Surface-based morphometry study of brain in patients with carbon monoxide poisoning

Wang, Tianhong; Jiang, Nan; Li, Jianlin; Lei, Junqiang; Guo, Shunlin

doi:10.1016/j.ejrad.2023.110711

Cited by 4 publications

(1 citation statement)

References 35 publications

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“…Another VBM study reported reduced gray matter (GM) volume in the bilateral basal ganglia, left postcentral gyrus, and left hippocampus, which was associated with decreased cognition in CO poisoning patients (Chen et al, 2013 ). Furthermore, our previous surface‐based morphometry (SBM) analysis demonstrated a significantly thinner cortical thickness in the SFG and rostral middle frontal gyrus (MFG), which was also related to lower MMSE scores in CO poisoning patients (Wang et al, 2023 ). These findings emphasize the crucial role of GM atrophy in the cognitive decline observed in patients with CO poisoning.…”

Section: Introductionmentioning

confidence: 96%

Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning

Zhang,

Wang,

Wang

et al. 2024

Human Brain Mapping

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Gray matter (GM) atrophy and white matter (WM) lesions may contribute to cognitive decline in patients with delayed neurological sequelae (DNS) after carbon monoxide (CO) poisoning. However, there is currently a lack of evidence supporting this relationship. This study aimed to investigate the volume of GM, cortical thickness, and burden of WM lesions in 33 DNS patients with dementia, 24 DNS patients with mild cognitive impairment, and 51 healthy controls. Various methods, including voxel‐based, deformation‐based, surface‐based, and atlas‐based analyses, were used to examine GM structures. Furthermore, we explored the connection between GM volume changes, WM lesions burden, and cognitive decline. Compared to the healthy controls, both patient groups exhibited widespread GM atrophy in the cerebral cortices (for volume and cortical thickness), subcortical nuclei (for volume), and cerebellum (for volume) (p < .05 corrected for false discovery rate [FDR]). The total volume of GM atrophy in 31 subregions, which included the default mode network (DMN), visual network (VN), and cerebellar network (CN) (p < .05, FDR‐corrected), independently contributed to the severity of cognitive impairment (p < .05). Additionally, WM lesions impacted cognitive decline through both direct and indirect effects, with the latter mediated by volume reduction in 16 subregions of cognitive networks (p < .05). These preliminary findings suggested that both GM atrophy and WM lesions were involved in cognitive decline in DNS patients following CO poisoning. Moreover, the reduction in the volume of DMN, VN, and posterior CN nodes mediated the WM lesions‐induced cognitive decline.

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Section: Introductionmentioning

confidence: 96%

Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning

Zhang,

Wang,

Wang

et al. 2024

Human Brain Mapping

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Environmental pollution and brain function

Gale,

Farrer,

Hedges

et al. 2025

Encyclopedia of the Human Brain

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Interaction Between DHCR24 and hsa_circ_0015335 Facilitates Cognitive Impairment in Cerebral Small Vessel Disease Patients

Shi,

Xu,

Wang

et al. 2024

CNS Neurosci Ther

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AimsThe study attempted to determine the underlying role and regulation mechanism of 3β‐hydroxysterol‐Δ24 reductase (DHCR24) in the pathophysiology of cerebral small vessel disease‐associated cognitive impairment (CSVD‐CI). An RNA high‐throughput sequencing and independent verification were conducted to identify potential circRNAs becoming the upstream regulator.MethodsRNA sequencing was performed in whole‐blood samples in cohort 1 (10 CSVD‐CI and 8 CSVD with cognitively normal [CSVD‐CN] patients). The DHCR24 and candidate circRNAs were verified in an independent cohort 2 (45 CSVD‐CI participants and 37 CSVD‐CN ones). The study also analyzed comprehensive cognitive assessments, plasma molecular index, and brain structure imaging.ResultsThe expression of DHCR24 and has_circ_0015335 in whole‐blood samples of CSVD‐CI patients was significantly reduced compared to CSVD‐CN patients in RNA sequencing and independent verification. Furthermore, the levels of DHCR24 and has_circ_0015335 were significantly related to global cognitive impairment in CSVD‐CI patients. Meanwhile, DHCR24 could regulate the correlation between has_circ_0015335 expression and alterations in brain cortex in surface area, thickness, and volume in CSVD‐CI patients. Additionally, hsa_circ_0015335 interacted with DHCR24 for plasma 24(S)‐hydroxycholesterol levels among CSVD‐CI patients.ConclusionInteraction between DHCR24 and hsa_circ_0015335 cognitively impaired CSVD by affecting brain cholesterol metabolism and brain structural changes.

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Surface-based morphometry study of brain in patients with carbon monoxide poisoning

Cited by 4 publications

References 35 publications

Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning

Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning

Environmental pollution and brain function

Interaction Between DHCR24 and hsa_circ_0015335 Facilitates Cognitive Impairment in Cerebral Small Vessel Disease Patients

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