Hi robbie,robbie wrote:Do you think Bob that with RRMS it is eaiser for companies to get better results because of the natural remission of attacks drugs or not.
My internet at home is down for a couple of days so I'm going to do a quick response from work which I hope is worthy of your questions. Obviously researchers have known for a while that permiable bbb, inflammation and lesions are involved in the RRMS process and considering that 85% of the people with MS have RRMS, those symptoms are what the researchers were aiming for when they designed the current drugs.
I think the problem is that the necessary solution would involve understanding the underlying MS disease process and designing treatments aimed at that, but researchers haven't identified the underlying mechanism so they can only direct treatments at secondary effects like the permiable bbb, inflammation and lesions.
Obviously that is like aiming a fire hose at the flames rather than the base of the flames. It does have an obvious effect but will never put out the fire.
Those treatments, which obviously have limited ability to do what they were intended to do and aren't aimed at the right mechanism, were used against other phases of MS with dissapointing results, which caused everyone to jump the gun and assume that there must be something vastly different about SPMS and PPMS.
I can't prove that their isn't something vastly different about SPMS and PPMS as opposed to RRMS but the evidence used to come to the conclusion that SPMS and PPMS are different was faulty on every count.
As far as I'm concerned the issue is back to a clean slate and there is no reason to think SPMS and PPMS wouldn't respond every bit as well to an "effective" treatment aimed at the "correct" mechanism.
With that in mind, there are a lot of people with SPMS and PPMS who are older and have advanced disability and what we are discussing at this point are treatments to stop the disease process. Stopping the disease process isn't going decrease everyone's EDSS. Probably isn't going to decrease MOST people's EDSS. It's not something I like but I think because of the effects of plasticity, older people and people with SPMS and PPMS are the least likely to experience decrease in EDSS after the disease process is stopped.
I hate to leave things this way robbie but my 1/2 lunch has already been an hour long!
Thanks for the post. Threads have a way of wandering off subject which is a good thing for discussion and sharing of ideas. I appreciate the focus, however briefly on the post subject. Interesting article. I have to wonder how a female hormone would react in a male recipient. I would hate to have the biggest cup size in the household.
In the spirit of getting the thread back on track I'm including this abstract I found interesting.
Dr Neil Scolding has always seemed to be a very knowledgeable and level headed researcher. One of my favorites.
Claire Rice1 and Neil Scolding1 Contact Information
(1) Dept. of Neurology, University of Bristol, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, BS16 1LE, UK
Received: 2 November 2006 Accepted: 3 November 2006 Published online: 7 March 2007
Abstract A number of factors more or less unique to multiple sclerosis have suggested that this disease may be particularly amenable to cell-based reparative therapies. The relatively focussed damage to oligodendrocytes and myelin at least in early disease implies that only a single population of cells need be replaced—and that the daunting problem of re-establishing connectivity does not apply. The presence of significant though partial spontaneous myelin repair in multiple sclerosis proves there to be no insurmountable barrier to remyelination intrinsic to the CNS: the therapeutic challenge becomes that of supplementing this spontaneous process, rather than creating repair de novo. Finally, the large body of available knowledge concerning the biology of oligodendrocytes, and the success of experimental myelin repair, have allowed cautious optimism that future prospects for such therapies are not unrealistic. Nonetheless, particular and significant problems are not hard to list: the occurrence of innumerable lesions scattered throughout the CNS, axon loss, astrocytosis, and a continuing inflammatory process, to name but a few. Here we review the progress and the areas where difficulties have yet to be resolved in efforts to develop remyelinating therapies for multiple sclerosis.
