{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T05:15:19Z","timestamp":1788498919961,"version":"build-2803163510"},"reference-count":74,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2022,9,1]],"date-time":"2022-09-01T00:00:00Z","timestamp":1661990400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp; Dementia"],"published-print":{"date-parts":[[2023,4]]},"abstract":"Abstract<\/jats:title>\n \n \n \n It remains unclear to what extent cerebrovascular burden relates to amyloid beta (A\u03b2) deposition, neurodegeneration, and cognitive dysfunction in mixed disease populations with small vessel disease and Alzheimer's disease (AD) pathology. In 120 subjects, we investigated the association of vascular burden (white matter hyperintensity [WMH] volumes) with cognition. Using mediation analyses, we tested the indirect effects of WMH on cognition via A\u03b2 deposition (\n 18<\/jats:sup>\n F\u2010AV45 positron emission tomography [PET]) and neurodegeneration (cortical thickness or\n 18<\/jats:sup>\n F fluorodeoxyglucose PET) in AD signature regions. We observed that increased total WMH volume was associated with poorer performance in all tested cognitive domains, with the strongest effects observed for semantic fluency. These relationships were mediated mainly via cortical thinning, particularly of the temporal lobe, and to a lesser extent serially mediated via A\u03b2 and cortical thinning of AD signature regions. WMH volumes differentially impacted cognition depending on lobar location and A\u03b2 status. In summary, our study suggests mainly an amyloid\u2010independent pathway in which vascular burden affects cognitive function via localized neurodegeneration.\n <\/jats:p>\n <\/jats:sec>\n \n Highlights<\/jats:title>\n \n \n \n Alzheimer's disease often co\u2010exists with vascular pathology.<\/jats:p>\n <\/jats:list-item>\n \n We studied a unique cohort enriched for high white matter hyperintensities (WMH).<\/jats:p>\n <\/jats:list-item>\n \n High WMH related to cognitive impairment of semantic fluency and executive function.<\/jats:p>\n <\/jats:list-item>\n \n This relationship was mediated via temporo\u2010parietal atrophy rather than metabolism.<\/jats:p>\n <\/jats:list-item>\n \n This relationship was, to lesser extent, serially mediated via amyloid beta and atrophy.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n 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