Publications by authors named "J Bouley"
Article Synopsis
- About 20% of familial ALS cases are linked to mutations in the SOD1 gene, and traumatic brain injury (TBI) is identified as a possible risk factor.
- Researchers studied the effects of repetitive TBI on ALS progression in SOD1 mouse models and the role of Sarm1, a regulator of axonal degeneration.
- Results showed that TBI worsened ALS symptoms and disease progression, but losing Sarm1 helped improve outcomes and reduced nerve damage, indicating potential for SARM1-targeted treatments.
Article Synopsis
- Moderate-to-severe repetitive traumatic brain injury (TBI) is linked to neurodegenerative disorders and is associated with the mislocalization of TDP-43 protein, which may trigger neurodegenerative processes.
- Research on mice showed that blocking the Sarm1 axon death pathway reduced pathological changes related to TDP-43 and improved neuronal health after TBI.
- Sarm1 knockout mice performed better in terms of neurological function and survival compared to Sarm1 wild type and hemizygous mice, suggesting that targeting the Sarm1 pathway could help in treating injuries caused by TBI.
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are fatal neurodegenerative diseases that represent ends of the spectrum of a single disease. The most common genetic cause of FTD and ALS is a hexanucleotide repeat expansion in the C9orf72 gene. Although epidemiological data suggest that traumatic brain injury (TBI) represents a risk factor for FTD and ALS, its role in exacerbating disease onset and course remains unclear.
View Article and Find Full Text PDFClinical observations indicate that body weight (BW) extremes are associated with worse outcome after traumatic brain injury (TBI); yet, it is uncertain whether the baseline BW (bBW) may affect outcome after mouse TBI. We retrospectively analyzed 129 similarly aged (9-12 weeks) male C57BL6/J mice that were subjected to repetitive closed head TBI (rTBI) using an established weight drop paradigm as well as 55 sham injured mice. We sought to determine whether the bBW as well as the post-TBI weight relative to baseline (%BW) were associated with a variety of post-rTBI outcomes, including acute model complications (skull fractures and macroscopic hemorrhage), impact seizures, return of the righting reflex (RR), the neurological severity score (NSS), post-rTBI BW-change, and 28-day mortality.
View Article and Find Full Text PDFTraumatic brain injury (TBI) constitutes one of the strongest environmental risk factors for several progressive neurodegenerative disorders of cognitive impairment and dementia that are characterized by the pathological accumulation of hyperphosphorylated tau (p-Tau). It has been questioned whether mouse closed-head TBI models can replicate human TBI-associated tauopathy. We conducted longitudinal histopathological characterization of a mouse closed head TBI model, with a focus on pathological features reported in human TBI-associated tauopathy.
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