AI Article Synopsis
Article Abstract
Objective: Traumatic brain injury (TBI) is a chronic, progressive condition associated with permanent disabilities, particularly cognitive impairments. Glial scar formation following TBI is considered a contributing factor to these persistent disabilities. Currently, limited research exists on pharmacological interventions targeting glial scar prevention that require a standard weight drop TBI model for glial scar formation. Since there is no established standard TBI model for glial scar formation, this study aims to validate and modify the height of the weight drop model to identify glial scar formation and cognitive impairments.
Methods: Fifteen male Sprague Dawley rats were randomly divided into sham, WD1, and WD2 groups. The weight drop model with a 10 g load was applied to the right exposed brain of the rats from a height of 5 cm (WD1) and 10 cm (WD2) using a modified Feeney's weight drop device. Cognitive impairments were confirmed using the novel object recognition (NOR) test with ethovision software on day 15. Subsequently, the rats were decapitated on day 16, and GFAP immunohistochemical staining was performed to confirm the presence of glial scarring.
Results: The WD1 and WD2 groups exhibited a significant increase in glial scar formation compared to the sham group, with the WD2 group resulting in even more pronounced glial scar formation. Only the WD2 model caused statistically significant cognitive damage. The negative correlation coefficient indicates that an increase in GFAP + cells will decrease the cognitive function.
Conclusion: Modification of the height of the weight drop model, by dropping a weight of 10 g from a height of 10 cm (WD2 group) onto the right brain exposed of the rat has been proven to induce the formation of a glial scar and cognitive impairment.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10722700 | PMC |
| http://dx.doi.org/10.1186/s12883-023-03494-y | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Effect of metabolic disorders on reactive gliosis and glial scarring at the early subacute phase of stroke in a mouse model of diabetes and obesity.
IBRO Neurosci Rep
June 2025
Université de la Réunion, INSERM, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), Saint-Pierre 97410, France.
It is well recognized that type II Diabetes (T2D) and overweight/obesity are established risk factors for stroke, worsening also their consequences. However, the underlying mechanisms by which these disorders aggravate outcomes are not yet clear limiting the therapeutic opportunities. To fill this gap, we characterized, for the first time, the effects of T2D and obesity on the brain repair mechanisms occurring 7 days after stroke, notably glial scarring.
View Article and Find Full Text PDFTemporal lobe epilepsy with isolated amygdala enlargement: anatomo-electro-clinical features and long-term outcome.
J Neurol
January 2025
Epilepsy Unit - Sleep Disorders Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
Background: Temporal lobe epilepsy with isolated amygdala enlargement (TLE-AE) still lacks a definite characterization and controversies exist.
Methods: We conducted a retrospective study identifying brain MRI scans with isolated AE between 2015 and 2021. We collected clinical and paraclinical data of patients with TLE-AE and evaluated the outcome.
Dyke-Davidoff-Masson syndrome: A rare case of hemiatrophy with chronic seizure disorder.
Radiol Case Rep
March 2025
Department of Radiology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education & Research, Sawangi, Meghe, Wardha, India.
Dyke-Davidoff-Masson syndrome (DDMS) is a rare neurological disorder characterized by cerebral hemiatrophy, leading to seizures, hemiparesis, and cognitive deficits. We report the case of a 20-year-old female with a history of chronic seizure disorder and left-sided hemiparesis. The patient experienced her first seizure at 6 months of age, followed by recurrent generalized tonic seizures throughout childhood.
View Article and Find Full Text PDFIncreased SOX10, p16, and Cyclin D1 Immunoreactivity Differentiates MAP Kinase-activated Low-grade Gliomas From Piloid Gliosis.
Am J Surg Pathol
January 2025
Department of Pathology, Johns Hopkins University, Baltimore, MD.
Low-grade gliomas and reactive piloid gliosis can present with overlapping features on conventional histology. Given the large implications for patient treatment, there is a need for effective methods to discriminate these morphologically similar but clinically distinct entities. Using routinely available stains, we hypothesize that a limited panel including SOX10, p16, and cyclin D1 may be useful in differentiating mitogen-activated protein (MAP) kinase-activated low-grade gliomas from piloid gliosis.
View Article and Find Full Text PDFRNA-Targeting CRISPR/CasRx system relieves disease symptoms in Huntington's disease models.
Mol Neurodegener
January 2025
Guangdong Key Laboratory of Non-Human Primate Research, Key Laboratory of CNS Regeneration (Ministry of Education), School of Medicine, GHM Institute of CNS Regeneration, Jinan University, Guangzhou, 510632, China.
Background: HD is a devastating neurodegenerative disorder caused by the expansion of CAG repeats in the HTT. Silencing the expression of mutated proteins is a therapeutic direction to rescue HD patients, and recent advances in gene editing technology such as CRISPR/CasRx have opened up new avenues for therapeutic intervention.
Methods: The CRISPR/CasRx system was employed to target human HTT exon 1, resulting in an efficient knockdown of HTT mRNA.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!