From: gts (gts_2000@yahoo.com)
Date: Sat Feb 08 2003 - 05:24:23 MST
Here is published evidence that selegiline (deprenyl) increases
life-expectancy in Parkinson's Disease, (something that Rafal considers
impossible.)
In this 9 year study, 564 of 941 PD patients were given selegiline as part
of their treatment. The patients treated with selegiline lived significantly
longer than those not treated with selegiline. This is strong evidence that
selegiline actually slows the progression of the disease in addition to
relieving its symptoms. While these results were not confirmed by another
similar study, they can hardly be discounted given the preponderance of
evidence from other studies that support the hypothesis that selegiline has
neuroprotective and antioxidant properties outside of PD, including evidence
from those other studies I've already posted here over the last week. -gts
ABSTRACT
Increased life expectancy resulting from addition of L-deprenyl to Madopar
treatment in Parkinson's disease: a longterm study.
J Neural Transm 1985;64(2):113-27 (ISSN: 0300-9564)
Birkmayer W; Knoll J; Riederer P; Youdim MB; Hars V; Marton J
In an open, uncontrolled study the longterm (9 years) effect of treatment
with Madopar alone (n = 377) or in combination with l-deprenyl (selegiline,
selective monoamine oxidase type B inhibitor) (n = 564) have been compared
in Parkinsonian patients. In patients who lost their response to
conventional Madopar therapy the addition of l-deprenyl resulted in a
significant recouping of levodopa effect. The survival analysis revealed a
significant increase of life expectancy in Madopar--l-deprenyl group
regardless of the fact whether or not the significant demographic
differences between the two groups were taken into account. Although the
mechanism underlying this action of l-deprenyl is not known, the results are
interpreted as indicating l-deprenyl's ability to prevent or retard the
degeneration of striatal dopaminergic neurons. l-Deprenyl is the first
anti-Parkinson drug having such a property. This hypothesis is not far
fetched since l-deprenyl selectively prevents the degeneration of striatal
dopaminergic neurons induced in animals by the illicit drug
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Since latter compound
is known to cause Parkinsonism in man and primates or Parkinson-like
neurochemical and pathological changes in other animals the implications of
the present study involving monoamine oxidase activity and l-deprenyl are
apparent.
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