Despite higher rates of hospitalization and mortality following traumatic brain injury (TBI) in patients over 65 years old, older patients remain underrepresented in drug development studies. Worse outcomes in older individuals compared to younger adults could be attributed to exacerbated injury mechanisms including oxidative stress, inflammation, blood-brain barrier disruption, and bioenergetic dysfunction. Accordingly, pleiotropic treatments are attractive candidates for neuroprotection. Taurine, an endogenous amino acid with antioxidant, anti-inflammatory, anti-apoptotic, osmolytic, and neuromodulator effects, is neuroprotective in adult rats with TBI. However, its effects in the aged brain have not been evaluated. We subjected aged male rats to a unilateral controlled cortical impact injury to the sensorimotor cortex, and randomized them into four treatment groups: saline or 25 mg/kg, 50 mg/kg, or 200 mg/kg i.p. taurine. Treatments were administered 20 min post-injury and daily for 7 days. We assessed sensorimotor function on post-TBI days 1-14 and tissue loss on day 14 using T-weighted magnetic resonance imaging. Experimenters were blinded to the treatment group for the duration of the study. We did not observe neuroprotective effects of taurine on functional impairment or tissue loss in aged rats after TBI. These findings in aged rats are in contrast to previous reports of taurine neuroprotection in younger animals. Advanced age is an important variable for drug development studies in TBI, and further research is required to better understand how aging may influence mechanisms of taurine neuroprotection.
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http://dx.doi.org/10.1007/s11682-018-9865-5 | DOI Listing |
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Zoology Department, Faculty of Science, Cairo University, Giza, Egypt.
Due to the continuous exposure to bisphenol-A (BPA), the current study was conducted to evaluate taurine's neuroprotective action against BPA's adverse effect on the brain. Rats were grouped into control, BPA-treated rats, and taurine + BPA-treated rats. At the end of the 35-day treatment period, the memory of the rats was evaluated using the novel object test and the Y-maze test.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Neuroscience, Laboratory of Prion Neurobiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
There is no cure for Marinesco-Sjögren syndrome (MSS), a genetic multisystem disease linked to loss-of-function mutations in the SIL1 gene, encoding a BiP co-chaperone. Previously, we showed that the PERK kinase inhibitor GSK2606414 delays cerebellar Purkinje cell (PC) degeneration and the onset of ataxia in the woozy mouse model of MSS. However, GSK2606414 is toxic to the pancreas and does not completely rescue the woozy phenotype.
View Article and Find Full Text PDFBehav Brain Res
March 2025
DELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Basic Medical Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Reducing antioxidant levels exacerbates the generation of reactive oxygen/nitrogen species, leading to alpha-synuclein aggregation and the degeneration of dopaminergic neurons. These play a key role in the onset of Parkinson's disease (PD), for which effective treatment remains elusive. This study examined the neuroprotective effects of taurine, an essential β-amino acid with antioxidant and antiinflammation properties, in Swiss male mice exposed to rotenone-induced PD.
View Article and Find Full Text PDFBiomedicines
November 2024
Department of Neurological Rehabilitation, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
: Long non-coding RNA taurine-upregulated gene 1 (TUG1) is involved in various cellular processes, but its role in cerebral ischemia-reperfusion injury remains unclear. This study investigated TUG1's role in regulating the nucleocytoplasmic shuttling of human antigen R (HuR), a key apoptosis regulator under ischemic conditions. : CRISPR-Cas9 technology was used to generate TUG1 knockout Sprague Dawley rats to assess TUG1's impact on ischemic injury.
View Article and Find Full Text PDFJ Control Release
January 2025
Department of Gastroenterology, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China. Electronic address:
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