Anavex Life Sciences Corp (AVXL)

[falconer66a]

Brain, Spinal Cord Similar, Same Sorts of Neurons

Is the brain composition different than nerves or are they close in their structure and composition?

Medical people will take great issue with my title, as there are numerous neuron types in the central nervous system, in the brain and spinal cord.

But regarding the neuron demyelination of multiple sclerosis, where the immune system mistakenly attacks and destroys the signal-insulating myelin sheath that surrounds all signal-sending neurons throughout the body, the neurons are effectively the same. They all have the insulating myelin sheaths. When those break down or are destroyed, electro-chemical nerve signals are weakened or lost, exactly similar to slicing off the rubber coating of electrical wires. Without those, electricity grounds out, leaking away from the current-carrying wire. Without an intact myelin sheath, nerve signals get lost; the primary pathology of multiple sclerosis.

Remyelination of a naked neuron is not a merely physical process (as would be wrapping some electrical type around an exposed electrical cord). A bit more complex. The new myelin sheath must be properly formed and connected to underlying nerve. Not as simple as physically wrapping some tape around a wire.

In honesty, I do not know the exact chemistry of remyelination (if anyone actually does — may involve some microchemical unknowns). And I can offer no precise explanations of how Anavex 2-73 causes or induces remyelination. I don’t see that the molecule would directly attach to the naked neuron and chemically bind dissolved or free-floating myelin to the neuron. I think Anavex 2-73 works further “upstream,” inducing the neuron to make proper enzymes that control sheath-making reactions. And the aberrant immune system must be turned off or turned away, to prohibit continued demyelination.

Practically, a precise understanding of how Anavex 2-73 causes remyelination and/or prevents demyelination is not needed for the drug to be approved and used by multiple sclerosis patients. It just needs to be approved for such by the FDA, and they will do that when they see solid clinical evidence of sustained or restored neuromuscular control by multiple sclerosis patients in a well-designed clinical trial.

The precise chemistry of how all of that happens is merely an intellectual question for academics. The exact mechanism of action is not required to be discovered to gain FDA approval; merely that the drug is safe and yields better symptomatic outcomes than any existing drug.