Melatonin treatment in PD [1-17-05]

The effect of melatonin treatment on sleep and
sleepiness in dopamine
agonist treated patients with Parkinson's disease
GA Dowling, MJ Aminoff, J Mastick, E Colling, JH
Carter, CM Singer
P297; S102

Low-dose melatonin improves sleep in PD patients
with sleep disturbance,
according to this study.

Twenty-seven patients received either placebo or
melatonin at 5 mg or 50
mg for 2 weeks, with crossover to each of the
other arms separated by a
1-week washout. Five mg but not placebo or 50 mg
improved total score on
the General Sleep Disturbance Scale and the
sleepiness subscale. At the 5
mg dose, approximately two thirds of patients
improved on the GSDS, and
three quarters on the sleepiness subscale.
----

2002 E-MOVE conference reports are made possible
in part through
unrestricted educational grants from these
sponsors:
Gold Level: Bertek Pharmaceuticals, Elan
Pharmaceuticals, Pharmacia
Corporation.
Silver Level: GlaxoSmithKline, Amarin
Pharmaceuticals
Bronze Level: Procter & Gamble Pharmaceuticals,
Schwarz Pharma.

Copyright 2002 WE MOVE
Editor: Richard Robinson (rrobinson@wemove.org)
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Pharmacology Biochemistry and Behavior
Volume 80, Issue 1 , January 2005, Pages 9-26

Pharmacol Biochem Behav. 2004 Nov;79(3):413-29.
    Recovery of experimental Parkinson's disease
with the melatonin
analogues ML-23 and S-20928 in a chronic,
bilateral 6-OHDA model: a new
mechanism involving antagonism of the melatonin
receptor.

    Willis GL, Robertson AD.

    The Bronowski Institute of Behavioural
Neuroscience, Coliban Medical
Centre, 19 Jennings Street, Kyneton, Victoria
3444, Australia.

    Over the past 10 years, there has been a
resurgence of interest in
examining the role of melatonin in health and
disease. While the brunt of
research in this area has portrayed melatonin in
a favorable light, there
is a growing body of evidence suggesting that
melatonin may possess
adverse effects contributing to the development
of various
neuropsychiatric disease states. In preclinical
models of Parkinson's
disease (PD), melatonin has been shown to enhance
the severity of this
condition while its antagonism, using constant
light or pinealectomy,
facilitates recovery. To test this hypothesis
further, the present study
employed the melatonin analogues ML-23 and
S-20928 in a post-6-OHDA
injection regime to determine whether they may
have a favorable effect on
the symptoms of this more chronic model of PD.
When ML-23 was injected
I.P. in a dose of 3 mg/kg twice daily for 3.5
days after 6-OHDA,
significant improvement in motor function and
regulatory deficits was
observed. Similarly, the injection of S-20928 in
a 1 mg/kg dose (I.P.), in
the same regimen, facilitated modest improvement
in motor function and
regulatory deficits while the larger dose
enhanced the severity of
behavioural deficits and produced severe side
effects causing
deterioration in condition during the course of
drug administration. ML-23
administration totally abolished the
6-OHDA-induced mortality, which
accompanies dopamine (DA) degeneration, while
S-20928 had no effect on
this parameter. These results suggest that some
melatonin analogues can
aid in recovery from DA depleting lesions after
DA degeneration has
commenced and the recovery is not attributable to
the antioxidative
properties of this hormone. While the exact
mechanism by which ML-23 and
S-20928 are exerting their therapeutic effect is
unclear, it is possible
that antagonism of melatonin receptors may play
some role and this should
be considered when assessing the potential of
melatonin analogues for
treatment of human neuropsychiatric disorders.

    PMID: 15582013 [PubMed - in process]