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Exploring the impact of exercise-induced BDNF on neuroplasticity in neurodegenerative and neuropsychiatric conditions.
Mol Biol Rep
January 2025
Department of Nursing Science, Faculty of Basic Medical Sciences, Adeleke University, Ede, Osun State, Nigeria.
This review investigates the intricate relationship between exercise, brain-derived neurotrophic factor (BDNF), neuroplasticity, and cognitive function, with a focus on implications for neuropsychiatric and neurodegenerative disorders. A systematic review was conducted by searching various databases for relevant studies that explored the connections between exercise, BDNF, neuroplasticity, and cognitive health. The analysis of eligible studies revealed that exercise increases BDNF levels in the brain, promoting neuroplasticity and enhancing cognitive functions.
View Article and Find Full Text PDFEdaravone Mitigates Hippocampal Neuronal Death and Cognitive Dysfunction by Upregulating BDNF Expression in Neonatal Hypoxic-Ischemic Rats.
Int J Dev Neurosci
February 2025
Department of Digestive and Nutrition, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological injury during infancy, often resulting in long-term cognitive deficits. This study aimed to investigate the neuroprotective effects of Edaravone (EDA), a free radical scavenger, and elucidate the potential role of brain-derived neurotrophic factor (BDNF) in mediating these effects in neonatal HIE rats. Using the Rice-Vannucci model, HIE was induced in neonatal rats, followed by immediate administration of EDA after the hypoxic-ischemic insult.
View Article and Find Full Text PDFThe impact of a high-carbohydrate diet on the cognitive behavior of mice in a low-pressure, low-oxygen environment.
Food Funct
January 2025
State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi 214122, China.
The effectiveness of high-carbohydrate diets (HCD) on cognitive impairment is still being debated. To clarify the impact of HCD on the cognitive behavior of mice under low-pressure hypoxic conditions, we studied 24 mice in different environments while subjecting them to dietary intervention for 5 weeks, and conducting behavioral tests. Under low-pressure hypoxic conditions, HCD intervention reversed the decline in spatial learning and memory abilities in mice caused by hypoxia, ameliorated pathological brain damage, and restored the integrity of the intestinal mucosa.
View Article and Find Full Text PDFBrain-derived neurotrophic factor alterations and cognitive decline in schizophrenia: Implications for early intervention.
World J Psychiatry
January 2025
Department of Digital Anti-aging Healthcare (BK21), Inje University, Gimhae 50834, South Korea.
This manuscript explores the recent study by Cui which assessed the interplay between inflammatory cytokines and brain-derived neurotrophic factor (BDNF) levels in first-episode schizophrenia patients. The study revealed that higher levels of interleukin-6 and tumor necrosis factor-α correlated with reduced BDNF levels and poorer cognitive performance. Schizophrenia is a severe psychiatric disorder impacting approximately 1% of the global population, characterized by positive symptoms (hallucinations and delusions), negative symptoms (diminished motivation and cognitive impairments) and disorganized thoughts and behaviors.
View Article and Find Full Text PDFRole of Adenosine A1 Receptor in Sleep Deprivation-Induced Neuroinflammation: Insights on Rapid Eye Movement Sleep and Fear Extinction Memory Recall in Rats.
Cureus
December 2024
School of Allied Health Sciences, Manav Rachna International Institute of Research and Studies, Faridabad, IND.
Introduction: Sleep deprivation (SD), stemming from a myriad of aetiologies, is a prevalent health condition frequently overlooked. It typically impairs memory consolidation and synaptic plasticity, potentially through neuroinflammatory mechanisms and adenosinergic signalling. It is still unclear whether the adenosine A1 receptor (A1R) modulates SD-induced neurological deficits in the hippocampus.
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