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 | Research: Component of Turkey (Tryptophan) Promising in MS |
 It is common myth that eating large amounts of turkey makes one sleepy. Science long ago uncovered that the key component of turkey meat that might cause drowsiness is an amino acid called tryptophan.
It seems what was once a piece of useless trivia may become very interesting with respect to multiple sclerosis. Working off the idea that tryptophan may be a powerful immune modulator, new research, from scientists in Germany and California has shown a successful reversal of paralysis in mice afflicted with the laboratory model of Multiple Sclerosis (known as EAE) by dosing the mice with a synthetic version of tryptophan.
The tryptophan synthetic was administered at the onset of paralysis that develops in the animals legs. Compared to placebo animals, the treated mice retained the ability to walk and had fewer and less severe relapses. Furthermore, their immune systems showed a reduction of inflammatory cells considered detrimental to multiple sclerosis patients. Even more intriguing-- when blood was transfused from a treated mouse to a placebo mouse, the recipient actually improved-- implying the change induced by the treatment might be causing the creation of immune cells that target the errant cells responsible for multiple sclerosis inflammation.
The synthetic drug is called tranilast, and is actually used in Japan to treat certain allergy conditions, as well as in various clinical trials worldwide. Certainly the research on mice does not yet indicate that multiple sclerosis patients would benefit from consuming tryptophan or its synthetic derivatives, but it does confirm this relatively common amino acid's role in mediating the immune system and inspires the evaluation of a potentially straightforward treatment strategy.
As with all animal trials, confirmation of efficacy, and most importantly, safety, needs to be established as a next logical step in the treatment's development strategy.
Click "read more" for links to source articles...
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Articles of Further Interest
Tryptophan no Turkey in Boosting Immune System
A Multiple Sclerosis Find
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Re: Component of Turkey (Tryptophan) Promising in MS (Score: 1)
by dignan on Tuesday, November 08 @ 16:06:26 EST
(User Info | Send a Message) | | Here's another, older study from Pubmed by the German team involved in this latest finding:
Biochem Pharmacol. 2003 Oct 1;66(7):1263-70.
Involvement of protein kinase Cdelta and extracellular signal-regulated kinase-2 in the suppression of microglial inducible nitric oxide synthase expression by N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast).
Platten M, Eitel K, Wischhusen J, Dichgans J, Weller M.
Department of Neurology, University of Tubingen, 72076 Tubingen, Germany.
Excess nitric oxide (NO) in the brain released by microglial cells contributes to neuronal damage in various pathologies of the central nervous system (CNS) including neurodegenerative diseases and multiple sclerosis. N-[3,4-Dimethoxycinnamoyl]-anthranilic acid (tranilast, TNL) is an anti-allergic compound which suppresses the activation of monocytes. We show that inducible nitric oxide synthase (iNOS) mRNA and protein expression and the release of NO from N9 microglial cells stimulated with the bacterial endotoxin lipopolysaccharide (LPS) are inhibited when the cells are exposed to TNL.
TNL fails to modulate LPS-stimulated nuclear factor-kappaB (NF-kappaB) reporter gene activity and phosphorylation of inhibitory kappaB (IkappaB), indicating that NF-kappaB is not involved in the TNL-mediated suppression of LPS-induced iNOS expression. Moreover, TNL inhibits LPS-induced phosphorylation of extracellular signal-regulated kinase 2 (ERK-2). Finally, TNL abolishes translocation of protein kinase Cdelta (PKCdelta) to the nucleus and suppresses the phosphorylation of the PKCdelta substrate, myristoylated alanin-rich C kinase substrate (MARCKS).
We conclude that the anti-allergic compound TNL suppresses microglial iNOS induction by LPS via inhibition of a signalling pathway involving PKCdelta and ERK-2.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14505805&query_hl=4 |
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