Topic: BDNF

Neurotrophins (NGF, BDNF, NT-3) are endogenous growth factors that exert neuroprotective effects by preventing neuronal death and promoting neurogenesis. They act by binding to their respective high-affinity, pro-survival receptors TrkA, TrkB or TrkC, as well as to p75NTR death receptor. While these molecules have been shown to significantly slow or prevent neurodegeneration, their reduced bioavailability and inability to penetrate the blood-brain-barrier limit their use as potential therapeutics. To bypass these limitations, our research team has developed and patented small-sized, lipophilic

In the central nervous system, neuronal activity is a critical regulator of development and plasticity. Activity-dependent proliferation of healthy glial progenitors, oligodendrocyte precursor cells (OPCs), and the consequent generation of new oligodendrocytes contributes to adaptive myelination. This plasticity of myelin tunes neural circuit function and contributes to healthy cognition. The robust mitogenic effect of neuronal activity on normal oligodendroglial precursor cells, a putative cellular origin for many forms of glioma, suggests that dysregulated or “hijacked” mechanisms of myelin

Pediatric high-grade gliomas (pHGG) are a devastating group of diseases that urgently require novel therapeutic options. We have previously demonstrated that pHGGs directly synapse onto neurons and the subsequent tumor cell depolarization, mediated by calcium-permeable AMPA channels, promotes their proliferation. The regulatory mechanisms governing these postsynaptic connections are unknown. Here, we investigated the role of BDNF-TrkB signaling in modulating the plasticity of the malignant synapse. BDNF ligand activation of its canonical receptor, TrkB (which is encoded for by the gene NTRK2),

Neuronal plasticity has for a long time been considered important for the recovery from depression and for the antidepressant drug action, but how the drug action is translated to plasticity has remained unclear. Brain-derived neurotrophic factor (BDNF) and its receptor TRKB are critical regulators of neuronal plasticity and have been implicated in the antidepressant action. We have recently found that many, if not all, different antidepressants, including serotonin selective SSRIs, tricyclic as well as fast-acting ketamine, directly bind to TRKB, thereby promoting TRKB translocation to synapt

The synapse is the core component of the nervous system and synapse formation is the critical step in the assembly of neuronal circuits. The assembly and maturation of synapses requires the contribution of secreted and membrane-associated proteins, with neuronal activity playing crucial roles in regulating synaptic strength, neuronal membrane properties, and neural circuit refinement. The molecular mechanisms of synapse assembly and refinement have been so far largely examined on a gene-by-gene basis and with a perspective fully centered on neuronal cells. However, in the last years, the invol

The functioning of a synapse depends on its accessibility to proteins and, thus, on the localization of protein sources along the dendrite (Westenbroek 2009, Vacher et al. 2008). Therefore, the behaviour of the synapse highly depends on the availability of proteins and ion channels and any perturbation in the localization and availability of these components would lead to a dysfunction of the synapse. Hence, understanding the localization and distribution of ion channels and proteins in the dendrite in relation to the synapse is crucial. Using super-resolution microscopy, Helm et al., 2021 der

Aims: Psychiatric morbidity and functional limitations are widespread in patients with thermal skin injury. Hyperbaric oxygen therapy (HBO) and antioxidant supplementation have been adjunctive therapy to promote wound healing. We evaluated the effects of HBO (100% O2 at 2.5 ATA for 60 minutes) and the antioxidant supplementation – Filipendula ulmaria (FU) extract (100 mg/kg b.w.), individually, in the treatment of anxiety-like behavior that occurs along the thermal skin injury in rat for seven days. Methods: Anxiety level estimation was performed in the open field and the elevated plus maze te

Parkinson’s Disease (PD) is a neurodegenerative disorder associated with the loss of dopaminergic neurons in the nigrostriatal circuit, and the development of motor and non-motor symptoms. Currently, no disease-modifying pharmacological treatments are available, and dopamine-based therapies help to mitigate symptoms but also cause side-effects. In this context, indirect evidence has suggested that activation of metabotropic Glutamate Receptor 3 (mGluR3) exerts neuroprotective effects in animal models of PD. However, the lack of selective agonists/ligands for this receptor has hindered more in-