Objective. To evaluate the efficacy of neuroprotective therapy in carotid ischemic stroke. Material and methods. An open comparative study of combined neuroprotective therapy in comparison with standard treatment has been carried out in 25 patients with carotid ischemic stroke of moderate severity in the acute period of disease. Patients received cytoflavin, gliatilin and actovegin, along with basic therapy, during 15 days. Patient's state was assessed every 5 days using the NIHSS. The Barthel index was estimated in the 21st day. Results and conclusion. By the end of treatment, the degree of neurological deficit was significantly lower in patients treated with the combination of the neuroprotectors. The better functional rehabilitation to the 21st day and the positive dynamics of inflammation indices and free-radical processes were shown in patients of the main group.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.17116/jnevro201411412238-42 | DOI Listing |
NPJ Parkinsons Dis
January 2025
Department of Neuroscience & Experimental Therapeutics, Texas A&M University College of Medicine, 8447 John Sharp Pkwy, Bryan, TX, 77807-3260, USA.
The smoking cessation drug cytisine exerts neuroprotection in substantia nigra pars compacta (SNc) dopaminergic (DA) neurons of female but not male 6-hydroxydopamine (6-OHDA) lesioned parkinsonian mice. To address the important question of whether circulating 17β-estradiol mediates this effect, we employ two mouse models aimed at depleting systemically circulating 17β-estradiol: (i) bilateral ovariectomy (OVX), and (ii) aromatase inhibition with systemically administered letrozole. In both models, depleting systemically circulating 17β-estradiol in female 6-OHDA lesioned parkinsonian mice results in the loss of cytisine-mediated neuroprotection as measured using apomorphine-induced contralateral rotations and SNc DA neurodegeneration.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Neurochem Res
January 2025
Department of Physiology, Faculty of Medicine, University of Ondokuz Mayıs, Samsun, Türkiye.
In the present study, the effects of the acetylcholinesterase (AChE) enzyme inhibitor rivastigmine (RIVA) on spike-wave discharges (SWDs), memory impairment, anxiety-like behavior, and the transient receptor potential vanilloid 1 (TRPV1) gene expression were investigated in genetic absence epileptic Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats. After tripolar electrodes were implanted on the WAG/Rij rats' skulls, single doses of 0.125, 0.
View Article and Find Full Text PDFJ Neural Transm (Vienna)
January 2025
Neurology Department, LR18SP03, Razi University Hospital, Tunis, Tunisia.
Amyotrophic Lateral Sclerosis(ALS) has traditionally been managed as a neuromuscular disorder. However, recent evidence suggests involvement of non-motor domains. This study aims to evaluate the impact of APOE and MAPT genotypes on the cognitive features of ALS.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Chiang Mai University/Neurophysiology Unit/Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai, Thailand.
Background: Our studies suggest that iron-overloaded rats developed neurotoxicity and cognitive impairment (1,2). An increase in brain mitochondrial fission and brain mitophagy have been considered as one of underlying mechanisms in brain with iron-overloaded condition (3,4). Hence, a pharmacological intervention focused on preventing brain mitochondrial pathologies is required.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!