ArticleNature communications2024
Genetic risk factors underlying white matter hyperintensities and cortical atrophy.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Associations of social isolation and loneliness with neurological disorders, psychiatric disorders, brain structures and behavioural phenotypes among UK Biobank participants.Nature communications · 2026Article
- Multiomics Profiling Supports Cathepsin B as a Protective Factor in Cerebral Small Vessel Disease.Research square · 2026Article
- Macrostructural, microstructural, and cellular effects of neuroinflammation on the mouse brain.Brain, behavior, & immunity - health · 2026Article
- T cell-microglial interactions that impair myelin maintenance and regeneration: cellular mechanisms on white-matter associated changes.Frontiers in immunology · 2026Review
- Specific genetic and biological patterns underlying cortical morphological alterations in vascular cognitive impairment.Alzheimer's research & therapy · 2025Article
- Polygenic risk for Alzheimer's disease in healthy aging: age-related and APOE-driven effects on brain structures and cognition.Genome medicine · 2025Article
- White matter hyperintensities drive propagating grey matter atrophy in cerebral small vessel disease.Brain communications · 2025Article
- Exploration of heterogeneity in risk factors associated with imaging subtypes of white matter hyperintensities on fluid-attenuated inversion recovery magnetic resonance imaging.Frontiers in neurology · 2025Article
- Association between white matter hyperintensities and gray matter volume in cerebral small vessel disease: insights from periventricular and deep white matter lesions.Frontiers in neurology · 2025Article
Corrections and comments
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Authors and funding
40 authors.
Funding
Abstract
White matter hyperintensities index structural abnormalities in the cerebral white matter, including axonal damage. The latter may promote atrophy of the cerebral cortex, a key feature of dementia. Here, we report a study of 51,065 individuals from 10 cohorts demonstrating that higher white matter hyperintensity volume associates with lower cortical thickness. The meta-GWAS of white matter hyperintensities-associated cortical 'atrophy' identifies 20 genome-wide significant loci, and enrichment in genes specific to vascular cell types, astrocytes, and oligodendrocytes. White matter hyperintensities-associated cortical 'atrophy' showed positive genetic correlations with vascular-risk traits and plasma biomarkers of neurodegeneration, and negative genetic correlations with cognitive functioning. 15 of the 20 loci regulated the expression of 54 genes in the cerebral cortex that, together with their co-expressed genes, were enriched in biological processes of axonal cytoskeleton and intracellular transport. The white matter hyperintensities-cortical thickness associations were most pronounced in cortical regions with higher expression of genes specific to excitatory neurons with long-range axons traversing through the white matter. The meta-GWAS-based polygenic risk score predicts vascular and all-cause dementia in an independent sample of 500,348 individuals. Thus, the genetics of white matter hyperintensities-related cortical atrophy involves vascular and neuronal processes and increases dementia risk.
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