TrkB x TrkA x p75NTR x BDNF

Last update 08 May 2025

Basic Info

Related Targets

TrkBTrkAp75NTR[+1]

Drugs associated with TrkB x TrkA x p75NTR x BDNF

AC-25793

Target

BDNF x TrkA x TrkB x p75NTR

Mechanism

BDNF modulators [+3]

Active Org.

AlzeCure Pharma AB [+1]

Originator Org.

AlzeCure Pharma AB

Active Indication

Alzheimer Disease

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TrkB x TrkA x p75NTR x BDNF

100 Translational Medicine associated with TrkB x TrkA x p75NTR x BDNF

0 Patents (Medical) associated with TrkB x TrkA x p75NTR x BDNF

Literatures (Medical) associated with TrkB x TrkA x p75NTR x BDNF

01 Jun 2025·Neurochemical Research

Alpha-Pinene Ameliorates Memory Deficits in 3-Nitropropionic Acid-Induced Rat Model of Huntington’s Disease

Article

Author: Hassanzadeh, Katayoun ; Rahmani, Helia ; Hashemi, Paria ; Moloudi, Mohammad Raman ; Vahabzadeh, Zakaria ; Izadpanah, Esmael

Memory impairment is one of the cognitive symptoms in Huntington's disease (HD) which appears before motor dysfunction in patients. Various molecular mechanisms, including disruptions in neurotrophins levels, are involved in the occurrence of memory problems in HD. Alpha-pinene (APN), a member of the monoterpene family, exhibited beneficial effects in animal models of neurodegenerative disorders. As a result, this study assessed the impact of APN on memory in the 3-nitropropionic acid (3-NP) induced model of HD in rats. Male Wistar rats received saline, 3-NP to model HD, or APN (1, 5, or 10 mg/kg) plus 3-NP for 21 days to assess APN's effects. Working and spatial memory were examined by the Y-maze and Morris-water-maze (MWM) tests. The mRNA levels of neurotrophins and their receptors in the brain cortex and hippocampus of the rats were quantitatively assessed through Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) analysis. The results showed that APN, at all three doses, significantly prevented the disease phenotype induced by 3-NP administration. In addition, APN treatment elevated the gene expression levels of BDNF, TrkA, TrkB, and CREB, while significantly decreasing P75 NTR showing a dose-dependent effect in the brain cortex and hippocampus, compared to the 3-NP group. These findings suggest that APN alleviates 3-NP-induced memory deficits by enhancing neurotrophins and their receptor levels in an animal model of HD.

01 Mar 2025·Journal of Biochemical and Molecular Toxicology

Insulin Receptor Regulates Neurotrophin and Neurotrophin Receptor Expression in the Differentiation of Neural Stem Cells: In Vitro Study

Article

Author: Langhnoja, Jaldeep ; Buch, Lipi ; Chruvattil, Ragitha ; Pillai, Prakash ; Gupta, Sarita

ABSTRACTAdult Neural stem cells (NSCs)/Neural Progenitor cells (NPCs) are known to play an important role in creating new neurons and glial cells. The self‐renewal, multipotent abilities of NSCs are attributed to several of cell‐intrinsic and extrinsic factors. Insulin is an important neuromodulator, particularly influencing neural survival, memory, and energy homeostasis. Insulin receptor is expressed in the adult NSC niche and also induces neurogenesis and gliogenesis and may be affected by neurotrophins. Neurotrophins have been demonstrated to play an active role in NSC differentiation into neurons and glial cells. Nerve growth factor (NGF) and brain‐derived neurotrophic factor (BDNF), both have significant roles in hippocampal plasticity and long‐term potentiation events. However, the crosstalk between insulin and neurotrophic signaling pathways is still unclear and requires studies to understand brain development in insulin resistance conditions. Preliminary data from the current study suggest that insulin receptor is involved in regulating the transcript levels of neurotrophins (NGF, BDNF) and Trk receptors (TrkA, TrkB and p75NTR). It is also able to regulate the secretion of BDNF by neural stem cells. In addition, the data from the present study also reveal insulin receptor knockdown significantly altered the expression levels of key early brain cell type development markers such as PDGFR‐α, GFAP, and Tuj1, which further confirms the essential role of crosstalk between insulin receptor and neurotrophins in brain development in regard to neural stem cell differentiation.

01 Jul 2024·Histology and histopathology

Differential roles of serotonin receptor subtypes in regulation of neurotrophin receptor expression and intestinal hypernociception.

Article

Author: Wu, Ming-Shiang ; Tu, Chia-Hung ; Lin, Li-Yu ; Hsin, Ling-Wei ; Hsieh, Yu-Ting ; Yu, Linda Chia-Hui ; She, Meng-Ping

OBJECTIVESAberrant serotonin (5-hydroxytryptamine, 5-HT) metabolism and neurite outgrowth were associated with abdominal pain in irritable bowel syndrome (IBS). We previously demonstrated that 5-HT receptor subtype 7 (5-HT₇) was involved in visceral hypersensitivity of IBS-like mouse models. The aim was to compare the analgesic effects of a novel 5-HT₇ antagonist to reference standards in mouse models and investigate the mechanisms of 5-HT₇-dependent neuroplasticity.METHODSTwo mouse models, including Giardia post-infection combined with water avoidance stress (GW) and post-resolution of trinitrobenzene sulfonic acid-induced colitis (PT) were used. Mice were orally administered CYY1005 (CYY, a novel 5-HT₇ antagonist), alosetron (ALN, a 5-HT₃ antagonist), and loperamide (LPM, an opioid receptor agonist) prior to measurement of visceromotor responses (VMR). Levels of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin receptors (NTRs) were assessed.RESULTSPeroral CYY was more potent than ALN or LPM in reducing VMR values in GW and PT mice. Increased mucosal 5-HT₇-expressing nerve fibers were associated with elevated Gap43 levels in the mouse colon. We observed higher colonic Ntrk2 and Ngfr expression in GW mice, and increased Bdnf expression in PT mice compared with control mice. Human SH-SY5Y cells stimulated with mouse colonic supernatant or exogenous serotonin exhibited longer nerve fibers, which CYY dose-dependently inhibited. Serotonin increased Ntrk1 and Ngfr expression via 5-HT₇ but not 5-HT₃ or 5-HT₄, while Ntrk2 upregulation was dependent on all three 5-HT receptor subtypes.CONCLUSIONSStronger analgesic effects by peroral CYY were observed compared with reference standards in two IBS-like mouse models. The 5-HT₇-dependent NTR upregulation and neurite elongation may be involved in intestinal hypernociception.

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