Ask about this productRelated genes to: BDNF protein
- 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 protein
Related articles to: BDNF protein
- Chronic unpredictable mild stress (CUMS) is a validated model of anxiety- and depression-like disorders and is associated with impaired neuroplasticity. Dysregulation of the plasminogen activator system, particularly elevated plasminogen activator inhibitor-1 (PAI-1), may disrupt tissue plasminogen activator (tPA)-dependent brain-derived neurotrophic factor (BDNF) signaling and contribute to stress-induced behavioral deficits. However, the therapeutic relevance of PAI-1 inhibition in mood disorders remains poorly defined. - Source: PubMed
Publication date: 2026/05/22
Bahi AmineDreyer Jean-Luc - To investigate the role of cardiomyocyte-derived BDNF as an endogenous regulator to decrease cardiac fibrosis, its underlying mechanism and therapeutic potential. - Source: PubMed
Publication date: 2026/04/28
Zhu YuRan YuanfeiFu TingtingZheng XinChen YanjunLiang ChunbaoLi YanmeiHuang RuijinZhao HuiPan XiudiYuan ZiqiangPu QinZeng ZhaohuaFeng ShanshanQi XufengLv LuochengZhan LixuanChen YilinCai Dongqing - Fibromyalgia, a syndrome characterized by hyperalgesia and 'negative emotionality', and major depressive disorder (MDD) demonstrate substantial overlaps in clinical, neurobiological, and therapeutic domains. Currently, treatment options for fibromyalgia remain limited; however, the epidemiology of this syndrome continues to grow worldwide. The use of animal models is indispensable for developing new treatment strategies for fibromyalgia. Meanwhile, the choice of animal paradigms is limited. Here, we used the ultrasound exposure of emotional stress on CBA, BALB/c, and C57BL/6 mouse strains to model this condition and to identify new molecular targets of fibromyalgia treatment. We exposed young male mice of three common strains to a three-week ultrasound stress (US) comprising emotionally negative and neutral frequencies of 20-25 kHz and 25-45 kHz, resulting in the development of altered pain sensitivity and signs of 'negative emotionality'. Specifically, mice were studied for timid-like/aggressive behaviors and the tail flick response. Serum levels of corticosterone, cortisol, β-Endorphin, and brain-derived neurotrophic factor (BDNF), as well as brain gene expression of interleukin-33 (), , and its receptor were investigated. Among the stressed mouse strains, C57BL/6 mice displayed augmented pain sensitivity, allodynia, and suppressed dominant behavior, whereas CBA and BALB/c mice demonstrated opposing changes. Glucocorticoid levels were increased in all stressed groups. Stressed C57BL/6 mice showed downregulated gene and protein expression of functionally inter-related BDNF and IL-33 molecules in the hippocampus, amygdala, and striatum, significantly correlating with behavioral outcomes, as well as lowered blood levels of β-Endorphin and elevated cortisol concentrations. Altogether, our study identified the BDNF/IL-33 regulatory pathway as a molecular correlate of fibromyalgia, and the use of US-exposed young C57BL/6 mice as a potential model that recapitulates this syndrome. - Source: PubMed
Publication date: 2026/04/30
Schroeter Careen APavlov DmitriiMunter Johannes P M deUmriukhin AlexeiCespuglio RaymondKuznetsova MariaDeykin Alexey VAskarova SholpanSicker MichaelGorlova AnnaStrekalova Tatyana - Acute coronary syndromes (ACS) remain time-critical clinical emergencies in which early diagnosis and accurate risk stratification determine management and outcomes. Although symptoms, electrocardiography, and high-sensitivity cardiac troponin (hs-cTn) provide a reliable framework for detecting myocardial injury, they offer limited insight into plaque instability, thromboinflammatory activity, vascular repair, and post-infarction remodeling. In this narrative review, we examine the biological rationale and current clinical evidence supporting brain-derived neurotrophic factor (BDNF) as a candidate biomarker in ACS, with particular attention to pre-analytical, analytical, and phenotypic sources of heterogeneity. Available studies show that circulating BDNF concentrations vary substantially according to biological matrix, timing of sampling, ACS subtype, and assay methodology, which likely contributes to inconsistent findings across cohorts. Overall, current evidence does not support BDNF as a diagnostic alternative to hs-cTn in rule-in or rule-out pathways. However, BDNF may have value in biological phenotyping and risk stratification by reflecting platelet activation, endothelial dysfunction, inflammatory signaling, and remodeling processes after ACS. Further progress will require standardized pre-analytical procedures, separate assessment of mature BDNF and proBDNF, serial sampling, and validation in large multicenter studies. - Source: PubMed
Publication date: 2026/04/25
Pruc MichalLopucki RafalCzarnek KatarzynaÇolak ŞahinMaslyk MaciejNiewiadomska IwonaUminska JuliaMamcarz ArturKubica JacekSzarpak Lukasz - Traumatic brain injury (TBI) initiates secondary injury cascades that can reduce brain-derived neurotrophic factor (BDNF), a key mediator of synaptic plasticity and repair. Erythropoietin (EPO) has nonhematopoietic neuroprotective effects and may upregulate BDNF, while serum BDNF is a feasible translational pharmacodynamic biomarker. The aim of this study was to evaluate whether repeated intraperitoneal EPO administration increased serum BDNF levels on post-injury day 7 in Wistar rats with experimental TBI. - Source: PubMed
Publication date: 2026/04/24
Hasan HasanSuryaningtyas WihastoParenrengi Muhammad ArifinWungu Citrawati Dyah Kencono