期刊
NEUROSCIENCE BULLETIN
卷 37, 期 6, 页码 789-803出版社
SPRINGER
DOI: 10.1007/s12264-021-00657-0
关键词
White matter hyperintensities; Cognitive impairment; Cortical thickness; Grey matter volume; Replication
资金
- National Natural Science Foundation of China [81801146, 81871438, 81771341]
- Natural Science Foundation of Hubei Province [2017CFB392]
- Beijing Natural Science Funds for Distinguished Young Scholars [JQ200036]
- Flagship Program of Tongji Hospital, China [2019CR106]
- Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health) [U01 AG024904]
- DOD ADNI (Department of Defense) [W81XWH-12-2-0012]
- National Institute on Aging
- National Institute of Biomedical Imaging and Bioengineering
- AbbVie
- Alzheimer's Association
- Alzheimer's Drug Discovery Foundation
- Araclon Biotech
- BioClinica, Inc.
- Biogen
- Bristol-Myers Squibb Company
- CereSpir, Inc.
- Cogstate
- Eisai Inc.
- Elan Pharmaceuticals, Inc.
- Eli Lilly and Company
- EuroImmun
- F. Hoffmann-La Roche Ltd
- Genentech, Inc.
- Fujirebio
- GE Healthcare
- IXICO Ltd.
- Janssen Alzheimer Immunotherapy Research & Development, LLC.
- Johnson & Johnson Pharmaceutical Research & Development LLC.
- NeuroRx Research
- Novartis Pharmaceuticals Corporation
- Pfizer Inc.
- Piramal Imaging
- Servier
- Transition Therapeutics
- Canadian Institutes of Health Research
- Neurotrack Technologies
- Lumosity
- Lundbeck
- Merck Co., Inc.
- Meso Scale Diagnostics, LLC.
- Takeda Pharmaceutical Company
The study found that gray matter atrophy in white matter hyperintensities patients may lead to cognitive decline, especially in those with mild cognitive impairment. The reduction in gray matter volume in the thalamus and fronto-insular cortices is associated with cognitive decline, and these results were further validated.
Grey matter (GM) alterations may contribute to cognitive decline in individuals with white matter hyperintensities (WMH) but no consensus has yet emerged. Here, we investigated cortical thickness and grey matter volume in 23 WMH patients with mild cognitive impairment (WMH-MCI), 43 WMH patients without cognitive impairment, and 55 healthy controls. Both WMH groups showed GM atrophy in the bilateral thalamus, fronto-insular cortices, and several parietal-temporal regions, and the WMH-MCI group showed more extensive and severe GM atrophy. The GM atrophy in the thalamus and fronto-insular cortices was associated with cognitive decline in the WMH-MCI patients and may mediate the relationship between WMH and cognition in WMH patients. Furthermore, the main results were well replicated in an independent dataset from the Alzheimer's Disease Neuroimaging Initiative database and in other control analyses. These comprehensive results provide robust evidence of specific GM alterations underlying WMH and subsequent cognitive impairment.
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