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Carl,

I have been thinking about your question about neuroprotectors.

Nothing per se has been written about CMT, except Creatine research

does show it might have some effect. Somewhere (and I'm sorry I can't

find the source right now) I also came across the use of ALA and

Vitamin E for general neuroprotective use in neuromuscular diseases,

not necessarily CMT specific. Potassium channel blockers and polyunsaturated

fatty acids are also known as neuroprotectors.

Please realize, of course, that the use of these does not stop/arrest syndromes

or disease, but in some instances can improve quality of life. I'd suggest

discussing the use of neuroprotectors with your neurologist before you start any

supplementation.

~ Gretchen - PS See below for a History of Neuroprotectors, it is 3

years old and the article is in Russian, so all I can give you is the

abstract on this.

Eksp Klin Farmakol. 2003 Mar-Apr;66(2):32-7.

[Evolution of the neuroprotection concept]

[Article in Russian]

Ostrovskaia RU.

Zakusov Institute of Pharmacology, Russian Academy of Medical

Sciences, Baltiiskaya ul. 8, Moscow, 125315 Russia.

Although the modern concept of neuroprotection has been formulated

quite recently, the basis of this approach was laid about four

decades ago when Zakusov initiated the study of mechanisms involved

in the neuroprotector action of GABA shunt metabolites (in

particular, alpha-hydroxybutyric acid and succinic semialdehyde)

during hypoxia. It was suggested to consider these agents as a system

of endogenous neuroprotectors. The interest of Zakusov in endogenous

regulators (including oligopeptides) had stimulated research in this

direction and gave impact to the investigations of A. P. Skoldinov

and T. A. Gudasheva initiated in the early 1980s. Proceeding from the

original concept of the possibility of imitation of the action of

neurotropic agents by their structural-conformational oligopeptide

analogs, a number of biologically active stable dipeptides were

obtained, based on pyroglutamate and proline, and high specific

bioaccessibility of these dipeptides for the brain was established.

Our investigations showed that these compounds not only possess

nootropic activity (in a dose 1000 times lower than that of

piracetam), but produce a pronounced neuroprotector action as well.

Most thoroughly studied in this respect were substituted acyl-prolyl

dipeptides, in particular, the drug noopept exhibiting a combined

neuroprotector effect both in vitro and in vivo. Noopept decreases

the extent of necrotic damage caused by photoinduced thrombosis of

cortical blood vessels. It was established that the neuroprotector

effect of noopept is related to its action upon the well-

known " triad " , whereby the drug reduces neurotoxic effects of excess

extracellular calcium, glutamate, and free radicals. Two additional

components of the neuroprotector action of noopept are related to the

antiinflammatory and antithrombotic activity. The prospects of using

direct and indirect action upon neurotrophin system for

neuroprotection purposes are considered. Taking into account common

secondary mechanisms of the neuronal damage, it is possible to

provide for pleotrophic brain protection with dipeptides in a broad

spectrum of pathological states, including strokes, cerebral traumas,

neurodegenerative processes, epilepsy, and schizophrenia.

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