Recombinant Human BDNF, 25 ug
- Known as:
- Recombinant Human BDNF, 25 ug
- Catalog number:
- PR15020-25
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Recombinant Human BDNF 25
Ask about this productRelated genes to: Recombinant Human BDNF, 25 ug
- Gene:
- BDNF NIH gene
- Name:
- brain derived neurotrophic factor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2016-06-01
- Gene:
- BDNF-AS NIH gene
- Name:
- BDNF antisense RNA
- Previous symbol:
- BDNFOS
- Synonyms:
- BT2A, BT2B, BT2C, BT2D, NCRNA00049, BDNF-AS1, BDNFAS
- Chromosome:
- 11p14.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2005-02-01
- Date modifiied:
- 2017-08-09
Related products to: Recombinant Human BDNF, 25 ug
Related articles to: Recombinant Human BDNF, 25 ug
- Alzheimer's disease (AD) is characterised by severe degeneration of cholinergic neurons within the basal forebrain complex (FBC) which is a key regulator of cognitive function. Cholinergic loss represents a central pathological hallmark of AD; however, the underlying molecular mechanisms remain incompletely understood. Although various in-vitro models are available, many are limited by species-specific differences, high cost, and technical complexity. Human neuroblastoma (SH-SY5Y) cells can be differentiated into neuron-like cells and represent a practical alternative for AD research. This study aimed to optimise retinoic acid (RA)-based differentiation conditions to enhance cholinergic characteristics in SH-SY5Y cells and evaluate their susceptibility to AD-related stressors as a simplified, cost-effective model for preliminary high-throughput AD studies. - Source: PubMed
Publication date: 2026/06/23
Zainuddin Muhammad-SafuanBai Magalingam KasthuriPamidi NarendraAzman Adzzie ShazleenBhuvanendran Saatheeyavaane - Previous studies have reported low circulating brain-derived neurotrophic factor (BDNF) concentrations in patients with coronary artery disease (CAD), but findings have been inconsistent and may be influenced by platelet-related factors. This study evaluated the association between plasma BDNF and CAD in patients undergoing coronary computed tomography angiography (CCTA). - Source: PubMed
Publication date: 2026/06/05
Tachibana TetsuroShiga YuheiMiura-Takahashi ErikaTashiro KoheiTsudome RikuKawahira YutoKuwano TakashiSugihara MakotoImaizumi SatoshiMiura Shin-Ichiro - Brain-derived neurotrophic factor (BDNF), a neurotrophin associated with neuronal survival and plasticity, has emerged as a significant player in cardiovascular biology. This review examines the evidence for BDNF as a regulator of hemostasis and thrombosis, integrating experimental, clinical, and genetic data to clarify its role in platelet function and thrombotic disease. - Source: PubMed
Publication date: 2026/06/11
Aubin CharlotteBlais JessicaPetkova YanitsaLordkipanidzé Marie - This study investigated the effects of intravitreal administration of brain-derived neurotrophic factor (BDNF) on the progression of form-deprivation myopia (FDM) in a guinea pig model and explored the associated molecular mechanisms. - Source: PubMed
Publication date: 2026/05/29
Xie Ruo-YiWang QiLiu HanLuo RuiLiu Chun-YiLi ShiChai YongXiong Fen - This narrative review integrates evidence from nutritional, metabolic, and neuroscientific research to examine whether brain-derived neurotrophic factor (BDNF) may represent a metabolically responsive molecular mediator linking fasting-induced metabolic adaptations with neuroplasticity and systemic metabolic regulation, and to discuss potential neurophysiological and clinical implications. Diet-related metabolic states are increasingly recognized as modulators of cognitive function and brain health. Fasting-based nutritional interventions may influence cognitive and metabolic disorders by promoting metabolic flexibility and engaging neuroplastic mechanisms. Among candidate mediators, BDNF has emerged as a key integrative signal at the intersection of metabolism, stress adaptation, and synaptic plasticity, with pleiotropic functions extending across central and peripheral systems; however, its regulation by fasting and interpretation as a biomarker in humans remains incompletely understood. Relevant experimental and clinical literature was synthesized to examine fasting-induced metabolic adaptations, BDNF regulation, and neuroplastic outcomes. Experimental evidence indicates fasting-related metabolic states engage cellular energy-sensing and stress-resistance pathways and are associated with enhanced neuroplasticity, partly mediated by BDNF-dependent mechanisms. In contrast, human findings remain limited and heterogeneous. Intermittent fasting interventions have been associated with inconsistent changes in circulating BDNF concentrations, influenced by baseline metabolic phenotype, inflammatory status, stress regulation, and methodological factors. Changes in circulating BDNF may reflect broader psychometabolic and inflammatory adaptations rather than direct induction of central neurotrophic signaling. Systems-level correlates of fasting-related metabolic adaptation and BDNF dynamics may be detectable using noninvasive neurophysiological approaches, such as electroencephalography, although direct causal links remain insufficiently established. Evidence positions BDNF as a context-dependent, metabolically responsive molecular bridge linking fasting-induced metabolic adaptations with neuroplastic potential, rather than a unidirectional marker of brain plasticity. Human data suggest fasting-related changes should be interpreted within broader metabolic and stress-related contexts. Well-controlled longitudinal studies integrating metabolic and neurobiological outcomes are needed to assess sustained brain health benefits. - Source: PubMed
Publication date: 2026/06/15
Kapłon KarolinaNapiórkowska-Mastalerz MartaBredelytė AelitaCiastek Barbara