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Cortical Morphometric Similarity Remodeling in Traumatic Brain Injury Links Cognitive Impairments with Transcriptional Changes and Type‐Specific Cells

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Title: Cortical Morphometric Similarity Remodeling in Traumatic Brain Injury Links Cognitive Impairments with Transcriptional Changes and Type‐Specific Cells
Authors: Yizhen Pan, Zhuonan Wang, Xiang Zhang, Wenpu Zhao, Haonan Zhang, Xuan Li, Xiaoyan Jia, Qiuyu Ji, Bo Yin, Guanghui Bai, Tingting Wu, Zhiqi Lee, Jierui Ding, Lei Shi, Jie Zhang, David H. Salat, Lijun Bai
Source: Adv Sci (Weinh)
Advanced Science, Vol 12, Iss 13, Pp n/a-n/a (2025)
Publisher Information: Wiley, 2025.
Publication Year: 2025
Subject Terms: Male, Adult, Cerebral Cortex, Adolescent, traumatic brain injury, Science, cortical structural abnormality, Middle Aged, Young Adult, Brain Injuries, Traumatic, morphometric similarity network, cells, Humans, Female, Cognitive Dysfunction, transcription, Transcriptome, Child, Brain Concussion, Research Article
Description: The heterogeneous injuries and resulting cognitive deficits pose significant challenges in the clinical management of mild traumatic brain injury (mTBI). However, the pathophysiological mechanisms related to heterogeneities of mTBI are still unclear. This study aims to explore the mechanisms underlying brain remodeling by examining the morphometric similarity (MS) alterations and corresponding transcriptomic signatures across adult and pediatric mTBI (adult mTBI: 112 acute patients, 47 follow‐up chronic patients, 66 healthy controls [HCs]; pediatric mTBI: 30 acute patients, 31 HCs). A healthy adult cohort (N = 840) is included to derive the modularized brain MS networks representing interregional cortical connectivity. Subsequently, cortical MS remodeling patterns are identified involving mostly MS increases in the frontal modules with typical high MS and decreases in the occipital module with typical low MS, with more pronounced changes observed in the developing brain with mTBI. The abnormal MS changes are correlated with variable cognitive impairments. Moreover, cortical MS remodeling is also associated with the genes enriched in CA1 pyramidal cells and neuron‐specific biological processes. The transcription‐related cortical remodeling in mTBI might reveal the disruption of brain cellular architecture. Therapeutic modalities to intervene in specific cortex and tackle CA1 over‐activation might better encircle the neurobiology of TBI.
Document Type: Article
Other literature type
Language: English
ISSN: 2198-3844
DOI: 10.1002/advs.202415262
Access URL: https://pubmed.ncbi.nlm.nih.gov/39921308
https://doaj.org/article/597ae3033230458d9f62a49b57dcdaf4
Rights: CC BY
Accession Number: edsair.doi.dedup.....07b0085765ef5324575a1541c6d3086b
Database: OpenAIRE
Description
Abstract:The heterogeneous injuries and resulting cognitive deficits pose significant challenges in the clinical management of mild traumatic brain injury (mTBI). However, the pathophysiological mechanisms related to heterogeneities of mTBI are still unclear. This study aims to explore the mechanisms underlying brain remodeling by examining the morphometric similarity (MS) alterations and corresponding transcriptomic signatures across adult and pediatric mTBI (adult mTBI: 112 acute patients, 47 follow‐up chronic patients, 66 healthy controls [HCs]; pediatric mTBI: 30 acute patients, 31 HCs). A healthy adult cohort (N = 840) is included to derive the modularized brain MS networks representing interregional cortical connectivity. Subsequently, cortical MS remodeling patterns are identified involving mostly MS increases in the frontal modules with typical high MS and decreases in the occipital module with typical low MS, with more pronounced changes observed in the developing brain with mTBI. The abnormal MS changes are correlated with variable cognitive impairments. Moreover, cortical MS remodeling is also associated with the genes enriched in CA1 pyramidal cells and neuron‐specific biological processes. The transcription‐related cortical remodeling in mTBI might reveal the disruption of brain cellular architecture. Therapeutic modalities to intervene in specific cortex and tackle CA1 over‐activation might better encircle the neurobiology of TBI.
ISSN:21983844
DOI:10.1002/advs.202415262