CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
This wpould fit an aetiology of Lyme induced ALS- ************************************************* 1: Med Hypotheses. 2007;69(4):836-7. Epub 2007 Mar 21. Links
Consideration of acamprosate for treatment of amyotrophic lateral sclerosis.
Kast RE, Altschuler EL. Department of Psychiatry, University of Vermont, College of Medicine, 2 Church Street, Burlington, VT 05401, USA. [email protected]
Amyotrophic lateral sclerosis (ALS) is a fatal disease of degeneration of motor neurons. There is no known cure or life extending treatment.
Much recent work has suggested that a possible cause of ALS is constitutive opening of the calcium pore in glutamate sensitive AMPA channels secondary to a failure of RNA editing that would change a crucial glutamate in the channel to arginine.
Here, we point out that the small molecule pharmaceutical acamprosate, usually used as a drug to maintain alcohol abstinence, may block this calcium pore--as do the related molecules endogenous polyamines such as putrescine, cadaverine, spermidine and spermine--and thus might have use in ALS.
PMID: 17368956
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
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Hi CaliforniaLyme. I don't see how you figured using acamprosate would make this treatment fit the etiology of Lyme. It protects glutaminergic neurons from excitotoxicity.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting both upper and lower motor neurons. Weakness may begin in the legs, hands, proximal arms, or pharynx. The course is relentless and progressive without remissions, relapses, or even stable plateaus. There is no effective drug therapy for ALS, although riluzole has been shown to prolong life in sufferers, without tracheostomy. A vitamin B12 analog, methylcobalamin, has a protective effect on cultured cortical neurons against glutamate-induced cytotoxicity.
We have shown the ultra-high-dose methylcobalamin (25 mg/day i.m.) slows down the progressive reduction of the CMAP (compound muscle action potential) amplitudes in ALS in the short term (4 weeks). The latencies of SSR (sympathetic skin response) were shorter after treatment (50 mg/day i.v., 2 weeks). In the long-term effect of methylcobalamin (50 mg/day i.m., twice a week), the survival time (or the period to become respirator-bound) was significantly longer in the treated group than in the untreated. Larger-scale randomized double blind trial was started in Japan in order to evaluate the long-term efficacy and the safety of ultra-high-dose methylcobalamin for sporadic or familial cases of ALS.
-------------------- "You know, the worst, meanest, nastiest, ticks in the world are politicks," - Steve Nostrum Posts: 242 | From South NJ | Registered: Dec 2006
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CaliforniaLyme
Frequent Contributor (5K+ posts)
Member # 7136
posted
Cat- this is a furin inhibitor and it could potentially prevent the flooding of calcium that makes the mitochondria destroy motor neurons!!!!!!!!
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
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