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Showing papers by "Fabrice Crivello published in 2022"



Journal ArticleDOI
01 Dec 2022
TL;DR: In this paper , the authors used multiscale diffusion imaging to explore genetic determinants of white matter microstructure across the adult lifespan and its relation with cerebral small vessel disease (cSVD).
Abstract: Cerebral small vessel disease (cSVD) is a leading cause of vascular cognitive impairment and dementia. Mounting evidence suggests that early life factors contribute to cSVD. Genetic risk loci for white matter hyperintensities (WMH), the most common MRI‐marker of cSVD in older age, were recently found to show strong associations with white matter microstructure on diffusion tensor imaging (DTI) already in young adults in their twenties. Here we aimed to use multi‐shell diffusion imaging to further explore genetic determinants of white matter microstructure across the adult lifespan and its relation with cSVD.

Posted ContentDOI
22 Mar 2022-bioRxiv
TL;DR: Gene ontology and enrichment analyses indicated that each of the three life-stages was associated with different biological processes and cellular components: synaptic modeling in early life, neurotransmission in mid-life, and neurodegeneration in late-life.
Abstract: Mechanisms underpinning age-related variations in cortical thickness in the human brain remain poorly understood. We investigated whether inter-regional age-related variations in cortical thinning (in a multicohort neuroimaging dataset from the ENIGMA Lifespan Working Group totalling 14,248 individuals, aged 4-89 years) depended on cell-specific marker gene expression levels. We found differences amidst early-life (<20 years), mid-life (20-60 years), and late-life (>60 years) in the patterns of association between inter-regional profiles of cortical thickness and expression profiles of marker genes for CA1 and S1 pyramidal cells, astrocytes, and microglia. Gene ontology and enrichment analyses indicated that each of the three life-stages was associated with different biological processes and cellular components: synaptic modeling in early life, neurotransmission in mid-life, and neurodegeneration in late-life. These findings provide mechanistic insights into age-related cortical thinning during typical development and aging.