Browse the latest research summaries in the field of pathology for spinal cord injury patients and caregivers.
Showing 1-10 of 22 results
Frontiers in Neuroanatomy, 2010 • July 13, 2010
The study provides a detailed immunohistochemical analysis of PlexinA4 expression in the adult rat CNS, revealing its widespread distribution in neurons and fibers throughout the brain and spinal cord...
KEY FINDING: PlexinA4 is widely expressed throughout the adult rat brain, including the cortex, hippocampus, brainstem, pontine and medullary nuclei.
JOURNAL OF NEUROTRAUMA, 2015 • August 1, 2015
This study investigates the mechanism of fibrotic scar formation after spinal cord injury (SCI), focusing on fibronectin matrix assembly. The findings indicate that fibronectin starts forming a matrix...
KEY FINDING: Fibroblasts are the major source of fibronectin in the fibrotic scar after spinal cord injury. Deletion of fibronectin in myeloid cells did not change fibronectin expression level, indicating that fibroblasts are likely the major source.
Neural Regeneration Research, 2016 • July 1, 2016
The study aimed to assess the neuroregenerative effects of bacterial melanin (BM) on central nervous system injuries in rats using a specific staining method. The results indicated that BM stimulated ...
KEY FINDING: BM accelerated the recovery of motor function in rats with central nervous system injuries.
Journal of Neuroinflammation, 2016 • April 14, 2016
The study investigates the role of APRIL in fibrotic scar formation after SCI, finding that APRIL and BCMA expression increases following SCI. Genetic deletion of APRIL resulted in reduced fibrotic sc...
KEY FINDING: APRIL expression, along with its receptor BCMA, increases following spinal cord injury.
iScience, 2024 • February 16, 2024
The study found that CD44 was upregulated during fibrotic scar formation after SCI. Blocking CD44 downregulated fibrosis-related extracellular matrix proteins and promoted axon regeneration, leading t...
KEY FINDING: CD44 is upregulated during the formation of fibrotic scar after spinal cord injury.
Neural Regeneration Research, 2017 • April 1, 2017
The study investigates the mechanism by which mitomycin C (MMC) reduces scar adhesion after surgical decompression for spinal cord injury, focusing on its effect on human epidural scar fibroblasts (HE...
KEY FINDING: MMC suppresses the growth of human epidural scar fibroblasts in a dose- and time-dependent manner.
Journal of Neuroinflammation, 2021 • June 9, 2021
The study demonstrates that S100A4 is upregulated in fibroblasts from ALS patients and in the spinal cord of hFUS mice, suggesting it is a common pathological trait of ALS. Silencing S100A4 in ALS fib...
KEY FINDING: S100A4 is upregulated in fibroblasts from ALS patients, regardless of the specific gene mutation, suggesting it is a common pathological trait.
Frontiers in Cellular Neuroscience, 2021 • August 26, 2021
This review summarizes the current understanding of fibrotic scar formation after spinal cord injury (SCI), its cellular origins, and its interactions with other cells in the injured area. It highligh...
KEY FINDING: Fibrotic scar tissue, composed of fibroblasts and excess extracellular matrix, forms after SCI and inhibits axonal regeneration.
PLoS ONE, 2017 • April 17, 2017
The study aimed to develop a safe surgical method for removing intramedullary hemorrhagic necrosis (IHN) after spinal cord contusion in rats to create a cavity for future therapeutic implants. A small...
KEY FINDING: Small surgical approach to debridement (SSAD) effectively removed hemorrhagic necrosis after acute cord contusion in rats.
International Journal of Immunopathology and Pharmacology, 2018 • August 28, 2018
Glial scar formation is a complex response to injury in the central nervous system, involving astrocytes, immune cells, and extracellular matrix deposition, which can both inhibit and promote neural r...
KEY FINDING: Glial scar formation involves the activation of resident astrocytes, which surround the lesion core and wall off intact neurons in neurological damages.