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DOI 10.1016/j.neurobiolaging.2025.03.002

Медицинская библиотека · Neurobiology of aging · 2025

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

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

СтатьяПоддержка NIH: внешняя программаПеревод в очереди

Аннотация

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.

Для цитирования: Singh-Reilly Neha, Pham Nha Trang Thu, Graff-Radford Jonathan, Machulda Mary M, Spychalla Anthony J, Senjem Matthew L, Petersen Ronald C, Lowe Val J, Boeve Bradley F, Jack Clifford R, Josephs Keith A, Kantarci Kejal, Whitwell Jennifer L. White matter hyperintensities in dementia with lewy bodies and posterior cortical atrophy.. Neurobiology of aging. 2025. DOI: 10.1016/j.neurobiolaging.2025.03.002.

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