The number of molecules that are currently in clinical trial or close to clinical trial that work at the root problem of many neurodegenerative disorders (protein aggregation) is growing day by day. I have to believe that in the coming years doctors will begin to discover “cocktails” of these meds that when taken together will be able to halt or slow the progression of many neurodegenerative disorders. I know we all want answers today, but honestly I believe in my heart that real relief is only a few short years away.
My son has gotten rid of all his symptoms. There are people with PD, HD, and ataxia well past the age when they should have symptoms, but they remain symptom free. Not everyone is so fortunate to have a mild and manageable disorder, but many do and are using science to take control of their own lives.
Did you read any of the linked research on Exenatide?
Riluzole was from the beginning intended to treat symptoms and not the underlying pathology. It affects glutamate pathways, but how it works has always been a bit of a controversy. There is even some evidence that one effect is the uptake of glutamate which would decrease the effectiveness of neuronal pathways.
Riluzole preferentially blocks TTX-sensitive sodium channels, which are associated with damaged neurons.[17][18] Riluzole has also been reported to directly inhibit the kainate and NMDA receptors.[19] However, the action of riluzole on glutamate receptors has been controversial, as no binding of the drug to any known sites has been shown for them.[20][21] In addition, as its antiglutamatergic action is still detectable in the presence of sodium channel blockers, it is also uncertain whether or not it acts via this way. Rather, its ability to stimulate glutamate uptake seems to mediate many of its effects.[22][23] In addition to its role in accelerating glutamate clearance from the synapse, riluzole may also prevent glutamate release from presynaptic terminals.[24] These effects combined could significantly reduce glutamate signaling and cause indirect antagonism without acting at glutamate receptors themselves. - Riluzole - Wikipedia
Perhaps people with access to doctors involved in the clinical trial might consider talking to them about these molecules that might actually treat the underlying pathology:
One should never begin taking a supplement based on comments from the internet without first doing their own research and talking with their doctor. Having said that I will say that I take 2 Tbs of trehalose daily in coffee plus I sniff a tiny pinch (about .3 g). I am under the careful watch of my doctor. I also now take 500 mg of Niagen and 250 mg daily of Pterostilbene. Here is an excellent article on trehalose: https://scienceofparkinsons.com/2017/10/23/trehalose/
Here are some articles to get you started on research of Niagen and Pterostilbene:
Hi Joy Can I remind you, we’re advised not to put private email addresses or telephone numbers on posts. Instead, invite people to send a private message This is for your own security Also, Protandim is classed as a Complimentary Therapy as far as posts are concerned xB
You can go to www.pubmed.gov and enter Protandim in search bar to see 23 peer reviewed published studies. You can also enter ataxia oxidative stress to see those studies.
but I think this article tells a much more complete story:
Protandim may in fact be beneficial, but the trouble for me is I would want to know which ingredient or mix of ingredients was helping and why. This is all but impossible with Protandim as the list of “active” ingredients is numerous.
No matter what I would emphasize again that no one should take any supplement based on internet comments alone, and one should do his own research and discuss the supplement(s) with a doctor before trying anything.
I knew nicotinamide riboside (Niagen) was headed for a human clinical trial for Cockayne Syndrome, but I had never found any underlying animal model research that led me to understand why researchers were interested. Today I finally found the paper. What is interesting for all ataxians is that the paper links to a plethora of additional research on ketogenic diets, NAD+ replenishment, and SIRT1 activation all of which have a great deal of research showing neuroprotective benefits. What was most striking to me is that pharmacological activation of SIRT1 was shown to have similar benefits to a ketogenic diet, and SIRT1 activation is just what nicotinamide riboside does that the other vitamin Bs do not. In addition there are other SIRT1 activators that are available today including my favorite, pterostilbene. Anyways, just thought I’d share.
this study I posted in several other locations, but I thought it was worth reposting in this thread since it is relevant here more than elsewhere . . .
NAD+ precursors have been shown to improve mTORC1 pathways in animal model research of Breast Cancer. Breast Cancer is one of several ailments for which a human clinical trial of Niagen is pending.
Specific enhancement of mitochondrial complex I activity inhibited tumor growth and metastasis through regulation of the tumor cell NAD+/NADH redox balance, mTORC1 activity, and autophagy . . . The results translate into a new therapeutic strategy: enhancement of the NAD+/NADH balance through treatment with NAD+ precursors inhibited metastasis in xenograft models, increased animal survival, and strongly interfered with oncogene-driven breast cancer progression in the MMTV-PyMT mouse model
The way this medication works may make it a good candidate for some ataxias. At a minimum people who have diabetes AND ataxia should most definitely talk to their doctors about this medicine as it is currently available for diabetes.
The studies below are in Parkinson, Alzheimers, and Huntingtons. What these diseases have in common are protein aggregation which is common in many ataxias as well. This could be big.
“They also asked the question ‘if Exenatide works for Parkinson’s, then why not other neurodegenerative disorders (such as, Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, multiple sclerosis) or other neurological diseases (including cerebrovascular disorders, traumatic brain injury).”
The way this medication works may make it a good candidate for some ataxias. At a minimum people who have diabetes AND ataxia should most definitely talk to their doctors about this medicine as it is currently available for diabetes.
The studies below are in Parkinson, Alzheimers, and Huntingtons. What these diseases have in common are protein aggregation which is common in many ataxias as well. This could be big.
“They also asked the question ‘if Exenatide works for Parkinson’s, then why not other neurodegenerative disorders (such as, Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, multiple sclerosis) or other neurological diseases (including cerebrovascular disorders, traumatic brain injury).”
Can I remind you, we’re advised not to put private email addresses or telephone numbers on posts. Instead, invite people to send a private message