I stumbled upon some research that discovered mice who were Ganglioside deficient developed what looks like sporadic PD...as in they did not need be injected with toxins to induce the MPTP kind of Parkinsonism. This toxin coerced PD model has yielded much data, but I have always questioned it- these animal models were far from developing sporadic PD, but hey it's all we had.

Now, we have an animal model that looks and acts just like the human version we know so well; it involves neurodegeneration, motor symptoms, but most amazingly the mice show alpha-synuclein aggregation in the brain. This is not forced on them as it is with all other animal models of PD. This is just like us- so I am doing a happy dance thinking finally some real progress in solving this riddle. What brought this on? A lack of Ganglioside. I have read the wikipedia article and still don't know what it a Ganglioside is...

but learned we need the GM1 type. Look at what GM1 does:

...impacts neuronal plasticity and repair mechanisms, and the release of neurotrophins in the brain.

Hey, it protects and encourages new neuron growth, and it passes the Blood Brain Barrier. Lookout GDNF

Then I get really excited when I read a couple abstracts on how mice in a different study with the older MPTP induced PD responded positively to treatment with GM1. Well, this is just mice, right. Once again, this a dead end.

Boy, I was wrong. Not only is there a study this year showing that PWP are Gangliodide deficient; better yet, we humans, respond really well to Ganglioside GM1 therapy. Needless to say I was thrilled to run across a study of this ganglioside in the treatment of PD and went to read over the abstract. I was astonished by what I read. This was not an early stage trial- it was a Placebo control trial showing both safety and efficacy; I quickly checked the date an read the trial results again. Here is the gist:

We have a natural substance that not only seems to halt degeneration but improved people in clinical trial long term over the course of five years. People in this study after five years treatment were better than baseline, that is off meds, five years later!

The date for this pub is 2010 but a five year study plus scant literature dating back to 1989 showing not only that this most likely would benefit us but people with Huntington's as well. This looks like Phase II of the trial.

We have what looks like a very promising disease modifying treatment that as a natural substance appears to be more important than dopamine loss and this was published two years ago. The substance can be taken orally and is tolerated well up to 1 gram daily though best range is 3-70 mg max.


GM1 ganglioside in Parkinson's disease: Results of a five year open study.

Is anyone else wondering why we do not know about this and feeling slightly punked? No one in the industry saw this as news worthy?

Am I over reacting? I hope others see something fundamentally wrong here. Why has this not been in press. When patients in a trial collectively fare BETTER off meds than they did five years upon taking this supplement doesn't that sort of tell us something beyond we need more studies. Does this have to do with the whole no patent no profit approach we have to improving the lives of those who suffer- right here and now- will it get tied up by the FDA again?

Sigh.

Laura