As I said in a different thread, there is so much reason to have hope. CCSVI is a major break-through, speaking from my experience and my understanding of it. Why not another major break-through, this time in the understanding of remyelination and axonal repair, for those who have sustained damage to the neurons from MS and CCSVI. We're not there yet but it could be coming.Normally neurons cannot regenerate damaged axons because of the presence of myelin, a substance that surrounds the axons, but the degradation-resistant "super" Id protein was able to promote axon growth even in the presence of myelin.
Dr. Iavarone added that there is no chance that such a therapy would cause cancer in the brain or spinal cord. "Neurons have completely lost the ability to create new cells so there's no danger of creating a tumor. The only growth they're capable of is regeneration of their axons," he said.
- Family Elder
- Posts: 3746
- Joined: Wed Mar 17, 2010 3:00 pm
- Location: Kanata, Ontario, Canada
I changed the name to 'axonal repair.'1eye wrote:This thread is misnamed. It is peripherally about myelin, but it is more about the regrowth of axons. Useful, I would guess, in things like spinal cord injury.
In MS the axons and gray matter are damaged early in the disease process (or maybe, same point in time, it's late in the disease process of congenital CCSVI). It's not a severing of the axons, but the Wallerian degeneration starting from the farthest end of the axon. Even in areas of normal appearing white matter.
Nature. 2006 Jul 27;442(7101):471-4. Epub 2006 Jun 28.
Degradation of Id2 by the anaphase-promoting complex couples cell cycle exit and axonal growth.
Lasorella A, Stegmüller J, Guardavaccaro D, Liu G, Carro MS, Rothschild G, de la Torre-Ubieta L, Pagano M, Bonni A, Iavarone A.
SourceInstitute for Cancer Genetics, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.
In the developing nervous system, Id2 (inhibitor of DNA binding 2, also known as inhibitor of differentiation 2) enhances cell proliferation, promotes tumour progression and inhibits the activity of neurogenic basic helix-loop-helix (bHLH) transcription factors. The anaphase promoting complex/cyclosome and its activator Cdh1 (APC/C(Cdh1)) restrains axonal growth but the targets of APC/C(Cdh1) in neurons are unknown. Id2 and other members of the Id family are very unstable proteins that are eliminated as cells enter the quiescent state, but how they are targeted for degradation has remained elusive. Here we show that Id2 interacts with the core subunits of APC/C and Cdh1 in primary neurons. APC/C(Cdh1) targets Id2 for degradation through a destruction box motif (D box) that is conserved in Id1 and Id4. Depletion of Cdh1 stabilizes Id proteins in neurons, whereas Id2 D-box mutants are impaired for Cdh1 binding and remain stable in cells that exit from the cell cycle and contain active APC/C(Cdh1). Mutants of the Id2 D box enhance axonal growth in cerebellar granule neurons in vitro and in the context of the cerebellar cortex, and overcome the myelin inhibitory signals for growth. Conversely, activation of bHLH transcription factors induces a cluster of genes with potent axonal inhibitory functions including the gene coding for the Nogo receptor, a key transducer of myelin inhibition. Degradation of Id2 in neurons permits the accumulation of the Nogo receptor, thereby linking APC/C(Cdh1) activity with bHLH target genes for the inhibition of axonal growth. These findings indicate that deregulated Id activity might be useful to reprogramme quiescent neurons into the axonal growth mode
- Similar Topics
- Last post