Molecular pathology of acute spinal cord injury in middle-aged mice

Abstract The median age at which spinal cord injuries occur has steadily increased from 29 to 43 over the last several decades. Although more pre-clinical studies in aged rodents are being done to address this shift in demographics, comprehensive transcriptomic studies investigating SCI pathobiology...

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Main Authors: Corey Fehlberg, Danny John, Brian Kang, James S. Choi, Susana Cerqueira, Alexis Brake, Jae K. Lee
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Journal of Neuroinflammation
Subjects:
Online Access:https://doi.org/10.1186/s12974-025-03494-4
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author Corey Fehlberg
Danny John
Brian Kang
James S. Choi
Susana Cerqueira
Alexis Brake
Jae K. Lee
author_facet Corey Fehlberg
Danny John
Brian Kang
James S. Choi
Susana Cerqueira
Alexis Brake
Jae K. Lee
author_sort Corey Fehlberg
collection DOAJ
description Abstract The median age at which spinal cord injuries occur has steadily increased from 29 to 43 over the last several decades. Although more pre-clinical studies in aged rodents are being done to address this shift in demographics, comprehensive transcriptomic studies investigating SCI pathobiology in middle-aged mice are lacking. To address this gap in knowledge, we compared behavioral, histopathological, and transcriptional outcomes in young (2–4 months old) and middle-aged (10–12 months old) mice. In contrast to most previous studies, open field tests showed no differences in locomotor recovery between the young and middle-aged mice over a one-month period. The injury site also demonstrated similar histopathology in terms of lesion size, and numbers of macrophages and fibroblasts. Acutely after injury, proliferation of macrophages, fibroblasts, and astrocytes were also similar between the two age groups. In addition, spatial transcriptomics showed similar, transcriptionally defined regions around the injury site at 3 days post-injury. However, single cell RNA-sequencing of the cells at the injury site and surrounding spared tissue showed differences in select cell subpopulations. Taken together, our results indicate that although young and middle-aged mice display similar locomotor recovery and histopathology after SCI, changes in cell subpopulations may underlie a decline in repair mechanisms that manifest after middle age.
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spelling doaj-art-84a8a0066b8b43dd918162b55fc0ea662025-08-20T03:05:16ZengBMCJournal of Neuroinflammation1742-20942025-07-0122112110.1186/s12974-025-03494-4Molecular pathology of acute spinal cord injury in middle-aged miceCorey Fehlberg0Danny John1Brian Kang2James S. Choi3Susana Cerqueira4Alexis Brake5Jae K. Lee6Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineMiami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineMiami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineMiami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineMiami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineMiami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineMiami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of MedicineAbstract The median age at which spinal cord injuries occur has steadily increased from 29 to 43 over the last several decades. Although more pre-clinical studies in aged rodents are being done to address this shift in demographics, comprehensive transcriptomic studies investigating SCI pathobiology in middle-aged mice are lacking. To address this gap in knowledge, we compared behavioral, histopathological, and transcriptional outcomes in young (2–4 months old) and middle-aged (10–12 months old) mice. In contrast to most previous studies, open field tests showed no differences in locomotor recovery between the young and middle-aged mice over a one-month period. The injury site also demonstrated similar histopathology in terms of lesion size, and numbers of macrophages and fibroblasts. Acutely after injury, proliferation of macrophages, fibroblasts, and astrocytes were also similar between the two age groups. In addition, spatial transcriptomics showed similar, transcriptionally defined regions around the injury site at 3 days post-injury. However, single cell RNA-sequencing of the cells at the injury site and surrounding spared tissue showed differences in select cell subpopulations. Taken together, our results indicate that although young and middle-aged mice display similar locomotor recovery and histopathology after SCI, changes in cell subpopulations may underlie a decline in repair mechanisms that manifest after middle age.https://doi.org/10.1186/s12974-025-03494-4Spinal cord injuryMiddle-ageAgingAge as a biological variableSingle-cell RNA sequencingSpatial transcriptomics
spellingShingle Corey Fehlberg
Danny John
Brian Kang
James S. Choi
Susana Cerqueira
Alexis Brake
Jae K. Lee
Molecular pathology of acute spinal cord injury in middle-aged mice
Journal of Neuroinflammation
Spinal cord injury
Middle-age
Aging
Age as a biological variable
Single-cell RNA sequencing
Spatial transcriptomics
title Molecular pathology of acute spinal cord injury in middle-aged mice
title_full Molecular pathology of acute spinal cord injury in middle-aged mice
title_fullStr Molecular pathology of acute spinal cord injury in middle-aged mice
title_full_unstemmed Molecular pathology of acute spinal cord injury in middle-aged mice
title_short Molecular pathology of acute spinal cord injury in middle-aged mice
title_sort molecular pathology of acute spinal cord injury in middle aged mice
topic Spinal cord injury
Middle-age
Aging
Age as a biological variable
Single-cell RNA sequencing
Spatial transcriptomics
url https://doi.org/10.1186/s12974-025-03494-4
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