Cardiovascular disease (CVD) is currently the leading cause of death in Brazil and worldwide. In 2016, CVD accounted for more than 17 million deaths, representing 31% of all deaths globally. Molecular and genetic mechanisms may be involved in vascular protection and should be considered in new therapeutic approaches. In this sense, recent studies have reported that brain-derived neurotrophic factor (BDNF) is reduced in individuals predisposed to develop CVD, and that aerobic physical training increases the amounts of circulating BDNF. BDNF is a neurotrophin found at high concentrations in the hippocampus and cerebral cortex and is considered a key molecule for the maintenance of synaptic plasticity and survival of neuronal cells. In addition to neuronal plasticity, BDNF is also important in vascular function, promoting angiogenesis through the regulation of reactive oxygen species (ROS). However, a variant of the BDNF gene in humans, the Val66Met polymorphism (substitution of the amino acid valine for a methionine at position 66 of the codon), occurring in 20-30% of the Caucasian population, may affect plasma BDNF concentrations and its activity in all peripheral tissues containing tyrosine kinase B receptors (TrkB), such as the endothelium. Thus, we will present a discussion about the role of serum BDNF levels in cardiovascular protection, Val66Met genetic variant in vascular reactivity and the effect of physical exercise.
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http://dx.doi.org/10.36660/abc.20190368 | DOI Listing |
Nanoscale
January 2025
James Watt School of Engineering, University of Glasgow, Glasgow G12 8QQ, UK.
Neurodegenerative diseases, characterized by the progressive deterioration of neuronal function and structure, pose significant global public health and economic challenges. Brain-Derived Neurotrophic Factor (BDNF), a key regulator of neuroplasticity and neuronal survival, has emerged as a critical biomarker for various neurodegenerative and psychiatric disorders, including Alzheimer's disease. Traditional diagnostic methods, such as Enzyme-Linked Immunosorbent Assay (ELISA) and electrochemiluminescence (ECL) assays, face limitations in terms of sensitivity, stability, reproducibility, and cost-effectiveness.
View Article and Find Full Text PDFJ Neurochem
January 2025
CNR Neuroscience Institute, Milano, Vedano al Lambro, Italy.
Mutations in the Transcription Factor 20 (TCF20) have been identified in patients with autism spectrum disorders (ASDs), intellectual disabilities (IDs), and other neurological issues. Recently, a new syndrome called TCF20-associated neurodevelopmental disorders (TAND) has been described, with specific clinical features. While TCF20's role in the neurogenesis of mouse embryos has been reported, little is known about its molecular function in neurons.
View Article and Find Full Text PDFEndocrinology
January 2025
Department of Cancer Biology & Genetics, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.
Prader-Willi syndrome (PWS) is a rare genetic disease that causes developmental delays, intellectual impairment, constant hunger, obesity, endocrine dysfunction, and various behavioral and neuropsychiatric abnormalities. Standard care of PWS is limited to strict supervision of food intake and growth hormone therapy, highlighting the unmet need for new therapeutic strategies. Environmental enrichment (EE), a housing environment providing physical, social, and cognitive stimulations, exerts broad benefits on mental and physical health.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Background: Traumatic brain injury (TBI) is characterized by high mortality and disability rates. Disease-associated microglia (DAM) are a newly discovered subtype of microglia. However, their presence and function in the acute phase of TBI remain unclear.
View Article and Find Full Text PDFToxicology
January 2025
School of Forensic Medicine, National Health Commission (NHC) Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan 650500, China. Electronic address:
Methamphetamine (METH), a synthetic stimulant, has seen an escalating abuse situation globally over the past decade. Although the molecular mechanism underlying METH-induced neurotoxicity has been explored, the dysfunction of brain-derived neurotrophic factor (BDNF) neuroprotection in the context of METH neurotoxicity remains insufficiently understood. Our previous studies have found that METH induced neurotoxicity and BDNF expression in rat primary neurons, necessitating further research into this paradox.
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