Treatments which affect chorea or psychological symptoms like depression are considered symptomatic treatments. Treatment that affect the progression of the disease (slowing, stopping, or reversing) are considered actual treatments.

The problematic word in interpreting research is 'improvement'. When you see 'improvement' in a press release or an abstract, you need to read the actual study to see what it means. It could mean that the patients got better but it could also mean that they stayed the same while the control group declined or even that they declined but at a slower rate than the control group.

The preliminary data on creatine shows cognitive improvement and a slowing of the progression of the disease so we're talking about a real potential treatment (not a symptomatic treatment).

Thanks, Marsha - I'll read the studies again.

remig, i dont understand your post. People with hd have too much glutamate, and it destroys brain cells, but i dont understand what you are saying.

I mean "reduced" in the sense of the opposite of oxidized, not in the sense of less. The more of the reduced form of glutathione the better.

So what do tylenol and fava beans do, do they increase or decrease glutamate? I tried to read the web you referred, but couldn't understand it. Thanks

Barb

I think there are several detrimental consequences of the HD mutation. Elevated glutamate is one consequence and loss of anti-oxidant protection is another. And there are yet other consequences. Memantine protects against the first consequence, elevated glutamine. Anti-oxidant supporters protect against the second. (Note that glutathione is not glutamate.)

but i think they're similar, but im not sure...thanks...smile

Nope...cognitive symptoms. An improvement could include a slower rate of decline or a lessening in the severity of symptoms as well. That is an improvement from natural progression. In the case of creatine for instance, so far there has been measurable improvement, in the pure sense of the word, in a percentage of those in the phaseII trials. Yes, actual, measurable improvement! A larger percentage showed no decline and the remaining showed slower than expected rate of decline. There is no reason to exclude the word improvement from the vocabulary anymore. I am very eager to watch phaseIII of creatine. I am also hoping they get testing of creatine for the pre-symptomatic started soon.

I keep seeing more research on minocycline. Some good, some bad. Does anybody have any thoughts on it. It seems by itself it has not produced the results people expected yet combined with other drugs it has better results.

Hi All,
I was wondering if someone has a definitive concise list of supplements they can share with me on the recommended dosages ? I have been reading thru the messages but am not sure what i should take and why or what else i should be avoiding ?
Any and all help would greatly be appreciated. Thanks in advance...>>LP

HD Lighthouse has a great section on supplements which includes dosages and what they do - [www.hdlighthouse.org]

The way I understood things from this and other readings is:

Creatine or Coenzyme Q10 work very similarly. Creatine results seem more positive. - 10G creatine daily - I use tablets, no coenzyme

Omega 3 - 2G of EPA

400U of Vitamin E daily (which I get in a daily multi vitamin)

Blueberries - 1 cup daily - I use a supplement

Trehalose - 75G daily



Edited 1 time(s). Last edit at 05/07/2007 12:18PM by ChiTom.

[www.hdac.org] minocycline that young man tried it and he has an email address if you press on his name . db



Edited 1 time(s). Last edit at 05/07/2007 01:17PM by db.

Barb

As to your observation that glutathione and glutamate are similar: yes and no. Glutathione is a very short protein constructed from three amino acids one of which does happen to be glutamate. That constituent glutamate is however unconnected to the glutamate released at nerve synapses as a neurotransmitter, whose excessive release in HD is mitigated by memantine. Interestingly glutamate competes with cysteine for transport into the cell and cysteine is also one of the amino acids in glutathione. The third amino acid is proline which, by its self, has been shown to inhibit the aggregation of proteins like the poly-glutamINE protein of HD that is the root cause of the disease. I have wondered if, since the amino acid glutamINE is manufactured in the cell from glutamATE, glutamine depletion in producing the aggregating protein might cause the cell to increase the levels of the enzymes in the glutamine synthesis pathway and thus cause the elevated glutamate seen in HD. Perhaps gluatimINE supplementation, a common practice of body builders, could be of benefit in HD for this reason. Also avoiding foods rich in glutamATE such as wheat, peanut, soy, bean and, of course, MSG might be similarly beneficial. (Or they could do the opposite - it really needs to be researched first).

Thank you for the easier read Ron, that was easy to understand. Well, i def stay away from msg and soy, i get migraines from them, and i don't think msg is good for hd.

Oops, did I say proline was a component of glutathione. Actually the third amino-acid is glycine, not proline. Nevertheless proline may work like trehalose is supposed to work in preventing protein aggregation - see [www.pnas.org]. And unlike trehalose it can enter the bloodstream and cross the blood-brain barrier intact. The body synthesizes the proline it needs from glutamate and may thus be somehow affected by the glutamate imbalances common to HD. Proline levels can be depressed under conditions of metabolic stress so its dietary supplementation might as worthy of study as trehalose in treating HD.