National Institutes for Quantum Science and Technology, Chiba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3354-5472","authenticated-orcid":false,"given":"Osamu","family":"Onodera","sequence":"additional","affiliation":[{"name":"Department of 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