Anavex Life Sciences Corp (AVXL)

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No, Multiple Sclerosis Is Not At Synapses

seems like its more like replacing a damaged female or male end of an electrical cord, to allow electrical current to run through the cord (again).

The location of multiple sclerosis pathologies is not at the nerve ends, it's along the nerve itself.

Nerve ends, of course, are the synapses, where two nerve cells connect, across which the nerve impulse must "jump," with a neurotransmitter.

That's how the existing Alzheimer's drugs work. Most of them (at least three) are acetylcholinesterase inhibitors. Acetylcholinesterase is a naturally-occurring enzyme that disables acetylcholine, an essential neurotransmitter that carries the nerve impulse across the tiny synapse gap between neurons along the nerve itself.

If acetylcholinesterase concentrates in the synapse, it destroys the acetylcholine neurotransmitter and nerve message transmission is inhibited.

In Alzheimer's, waste proteins, beta-amyloid plaques and tau tangles, can allow (among other pathologies) for the accumulation of acetylcholinesterase enzymes. The Alzheimer's drugs inhibit the production of the nerve message-disrupting proteins.

But only for a period, and never very completely. Eventually, nerve transmissions are again disrupted and the lethal course of Alzheimer's resumes.

Of course, as related previously, Anavex 2-73 works (against Alzheimer's) very differently, by restoring normal internal neuron cell processes and functions.