BDNF
- Known as:
- BDNF
- Catalog number:
- PA1014
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- SDlabs
- Gene target:
- BDNF
Related genes to: BDNF
- 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: BDNF
Related articles to: BDNF
- 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 - Autism spectrum disorder (ASD) is classified as a neurodevelopmental disorder with an increasingly high incidence rate. Increasing awareness, changing diagnostic criteria and social attitudes, as well as financial considerations, will affect the prevalence of diagnosis. The symptoms of ASD vary widely, making it difficult to detect. It represents a spectrum of alterations ranging from mild indications to severe impairments and diagnosis is based on a very rigorous behavioral assessment. Nevertheless, certain neuropathological changes are common, although the background of this disorder remains still unknown. Therefore, some research aimed at better understanding the pathology of the neurological alterations in ASD, as well as the possibilities for early diagnosis and treatment of this disorder, is urgently needed. This review summarizes the current evidence on some selected proteins such as tau protein, NFL, and BDNF as well as IGF-1 that appear to be the best protein candidates for better understanding the causes of autism, as well as for use as fluid biomarkers in the diagnosis and monitoring of ASD. - Source: PubMed
Publication date: 2026/06/03
Rutkowski PiotrRomanowicz AdriannaMroczko JanGudowska-Sawczuk MonikaMroczko Barbara - Adult hippocampal neurogenesis persists throughout the human lifespan, yet declines in Alzheimer's disease and major depression, associated in part with reduced brain-derived neurotrophic factor (BDNF) levels. For rodents, environmental enrichment, dichotomised primarily as physical activity and spatial complexity, robustly promotes adult hippocampal neurogenesis, but no framework has translated these findings to human environments. This review is the first to synthesise evidence across the full translational pathway, arguing that spatial complexity and physically active navigation in neighbourhoods and buildings constitute a humanised form of environmental enrichment. It proposes that standard indoor environments may represent a functionally impoverished condition for the human hippocampus, paralleling standard laboratory caging. An applied model is presented, mapping built environment features onto the neurobiological mechanisms regulating adult hippocampal neurogenesis, with BDNF as the central translatable biomarker linking environmental exposures to neurogenic outcomes. A methodological roadmap for future empirical validation is also outlined. This framework repositions the built environment as a modifiable determinant of adult hippocampal neurogenesis in humans, with implications for mitigating the risk of depression, cognitive impairment, and Alzheimer's disease. - Source: PubMed
Publication date: 2026/05/26
Khalil Mohamed Hesham - Polycystic ovary syndrome (PCOS) in adolescence is characterized by hormonal imbalance, low-grade inflammation, oxidative stress, and metabolic dysfunction. Brain-derived neurotrophic factor (BDNF) regulates energy homeostasis and neuroimmune signaling and may act as a neuroimmunometabolic integrator in PCOS. - Source: PubMed
Publication date: 2026/05/21
Mizgier MałgorzataFormanowicz DorotaSansoni VeronicaJarząbek-Bielecka GrażynaLombardi GiovanniKędzia WitoldOpydo-Szymaczek Justyna