From: gts (gts_2000@yahoo.com)
Date: Wed Feb 05 2003 - 16:26:32 MST
Rafal wrote:
> As a practicing neurologist I can tell you that selegiline is not
> prescribed in our movement disorders clinic, precisely because of the
> absence of such studies, and the results of DATATOP, currently the
> last word on selegiline in PD.
How strange. Did your people actually read the studies?
As stated in the following abstract, from DATATOP, "The study found that
deprenyl [selegiline] treatment almost halved the risk of reaching a
stage of Parkinsonism at which the start of levodopa treatment becomes
imperative for lessening disability."
That looks like potent neuroprotection to me.
ABSTRACT:
Deprenyl's effect at slowing progression of parkinsonian disability: the
DATATOP study. The Parkinson Study Group.
LeWitt PA
Acta Neurol Scand Suppl 1991 136:79-86
Studying a cohort of 800 mildly-affected parkinsonians, the North
American DATATOP* project has concluded that progression in disability
can be attenuated by the use of deprenyl, 10 mg/day. Interim results of
this controlled clinical trial were reported after participants received
treatment for an average of 12 months. The study found that deprenyl
treatment almost halved the risk of reaching a stage of Parkinsonism at
which the start of levodopa treatment becomes imperative for lessening
disability. In addition to this study end-point, other ratings supported
an improved clinical outcome from the chronic deprenyl (DP) regimen. The
34 investigators conducted clinical evaluations both while subjects
received medication and after a 4-week wash-out. Though some subjects
experienced mild symptomatic improvements of Parkinsonism from DP, these
effects were insufficient to account for the DP-treated group's delay at
reaching the study end-point. In addition to DP, this placebo-controlled
double-blind study also assessed the possibility of protective effects
from another antioxidative strategy, a 2,000 I.U./day regimen of
alpha-tocopherol. To date, results of the latter trial have not been
reported. Monoamine oxidase type-B (MAO-B) metabolism of dopamine
generates hydrogen peroxide and, thereby, an oxidative stress on the
nigrostriatal dopaminergic neuron. The inhibition of MAO-B by DP may
have been the means by which progression of Parkinsonism was attenuated,
although other mechanisms are also tenable. DATATOP has pointed to the
potential for arresting the progression of Parkinson's disease, and has
provided an unparalleled opportunity to study the clinical course and
neurochemical indices of untreated Parkinsonism.(ABSTRACT TRUNCATED AT
250 WORDS)
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