The Role of Brain-Derived Neurotrophic Factor in Autism Spectrum Disorder: Current Findings and Future Directions

Brain-derived neurotrophic factor (BDNF) is a crucial neurotrophic factor that plays an essential role in neuroplasticity and neurodevelopment. Autism spectrum disorder (ASD) is a neurodevelopmental disorder that affects social interaction, communication, and behavior. The relationship between BDNF and ASD has been studied extensively, with conflicting results. While some studies suggest that decreased BDNF levels may contribute to the development of ASD, others do not confirm this finding. The effects of BDNF on synaptic plasticity and cognitive functions have also been investigated, with some studies indicating that BDNF may be associated with impairments in learning, memory, and attention in individuals with ASD. Additionally, physical exercise and cognitive and behavioral therapies may help alleviate ASD symptoms by increasing BDNF levels and enhancing neuroplasticity. Further research is needed to better understand the mechanisms underlying the relationship between BDNF and ASD and to develop more effective treatment strategies for individuals with ASD

Rottlerin and Genistein Suppress Cell Proliferation, Invasion, Cell Cycle and Induce Apoptosis in Neuroblastoma Cells

WOS: 00041980620007

Levodropropizine suppresses seizure activity in rats with pentylenetetrazol-induced epilepsy

WOS: 000461404200005PubMed ID: 30610970Background: Millions of individuals worldwide suffer from epilepsy, and up to 25% of patients have seizures that are resistant to currently available antiepileptic drugs. Hence, there continues to be a need for more seizure medications that are effective yet tolerable. Levodropropizine (LVDP) is an established antitussive drug that, based on preclinical data, may also have antiepileptic activity. Methods: We treated rats with either intraperitoneal (IP) LVDP at two different doses or placebo in randomized fashion and then exposed them to IP pentylenetetrazol (PTZ), a potent seizure-inducing compound. We measured the rats' subsequent seizure activity with electroencephalography (EEG), Racine's convulsion scale (RCS) and time to first myoclonic jerk (TFMJ) to determine whether LVDP has antiepileptic properties in our murine model for epilepsy. Results: When compared to placebo, LVDP at both doses significantly suppressed seizure activity. Mean EEG spike wave percentage score decreased from 76.8% (placebo) to 13.1% (lower dose) and 7.6% (higher dose, both p < 0.0001). RCS decreased from a mean of 5.8 (placebo) to 1.83 (lower dose) and 1.16 (higher dose, both p < 0.05). TFMJ had increased from a mean of 65.1 s (placebo), to 247.3 s (lower dose) and 295.5 s (higher dose, both p < 0.0001). Conclusions: Levodropropizine, a common antitussive drug, suppresses seizure activity in rats with PTZ-induced status epilepticus. Given the ongoing need to find effective therapies for refractory epilepsy, the possibility of using levodropropizine as an antiepilepticshould be further explored

The Protective Effects of Carvedilol on Diabetic Nephropathy in A Streptozotocin-Induced Diabetic Rat Model

WOS: 000532415800094[No abstract available

Erythropoietin shows gender dependent positive effects on social deficits, learning/memory impairments, neuronal loss and neuroinflammation in the lipopolysaccharide induced rat model of autism

Alnak, Alper/0000-0002-3515-8217; Erdogan, Mumin/0000-0003-0048-444XWOS: 000571919100007PubMed: 32736811We aimed to evaluate the effects of EPO in the lipopolysaccharide (LPS) induced rat model of autism in terms of social deficits, learning and memory impairments, as well as their neurochemical correlates. Sixteen female Sprague Dawley rats randomly distributed into two equel groups, then were caged with fertile males for mating. At the 10th day of pregnancy, 0.5 ml %0,9 NaCl saline was given to first group, 100 mu g/kg LPS was given to second group to induce autism. on postnatal 21th day, forty-eight littermates were divided into four groups as; 8 male, 8 female controls, 16 male and 16 female LPS-exposed. Then, LPS groups were also divided in to two groups as saline (1 mg/kg/day) and EPO 600 U/kg/day groups, and animals were treated 45 days. At 50th day, after behavioral evaluations, brain levels of TNF-alpha, nerve growth factor (NGF) were measured. Histologically, hippocampal neuronal density and GFAP expression were assessed. Three-chamber sociability and social novelty test, passive avoidance learning test were revealed significant differences among the EPO and control groups. Histologically, hippocampal CAl & CA3 regions displayed significant alterations regarding gliosis (GFAP-positive cells) and regarding frontal cortical thickness in EPO groups compare to controls. Biochemical measurements of the brain levels of TNF-alpha and NGF levels showed significant differences between controls and EPO groups. According to our findings EPO treatment has beneficial effects on ASD-like symptoms, learning and memory processes, neuronal loss and neuroinflammation in the LPS induced rat model of autism, with some gender differences through inflammatory and neurotrophic pathways

