White matter hyperintensities in dementia with lewy bodies and posterior cortical atrophy.

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Tác giả: Bradley F Boeve, Jonathan Graff-Radford, Clifford R Jack, Keith A Josephs, Kejal Kantarci, Val J Lowe, Mary M Machulda, Ronald C Petersen, Nha Trang Thu Pham, Matthew L Senjem, Neha Singh-Reilly, Anthony J Spychalla, Jennifer L Whitwell

Ngôn ngữ: eng

Ký hiệu phân loại: 383.1205 Mail handling

Thông tin xuất bản: United States : Neurobiology of aging , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 693578

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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