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>    Subject: Re: Sinemet
>    From: Schaaf Angus / Meadow Creek Ranch <[log in to unmask]>
>    Date: Wed, 11 Jul 2001 00:11:25 -0600

All well and good, but  studies like this just happen to omit the  other
things like the dystonia, dyskinesia, etc. that seem to crop up after a
while ....... Rob
----- Original Message -----
From: "ervinmccarthy" <[log in to unmask]>
To: <[log in to unmask]>
Sent: Tuesday, July 10, 2001 7:39 PM
Subject: Sinemet


> Subject: Chronic LD not toxic, may promote neural recovery
> Date: 1/19/99
>
> Chronic levodopa is not toxic for remaining dopamine neurons, but instead
> promotes their recovery, in rats with moderate nigrostriatal lesions
>
> MG Murer, G Dziewczapolski, LB Menalled, MC Garcia, Y Agid, O Gershanik, R
> Raisman-Vozari
>
> Annals of Neurology, 1998, Vol 43, Iss 5, pp 561-575
>
> Six months of oral l-dopa caused no excess loss of dopaminergic neurons
> versus untreated controls, and may have promoted recovery of surviving
> neurons, according to this study on OHDA-lesioned rats. Rats were
> unilaterally injected with either saline or one of two quantities of OHDA
> (to produce moderate vs. severe lesions). Members of each group were
> randomly assigned to receive either vehicle or oral l-dopa. Neuronal
> survival was quantified by immunoautoradiography of tyrosine hydroxylase,
> vesicular monoamine transporter, and dopamine transporter.
>
> Results showed:
> a) L-dopa treatment caused no loss of dopaminergic neurons in either
> sham-lesioned or OHDA-lesioned rats compared to sham-lesioned,
> non-treated controls
> b) L-dopa treatment caused no reduction in terminal axonal arborization
> c) In the moderately lesioned group, treated rats showed, "in the
> denervated regions of the striatum, significantly higher levels of the
> three dopaminergic markers than their corresponding vehicle-treated
> control group, and also an increased density of TH-immunoreactive
> fibers."
>
> The authors suggest the recovery is likely to be due to axonal sprouting
of
> surviving dopaminergic neurons. They also note that their study provided
no
> evidence of accompanying functional recovery in this subgroup. In
discussing
> the relevance of these findings to human PD
> patients, they state "our results cannot be considered as definitive
> evidence of an absence of toxicity of chronic levodopa in PD patients" but
> note that other recent findings support the absence of l-dopa toxicity as
> well.
>
> An editorial by Stanley Fahn accompanies the article.
>
>
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