Aaron Boster

So just a little bit of like neuroanatomy type stuff.

We have different cells that provide myelin in the central compartment compared to in the periphery.

So in the central compartment, we myelinate the central nervous system nerves with oligodendrocytes.

And in the peripheral nervous system, we don't use oligodendrocytes.

We use these Schwann cells, these other cells.

And the demyelination and axonal damage that you see in the setting of multiple sclerosis is limited to the central nervous system.

So brain, spinal cord, optic nerves.

There are different autoimmune conditions like Guillain-Barre or AIDP, CIDP, which can cause demyelination of the peripheral nerves.

Mm-hmm.

And what's interesting is even though they sound rather similar in neurology, when we subdivide into like our little areas, it's on the other side of the nervous system.

So the guys and gals that manage autoimmune peripheral demyelination and I, we never talk.

You can use an immunosuppressant to treat any autoimmune condition because you can dampen the immune response.

But when you get into the details in some of the more targeted therapies, they're rather specific for multiple sclerosis.

Now, the question of why?

Well, the thought is, and there's actually a really cool study that I recently looked at, when you develop EBV, mono, and you make an antibody which binds to one of the proteins on mono,

that same antibody identifies one of the proteins on oligodendrocyte myelin.

And so that's that cross-reactivity that we were talking about.

So it's rather specific, we believe.

Now, you also touched on arguably one of the holy grails of MS therapies, which is remyelination.

So demyelination is when you strip the plastic coating off the wire.