I contacted them about volunteering for Phase 1. I got no response.You/us should wait for this Phase 1 to pop up. They will be looking for healthy
volunteers for the Phase 1.
I contacted them about volunteering for Phase 1. I got no response.You/us should wait for this Phase 1 to pop up. They will be looking for healthy
volunteers for the Phase 1.
It doesn't matter. I love proactivity, my friend!I contacted them about volunteering for Phase 1. I got no response.
You clearly took it too far. Reaching out to personal email addresses, Facebook profiles, and Whatsapp is going into the stalking territory.I tried to reach out to the CEOs of Axonis, a married couple originally from Poland. I sent them emails to their personal addresses, reached out to them on Facebook, and even sent one of them a message on WhatsApp.
10-15 years timeI believe this will be a go-to treatment for tinnitus when it comes out in 10-15 years, but to make sure, let's wait until Axonis announces its trials if they ever do, and see if anyone reports improvements in their tinnitus levels.
It's not worth worrying about. By then, several treatments will be available. There will probably be 2-3 treatments and at least 1 objective test by 2028-2029.believe this will be a go-to treatment for tinnitus when it comes out in 10-15 years,
Looking at their website, they've listed 25 potential disorders that their KCC2 development might address, but no mention of tinnitusI believe this will be a go-to treatment for tinnitus when it comes out in 10-15 years, but to make sure, let's wait until Axonis announces its trials if they ever do, and see if anyone reports improvements in their tinnitus levels.
→ Activation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2Abstract said:In healthy adults, activation of γ-aminobutyric acid (GABA)A and glycine receptors inhibits neurons as a result of low intracellular chloride concentration ([Cl–]i), which is maintained by the potassium-chloride cotransporter KCC2. A reduction of KCC2 expression or function is implicated in the pathogenesis of several neurological disorders, including spasticity and chronic pain following spinal cord injury (SCI). Given the critical role of KCC2 in regulating the strength and robustness of inhibition, identifying tools that may increase KCC2 function and, hence, restore endogenous inhibition in pathological conditions is of particular importance. We show that activation of 5-hydroxytryptamine (5-HT) type 2A receptors to serotonin hyperpolarizes the reversal potential of inhibitory postsynaptic potentials (IPSPs), EIPSP, in spinal motoneurons, increases the cell membrane expression of KCC2 and both restores endogenous inhibition and reduces spasticity after SCI in rats. Up-regulation of KCC2 function by targeting 5-HT2A receptors, therefore, has therapeutic potential in the treatment of neurological disorders involving altered chloride homeostasis. However, these receptors have been implicated in several psychiatric disorders, and their effects on pain processing are controversial, highlighting the need to further investigate the potential systemic effects of specific 5-HT2AR agonists, such as (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl)methylamine hydrobromide (TCB-2).
The picture down below is from the OV350 website, presenting what is written above.These studies suggest that the mechanisms of GABAergic homeostatic plasticity involve not only the secretion of GABA or the GABA receptors, but also the KCC2, which eventually "decides" if GABA is inhibitory or excitatory.