Mouse BDNF ELISA Kit
- Known as:
- Mouse BDNF Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- EK007
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- Olaf Pharmaceuticals
- Gene target:
- Mouse BDNF ELISA Kit
Related genes to: Mouse BDNF ELISA Kit
- 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: Mouse BDNF ELISA Kit
Related articles to: Mouse BDNF ELISA Kit
- A converging mechanistic theme across mental disorders involves impaired neuroplasticity and reduced brain-derived neurotrophic factor (BDNF). Glucagon-like peptide-1 receptor agonists (GLP-1RAs), used for type 2 diabetes and obesity, have shown neuroprotective potential, but whether these effects are mediated by BDNF is unclear. - Source: PubMed
Publication date: 2026/01/29
Xu TianyiZheng Yang JingWong SabrinaDri Christine EZhou Xin TongTeopiz Kayla MLe Gia HanMcIntyre Roger S - Depressive disorders often show recurrent courses that cannot be sufficiently prevented by existing therapeutic protocols. In other affective disorders, recurrence has been linked to three mechanisms -spontaneous recovery, accelerated new/relearning, and reinstatement- which are related to the preservation of disorder-related memory traces even through successful extinction-based interventions. Reconsolidation-interference protocols aim to directly alter such traces by reactivating and destabilizing them before intervention. While this approach has shown benefits in fear, craving, and trauma-related symptoms, its application to depression remains untested. To our knowledge, this study provides the first experimental evidence of its utility in depression-like states. Sixty participants took part in a three-day, three-group, double-blind randomized controlled trial. On day one, helplessness was induced using a modified unsolvable anagram task. On day two, participants were randomized into three groups undergoing different interventions while completing another cognitive demanding task: (1) extinction, where participants experienced success from start to finish; (2) reconsolidation, where participants briefly reexperienced failure before succeeding; or (3) reactivation, where failure repeated. On day three, the helplessness task was presented again to evaluate susceptibility for recurrence across conditions. Behavioral, self-report, and EEG data were collected. Across test days, participants showed reduced motivation and performance, attributing failure to personal ability, confirming successful helplessness induction. However, interventions at day two produced no robust group differences on behavioral, self-report, or EEG measures. Exploratory analyses suggested that brain-derived neurotrophic factor (BDNF) levels may have mediated outcomes. Findings do not confirm reconsolidation-based behavioral interference as effective for depression-like helplessness. Nonetheless, exploratory results highlight BDNF as a potential mediator, warranting further study on its role in postretrieval extinction effects in depression. - Source: PubMed
Forster AndréRodrigues JohannesSperlich BillyHewig Johannes - This study investigated whether employment status moderates associations between baseline serum biomarkers and antidepressant remission at 12 weeks and 12 months. - Source: PubMed
Publication date: 2026/01/09
Kim Jae-MinKang Hee-JuKim Ju-WanJhon MinLee Ju-YeonKim Sung-WanShin Il-Seon - DNA double-strand break repair has emerged as a vital pathway to repair DNA damage seriously related to the risk of colorectal cancer (CRC). - Source: PubMed
Publication date: 2026/01/19
Liu DaxuFan ZhijunZhang TengLi XiaoxiaMing CuiWu JiahangLu XiaoboSun Deyu - In this study, the neurorehabilitation potential of combined and isolated intermittent hypercapnia and hypoxia exposure was evaluated following photochemically induced cerebral thrombosis in rats. Particular attention was given to the roles of possible neuroplasticity mechanisms mediated by VEGF and BDNF, as well as the potential of hypercapnic-hypoxic interventions to synergistically amplify the therapeutic effects of pharmacological neuroprotectants during recovery. A total of 50 male Wistar rats were randomly assigned to five equal groups ( = 10 per group), each undergoing a course of respiratory interventions lasting 30 min per day for 15 sessions. The groups included (1) a normobaric hypoxia (PO ≈ 90 mmHg) group, (2) a permissive hypercapnia (PCO ≈ 50 mmHg) group, (3) a combined hypercapnic hypoxia (PO ≈ 90 mmHg, PCO ≈ 50 mmHg) group, (4) a control group, and (5) a sham-operated group. Following the rehabilitation protocol, animals exposed to hypercapnic hypoxia exhibited a two-fold reduction in stroke volume compared with controls, significant improvement in motor coordination (as assessed via the rotarod test), and marked upregulation of VEGF and BDNF expression within the ischemic brain region. Notably, only the HH group showed a decrease in serum neuron-specific enolase (NSE) levels. These findings indicate that hypercapnic hypoxia exerts a possible neurorehabilitative effect after focal ischemic injury, superior to that of isolated hypoxia or hypercapnia. Possible mechanisms underlying this outcome may involve activation of neurotrophic (BDNF) and angiogenic (VEGF) signaling pathways. - Source: PubMed
Publication date: 2025/12/13
Tregub Pavel PChekulaev Pavel AZembatov Georgy MNamiot Eugenia DIgnatyuk Michael AAtiakshin Dmitrii ABerdnikov Arseniy KManasova Zaripat ShLitvitskiy Peter FKulikov Vladimir P