Exenatide, a GLP-1 analog, has healing effects on LPS-induced autism model: Inflammation, oxidative stress, gliosis, cerebral GABA, and serotonin interactions

Erdogan, Mumin/0000-0003-0048-444XWOS: 000558438600001PubMed: 32745285Previous studies have established anti-inflammatory, antioxidant, and neuroprotective effects of Exenatide in the central nervous system. Since these mechanisms are thought to have important roles in the pathophysiology of autism, we hypothesized that Exenatide may have healing effects in autism. We tested this hypothesis by examining the effects of Exenatide in an experimental autism model created by lipopolysaccharide (LPS) exposure in the womb, with behavioral tests, histopathological examinations, and biochemical measurements. the autism model was created by administration of LPS (i.p) to pregnant rats on the 10th day of their pregnancy at a dose of 100 mu g/kg. on postnatal 21st day, a total of four groups were formed from offspring with regard to sex distribution and treatment. After a 45-day treatment, behavioral analysis tests were performed on rats. Subsequently, the rats were sacrificed and biochemical analysis [superoxide dismutase, tumor necrotizing factor alpha, nerve growth factor, 5-hydroxyindoleacetic acid, and glutamic acid decarboxylase-67] and histopathological analysis were performed. on the 10th day of the intrauterine period, LPS exposure was found to disrupt behavioral findings, increase inflammation and hippocampal gliosis, and decrease 5-HIAA, GAD-67, and NGF, especially in male rats. However, among the rats exposed to LPS in the intrauterine period, recipients of Exenatide demonstrated significant amelioration of findings. Exenatide therapy shows positive effects on behavioral disorders in an LPS-induced autism model. This agent probably exerts its effects by suppressing inflammation and oxidative stress and reducing hippocampal gliosis. in addition, Exenatide has also been shown to positively affect cerebral serotonergic and GABAergic effects

Neuroprotective effects of dexpanthenol on streptozotocin-induced neuronal damage in rats

Aim Although the most common age-related neurodegenerative disease defined by memory loss is Alzheimer's disease (AD), only symptomatic therapies are present. A complex pathway for the AD pathogenesis that includes an increase in inflammation has recently been suggested. Since in previous animal experiments dexpanthenol has anti-inflammatory and neuroprotective activities, effects and role of dexpanthenol in an intracerebroventricular (ICV)-streptozotocin (STZ) induced sporadic-AD(memory impairment) animal model have been examined. Design and methods In total, 18 adult sprague-dawley rats were classified into 3 groups; control (n = 6), STZ + Saline (n = 6) and STZ + Dexpanthenol (n = 6). Twelve AD-induced rats through STZ-injection (3 mg/kg) into both lateral ventricles via stereotaxy were separated into two groups five days after STZ administration: one of these groups was treated with dexpanthenol (1000 mg/kg/day, i.p.) for 3 weeks and the other with saline. A passive avoidance learning (PAL) test was used after treatment, followed by brain tissue extraction in all subjects. Brain levels of tumor necrosis factor-alpha (TNF-alpha) and choline acetyl transferase (ChAT) were measured and Cresyl violet staining was used to count neurons in cornu ammonis-1 (CA1) and cornu ammonis-3 (CA3). Results It was observed that ICV-STZ significantly shortened PAL latency, increased levels of TNF-alpha in brain, decreased activity of ChAT in brain, and number of hippocampal neurons. However, dexpanthenol significantly reduced all of those STZ-induced harmful effects. Conclusion Dexpanthenol significantly prevented the memory deficit induced by ICV-STZ through mitigating neuronal loss in hippocampus, cholinergic deficiency and neuroinflammation in rats. These findings suggest that dexpanthenol may be beneficial for treating memory impairment