Injury to the neurovasculature is a feature of brain injury and must be addressed to maximize opportunity for improvement. Cerebrovascular dysfunction, manifested by reduction in cerebral blood flow (CBF), is a key factor that worsens outcome after traumatic brain injury (TBI), most notably under conditions of hypotension. We report here that a new class of antioxidants, poly(ethylene glycol)-functionalized hydrophilic carbon clusters (PEG-HCCs), which are nontoxic carbon particles, rapidly restore CBF in a mild TBI/hypotension/resuscitation rat model when administered during resuscitation--a clinically relevant time point. Along with restoration of CBF, there is a concomitant normalization of superoxide and nitric oxide levels. Given the role of poor CBF in determining outcome, this finding is of major importance for improving patient health under clinically relevant conditions during resuscitative care, and it has direct implications for the current TBI/hypotension war-fighter victims in the Afghanistan and Middle East theaters. The results also have relevancy in other related acute circumstances such as stroke and organ transplantation.
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http://dx.doi.org/10.1021/nn302615f | DOI Listing |
Neurourol Urodyn
January 2025
Department of Neurology, Hochzirl Hospital, Zirl, Austria.
Introduction: Neurogenic bladder dysfunction is a prevalent condition characterized by impaired bladder control resulting from neurological conditions, for example, spinal cord injury or traumatic brain injury (TBI). Detrusor overactivity is a typical symptom of central nervous system damage. A lesion affecting the pontine neural network typically results in loss of tonic inhibition exerted by the pontine micturition center and causes involuntary detrusor contractions.
View Article and Find Full Text PDFEur J Neurol
January 2025
Epilepsy Center, Department of Neurology, Fondazione IRCCS San Gerardo Dei Tintori, Monza, Italy.
Background: Epileptiform activity, including status epilepticus (SE), occurs in up to one-third of comatose survivors of cardiac arrest and may predict poor outcome. The relationship between SE and hypoxic-ischemic brain injury (HIBI) is not established.
Methods: This is a single-center retrospective study on consecutive patients with post-anoxic super-refractory SE.
Drug Des Devel Ther
January 2025
Department of Pharmacology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, 610041, People's Republic of China.
Objective: Neuronal damage is criminal to cognitive dysfunction, closely related to endoplasmic reticulum stress (ERS). However, due to the pathogenesis of endotoxin-induced long-term cognitive dysfunction is not fully clarified, there is still a lack of effective treatment. This study was conducted to explore the protective effects and mechanism of rosmarinic acid (RA) against ERS in endotoxin-induced cognitive dysfunction in mice and neuronal injury in cells.
View Article and Find Full Text PDFIBRO 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 PDFGen Physiol Biophys
January 2025
Shanghai University of Traditional Chinese Medicine, Shenzhen Hospital, Shenzhen, Guangdong, China.
Cerebral ischemia-reperfusion (I/R) is a serious complication in patients with ischemic stroke. Senkyunolide A (SenA) can alleviate neuronal cell damage induced by cerebral I/R; however, the exact action mechanism remains unclear. An in vitro cellular injury model was established by inducing PC-12 cells with OGD/R.
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