Originally posted by Pepeluacho
If you guys just read the comments on the article, they would clarify that this will lead to treatment for those with nerve damage from injury.
"Neuroscience, is a completely different ballgame..."
I wanted to quote this, as it seems that a lot of people in this thread are a bit confused about what this research is actually saying.
MS is a disease that results of the progressive degeneration of the insulation (called myelin) that surrounds the axons of most of the neurons in our
body. It is a disease of the central nervous system (CNS) and not the peripheral nervous system (PNS), which is what this research was focused on. As
well, regeneration of the myelin sheath I don't think is the same thing as regeneration of the axons. My understanding is that they can occur as two
separate processes.
Along a similar vein and in response to a few other comments, axonal regeneration is *not* the same as regeneration of an entire neuron.
This is a cartoon image of a neuron (found
here):
Axons are elongated structures that radiate out from the cell body and carry electrical signals, usually in the form of action potential, throughout
the body. Damage to these presents obvious problems, since it curbs propagation of nerve impulses to the intended target. The result of this is seen
in a number of diseases as well as in some physical injuries in which feeling and motor control is lost. Regeneration of axons is actually quite
common in a lot of species - typically invertebrates and lower-order vertebrates - but it's much more restricted in our central nervous system (and in
mammals in general) for reasons that are slowly becoming understood.
What this paper has done is demonstrate that there may be some truth to mechanisms for the regeneration of axons put forward by other research.They
achieved this by performing what are called knockdown experiments in fruit fly larvae, which essentially means they made one or both (or neither, in
the case of the control group) copies of the gene encoding the spastin protein non-functional. Following this, they severed peripheral axons (i.e. not
those in the central nervous system), which are more susceptible to injury, and observed the severed axons at various stages.
The results were quite clear: regenerative growth (both proximal and distil) is inhibited both by over expression of the spastin gene and by the loss
of even a single copy of the gene. This is unlike normal axonal outgrowth, which is unaffected by the lack of the spastin gene.
Again, this research, while promising in its own right, will not help sufferers of MS or other types of brain damage like Alzheimer or Parkinson's. It
does shed some light on a disease called hereditary spastic paraplegia (mentioned in the article linked int he OP), for which the most common cause is
mutations in the gene encoding spastin for humans. It may also help with a number of other things involving nerve injury.
Edit: for those interested, the OP's article does provide a link to the actual paper, which is free to download. It's a bit heavy on the jargon, but
worth a read if you're up for it:
Normal Spastin Gene Dosage Is Specifically Required for Axon Regenerationedit on
5-11-2012 by hypervalentiodine because: (no reason given)
) but I could see
it happening. 
