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This sounds like a fantastic advancement. I don't think it'll help us much in MS because in MS, axons are not severed, so there's nothing to relink. Wallerian degeneration starts at the end of the axon and degenerates inward toward the neuron.

Cece wrote:I don't think it'll help us much in MS because in MS, axons are not severed, so there's nothing to relink.

I don't think that's correct. Axonal damage is characteristic of MS.

See this: Acute axonal damage in multiple sclerosis

--Tracy

I don't know why but the link wouldn't open for me. Axonal damage such as wallerian degeneration is present in MS. You are suggesting that axons are severed in MS? This advancement is specifically a way to get a severed axon to reattach to the neuron body. Typically a severed axon shrivels up and dies, and a new one must be regrown. As I understand it the problem in MS is not that the axons are severed, but that they are damaged. There is not a perfectly healthy axon that needs to be reattached, there is a half dead axon that is attached but not getting the nutrients including oxygen that it needs or that is suffering damage from leukocyte attack.

Cece wrote:You are suggesting that axons are severed in MS? This advancement is specifically a way to get a severed axon to reattach to the neuron body.

I jumped to the conclusion that your original post was stating axonal damage is not an important factor in MS, hence the link I added. I agree that the type of axonal damage that occurs with MS may not benefit directly from the recent accomplishment of repair of severed nerves.

From Oxford Brain Journal wrote:In recent years, it has become more evident that axonal damage is the major morphological substrate of permanent clinical disability. In our study, we investigated the occurrence of acute axonal damage determined by immunocytochemistry for amyloid precursor protein (APP) which is produced in neurones and accumulates at sites of recent axon transection or damage.

--Tracy

http://www.nejm.org/doi/full/10.1056/NE ... 1293380502

Transected axons were a consistent feature of the lesions of multiple sclerosis, and their frequency was related to the degree of inflammation within the lesion. The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appearing white matter from the control brains.

I stand corrected!

Axonal transection occurs at sites of inflammation and begins at disease onset but is clinically silent in RR-MS because the CNS compensates for neuronal loss. Once a threshold of axon loss is ex ceeded, MS patients enter an irreversible secondary progressive stage. In SP-MS, axonal degeneration is caused by chronic demyelination and may be irreversibly progressive. This view of MS provides a concep tional framework that explains conversion of RR-MS to SP-MS and provides a rationale for early aggressive anti-inflammatory and neuroprotective therapies.

http://nro.sagepub.com/content/5/1/48.abstract
So axonal transection means the same as severing of the axon.
Now I have to reread the link dania posted. Would there be a possible solution to ongoing axonal severing such as this, or would it only be practical in one-time traumatic instances of axonal severing, such as spinal cord accidents? Would the presence of inflammation interfere with reconnection of the severed axons?

I don't know, but I thought my 'black holes' or hypointense areas on my MRI, were dead areas (no water in dead cells). I thought that was probably due to nerve death. To me the thing that was singular about them was that they were very round, compared to the hyperintense lesions, the perivenous ones. They seemed to have a more well-defined 'sharper' edge. They made my brain look like a sponge-cake. That was one reason I thought it must be caused by a germ of some kind, but what do I know?