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Neurobiol Aging. 2014 Oct;35(10):2369-81. doi: 10.1016/j.neurobiolaging.2014.02.025. Epub 2014 Mar 1.

Brain lipidomes of subcortical ischemic vascular dementia and mixed dementia.

Author information

1
State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China; Department of Biological Sciences, National University of Singapore, Singapore.
2
NGS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore.
3
Life Science Institute, National University of Singapore, Singapore.
4
Department of Biological Sciences, National University of Singapore, Singapore; Department of Biochemistry, National University of Singapore, Singapore.
5
Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.
6
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Memory, Aging and Cognition Centre, National University Health System, Singapore.
7
State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China. Electronic address: ghshui@genetics.ac.cn.

Abstract

Despite its importance as the leading cause of vascular dementia, the primary pathogenic mechanisms in subcortical ischemic vascular dementia (SIVD) have remained elusive. Because of the lack of approved therapeutic agents for SIVD, there is a pressing need to identify novel therapeutic targets. Comparative lipidomic analyses of SIVD and mixed dementia (i.e., SIVD and Alzheimer's disease, MixD) may also confer new insights pertaining to the possible interaction between neurodegenerative and vascular mechanisms in the pathogenesis of dementia. Liquid chromatography coupled to mass spectrometry was used to comprehensively analyze the lipidomes of white and gray matter from the temporal cortex of nondemented controls, SIVD, and MixD subjects. Detailed molecular profiles highlighted the pathologic relevance of gray matter sphingolipid fatty acyl chain heterogeneity in dementia. In addition, the levels of sulfatides and lysobisphosphatidic acids were progressively increased in the temporal cortex gray matter from control to SIVD to MixD. White matter phospholipid profiles indicated possible adaptive mechanisms (i.e., increased unsaturation) to chronic ischemia in SIVD and elevated membrane degradation in MixD.

KEYWORDS:

Alzheimer's disease; Lipidomics; Mass spectrometry; Mixed dementia; Phospholipids; Sphingolipids; Subcortical ischemic vascular dementia

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