What is the next breakthrough drug in MS? #ShiftMS #MSBlog #ClinicSpeak
“The following is the next MS Report as part of our collaboration with Shift.ms. The topic addresses the issue of new drugs to treat MS.”
CoI: this work has been generously funded by the Wellcome Trust, Thank You.
Congratulations on these video clips – they are really good.Question – even if more effective drugs for progressive MS are found and eventually get approved, how can the problem of not getting diagnosed until years after MS onset (and much damage and disability is already present) be dealt with? This video contains positive words from Prof G, but it's a bit hard when you are already EDSS 3 at time of diagnosis (and 2 years later still getting worse – crutches not yet required but it's a struggle to walk more than 100-150 metres)
Re: drugs are started to late to have an impact on progressive disease. If brain atrophy is present even before first symptoms appear how can therapy be initiated? Once the first, full blown attack occurs the "horse is out of the barn". Closing the door with anti-inflammatories will not prevent atrophy. An example is the trial with Natalizumab in progressive disease. Brain atrophy was not affected. Do the DMTs slow down brain volume loss? We know they reduce lesion load but are lesion formation and CNS atrophy do separate mechanisms?
I appreciate this post Dr. G but respectfully disagree. The single most obvious choice for next breakthrough drug will be the remyelinating drugs, like RHiGM22 from Mayo Clinic, the anti-lingo drugs or even Biotin, if the hype is true. They will restore some, not all, function in every type of MS and are close to completion of their trials. I think that there is a disconnect, in terms of urgency, between MS patients and researchers. The 2.5 million MS patients want something today and not 10-20 years from now when some drug moves from the mouse to humans after clinically trials.
With respect you can't remyelinate nerves if the nerve is already dead. Therefore firstly we need robust neuroprotectants to save as many nerves as possible before we can think about giving remyelination agents to pwMS.
MD 2-this is very true, but many of the demyelinated nerves are not, in fact, dead, rather they exist and are inefficient in their transmission of electrical pulses-"saltatory conduction". I believe this is how Ampyra (5-AP) works by improving conduction along existing nerves. I think most MS patients and their physicians would be very happy to gain some of their function back by repairing existing demyelinated nerves. Also, it is believed that re-addition of of myelin through oligodendrocytes protects further damage to neurons (ie. neuroprotection). Again, in a perfect world it would be theoretically nice to have a 100% effective neuroprotectant before major demyelination happens but this would mean that almost every MS patient today will not see any improvements during their lifetime. How far off do you think this robust neuroprotectant drug is MD2?
It depends on how good repurposing is, there are compound avilable now if they can be shown to work but without pharma can this be done