Algernon Pharmaceuticals Inc (AGNPF)

[medchem]

Furthermore, for those interested in the science:

Coronavirus infection induces increased production of proinflammatory cytokines and neuronal degeneration as a consequence of glutamate excitotoxicity. In physiological conditions, glutamate is mainly synthesized by neurons and released in the synaptic cleft as the primary excitatory neurotransmitter of the CNS that activates the ligand-dependant receptor AMPAr, which allows the entry of sodium ions and the passage of the nerve impulse in the post-synaptic neuron, leading to activation of the NMDA receptor (N-methyl-D-aspartate receptor) that allows the entry of calcium ions. During infection of neurons by coronavirus, microglial cells detect the presence of virus and produce pro-inflammatory cytokines (TNF-alpha, IL-1 beta and IL-6) that down-regulate the astrocytic receptor GLT-1 (glutamate transporter 1) and prevent the efficient recapture of glutamate. This situation disturbs the regulation of glutamate homeostasis and theexcess of this neurotransmitter in the synaptic cleft leads to excitotoxicity associated with a massive entry of calcium which eventually leads to degeneration of and death of neuronal cells.

This is why NMDA ANTAGONIST IFENPRODIL is going to be helpful for saving neurons!