ArticleNeurobiology of aging2025
White matter hyperintensities in dementia with lewy bodies and posterior cortical atrophy.
Article in Neurobiology of aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- Compensatory hallucinogenesis across three neuropsychiatric disorders: a Bayesian account.Brain communications · 2026Review
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13 authors.
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Abstract
Dementia with Lewy bodies (DLB) and posterior cortical atrophy (PCA) are neurodegenerative disorders that can overlap clinically and in patterns of regional hypometabolism and show elevated white matter hyperintensity (WMH) burden. Little is known about the regional WMH burden in DLB patients without any interference of AD pathology and how these patterns compare to PCA patients. Twenty-two amyloid-negative DLB patients, 40 amyloid-positive PCA patients, and 49 amyloid-negative cognitively unimpaired (CU) healthy individuals were recruited at Mayo Clinic, Rochester, MN. They underwent a 3 T head MRI, a Pittsburgh Compound B (PiB) PET scan, and a fluid-attenuated inversion recovery scan (FLAIR). The relationship between regional WMH volume and diagnosis was evaluated while adjusting for age and sex. DLB showed greater periventricular WMH burden in the temporal, occipital, and frontal lobes and greater WMH burden in the posterior corpus callosum compared to CU. PCA showed greater subcortical WMH burden in temporal, parietal, and occipital lobes, and greater periventricular WMH burden in the temporal, occipital, and frontal lobes, compared to CU. On comparing both dementia groups, PCA showed greater subcortical WMH burden in the temporal and occipital lobes compared to DLB, while DLB showed greater WMH burden in the posterior corpus callosum compared to PCA. Hence, DLB and PCA are both associated with periventricular WMHs, with deep subcortical WMHs being more characteristic of PCA, and callosal WMHs more characteristic of Aβ-negative DLB patients, suggesting different pathophysiological mechanisms underlying the development of WMHs in these two neurodegenerative diseases.
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