It talks of transplants into actual HUMANS! with MS, back in 2002. I seached, but could not find the results.
http://www.sciencedaily.com/releases/20 ... 071547.htm
In this case, I took no news as bad news. I searched google scholar for the Dr's names, and they have published many articles since on rat studies.Second Patient With Multiple Sclerosis Undergoes Groundbreaking Surgery At Yale
Science Daily — New Haven, Conn. A 29-year-old man with multiple sclerosis is the second patient to undergo transplantation surgery at Yale in an effort to repair myelin, the protective brain and spinal cord sheath that is destroyed by the disease, Yale researchers have reported. The surgery took place in two stages March 6-7 and the patient was discharged from Yale-New Haven Hospital March 10. The young man is the second of five patients who are scheduled to participate in the groundbreaking clinical trial.
Vollmer said he and his team hope to perform the procedure on a third patient next month.
The purpose of the Phase One trial is to determine whether cells found in the body's peripheral nerves, in this case, the ankle, can safely repair the damaged cells in the brain and spinal cord that result in neurologic disability in patients with multiple sclerosis and other disorders of myelin.
In the first procedure on March 6, the surgical team harvested Schwann cells from the patient's ankle. Animal studies show that Schwann cells can replace the cells that generate the myelin. The second day, the cells were injected into the left posterior aspect of the patient's brain, which has lesions.
Vollmer said he and his team want to determine whether the Schwann cells survive in the brain and if they are able to restore myelin on the nerve fibers in the brain. The patient's progress is then monitored for six months using neuroimaging and other tests. After six months a small biopsy is taken to determine whether the cells survived and whether they made any myelin.
The six month results on the first patient will not be made public until they are published in a peer-reviewed medical journal.
Vollmer's team includes Jeffrey Kocsis, Dennis Spencer, M.D., Stephen Waxman, M.D., Adam Anderson, John Gore and others. The research is fully funded by The Myelin Project in Washington, D.C.
Thanks Cure.CureOrBust wrote: In this case, I took no news as bad news. I searched google scholar for the Dr's names, and they have published many articles since on rat studies.
I agree with the "no news is good news" but it's odd not hearing any more about it since 2002. Maybe they found that it isn't beneficial??
As expected from previous work, Schwann cell implants survive poorly unless the cells find axons to myelinate, the cells do not migrate significantly from the implantation site, fail to integrate with host oligodendrocytes and astrocytes, and form little myelin when challenged with astrocyte-rich environment in the retina.
Thanks dignan, you're right. Reading that part does stick in my mind but I didn't associate it with less than glowing trial results when I read it the first time.dignan wrote: As expected from previous work, Schwann cell implants survive poorly unless the cells find axons to myelinate, the cells do not migrate significantly from the implantation site, fail to integrate with host oligodendrocytes and astrocytes, and form little myelin when challenged with astrocyte-rich environment in the retina.
I hope we don't forget there are a couple more things that may support myelin repair:
andthyroid hormone enhances and accelerates remyelination in an experimental model of chronic demyelination
Thyroid hormone, when administered during the acute phase of the disease, increases expression of platelet-derived growth factor alpha receptor, restores normal levels of myelin basic protein mRNA and protein, and allows an early and morphologically competent reassembly of myelin sheaths. Moreover, thyroid hormone exerts a neuroprotective effect with respect to axonal pathology.
In addition to its traditional role in reproduction, progesterone (PROG) has demonstrated neuroprotective and promyelinating effects in lesions of the peripheral and central nervous systems, including the spinal cord.
Earlier research :
And, guys, progesterone is not just for women. As you’ll see here (TBI Research)PROG also promotes myelination in the brain, as shown in vitro in explant cultures of cerebellar slices and in vivo in the cerebellar peduncle of aged rats after toxin-induced demyelination.
Local synthesis of PROG in the brain and the neuroprotective and promyelinating effects of this neurosteroid offer interesting therapeutic possibilities for the prevention and treatment of neurodegenerative diseases, for accelerating regenerative processes and for preserving cognitive functions during aging.
Take careBoth ovariectomized female and male animals treated with progesterone showed a profound reduction in axonal injury (seen via diminished APP immunoreactivity) when compared to controls.
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