..Any body taking it?
There is plenty of research for it including the following :

http://en.wikipedia.org/wiki/Melatonin
"In animal models, melatonin has been demonstrated to prevent the damage to DNA by some carcinogens, stopping the mechanism by which they cause cancer.[30] It also has been found to be effective in protecting against brain injury caused by ROS release in experimental hypoxic brain damage.[31] The antioxidant activity of melatonin may reduce damage caused by some types of Parkinson's disease, may play a role in preventing cardiac arrhythmia and may increase longevity; it has been shown to increase the average life span of mice by 20% in some studies.[32][33][34]"

i don't have pd...but i take melatonin every night. i had insomia for years. would average 2- 3 hours of sleep a night. take me forever to fall asleep.

now i take melatonin and a calcium & magnesium supplement before going to bed. 30 minutes or less..and i'm out. i still wake up from pain, but i can now usually fall back asleep.

.. Can you tell me what dose of Melatonine / Ca/ Magnesium you are taking? and how long have you been taking it?

the melatonin 3 mg

i just check the bottle of my calcium..it also has vit d.
calcuim 600 mg
vit d 200 iu
magnesium 100 mg

i started this about 6 months ago.

imark
I also use melatonin but have to take only 300mg or at max 600mg per night

if I take any higher dose it has the opposite effect and makes me very edgy and restless

my doc says that it is likely to do with serotonin levels that different people require such a wide range of doses

It seems best to start on a low dose and then work up if needed

Cheri

In the mornings, too much melatonin can block the release of the first dopamine of the day. Sleep deprivation (which lowers melatonin) has been used to improve both PD and depression. As suggested above, start low and gradually increase.

WHAT? I'm stunned. Some anti-depressants improve sleep and help with depression. Lack of sleep seems to worsen PD symptoms. I thought that was true for everyone.

Prog Neuropsychopharmacol Biol Psychiatry. 1999 Jul;23(5):753-84.
Sleep deprivation therapy in depressive illness and Parkinson's disease.
Demet EM, Chicz-Demet A, Fallon JH, Sokolski KN.

Mental Health Care Group, VA Medical Center, Long Beach, CA, USA.

1. Sleep deprivation is commonly associated with feelings of fatigue and cognitive impairment. 2. Patients with depressive illness, however, often experience mood improvements under these same conditions. 3. Other studies now show that tremor and rigidity, in patients with Parkinson's disease, are also improved by sleep depression therapy. 4. The neural substrates which underlie these effects are unclear. Some recent evidence, however, suggests that sleep deprivation may activate mechanisms which are otherwise typical of conditions of metabolic stress. 5. A common feature of these mechanisms is the suppression of cholinergic activity which is thought to be excessive, in relation to monoamine transmission, in both depression and Parkinson's disease.

PMID: 10509373 [PubMed - indexed for MEDLINE]

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The effect of sleep deprivation on motor impairment and retinal adaptation in Parkinson's disease

Authors: Reist C.; Sokolski K.N.; Chen C.-C.; Coskinas E.; Demet E.M.1

1. Sleep deprivation has previously been reported to result in a temporary improvement of motor deficits in Parkinson's disease patients.2. The mechanism of this action is unclear but may involve an activation of dopamine pathways.3. Other studies suggest that light adaptive changes in the retinal pigment epithelium may serve as a model of dopamine sensitivity.4. The present study examined the effects of one night of total sleep deprivation on RPE potentials and motor abnormalities in Parkinson's patients.5. Sleep deprivation significantly improved motor deficits and these changes were strongly correlated with increases in light adaptive RPE potentials.

Effect of sleep deprivation on motor performance in patients with Parkinson's disease

Movement Disorders

Volume 16, Issue 4 , Pages 616 - 621

Published Online: 16 Jul 2001

Abstract
Animal research provides evidence that sleep deprivation influences the dopamine system. Knowledge about the effect of sleep deprivation on motor performance in patients with Parkinsons disease is scarce.

This study examines the influence of total and partial sleep deprivation compared to normal sleep on motor state and performance in Parkinson's disease. Fifteen nondepressed patients with Parkinson's disease underwent one night of total sleep deprivation (TSD), one night of partial sleep deprivation (PSD) after 3 a.m., and one control night of normal sleep (S), performed in a random, nonconsecutive order.

Over a period of 3 hours the following morning, motor evaluations (United Parkinson's Disease Rating Scale, [UPDRS] and tapping rate) were performed before and every 30 minutes after intake of the usual morning dopaminergic drug dose.

All patients underwent polysomnography apart from the sleep deprivation protocol. Mean UPDRS motor scores and tapping velocities did not differ significantly after each of the schedules, but a subgroup of four patients improved their motor score after partial sleep deprivation.

These data do not confirm previous findings of an overall positive influence of sleep deprivation on motor function in Parkinson's disease.

However, the results indicate that different response types to sleep deprivation may exist and that a subgroup of patients could benefit from partial sleep deprivation. © 2001 Movement Disorder Society.

MINIREVIEW
Regulation of antioxidant enzymes: a significant role for melatonin

http://www.blackwell-synergy.com/doi....x?cookieSet=1

ABSTRACT:

Antioxidant enzymes form the first line of defense against free radicals in organisms. Their regulation depends mainly on the oxidant status of the cell, given that oxidants are their principal modulators.

However, other factors have been reported to increase antioxidant enzyme activity and/or gene expression. During the last decade, the antioxidant melatonin has been shown to possess genomic actions, regulating the expression of several genes.

Melatonin also influences both antioxidant enzyme activity and cellular mRNA levels for these enzymes.

In the present report, we review the studies which document the influence of melatonin on the activity and expression of the antioxidative enzymes glutathione peroxidase, superoxide dismutases and catalase both under physiological and under conditions of elevated oxidative stress. We also analyze the possible mechanisms by which melatonin regulates these enzymes.

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"melatonin preserves the integrity of the mitochondria and helps to maintain cell functions and survival."

http://www.sciencedirect.com/science...991f4cf7fdf293

TOO MUCH MAY BE DANGEROUS:

Annals of the New York Academy of Sciences 993:351-361 (2003)
© 2003 New York Academy of Sciences

Gene and Protein Expression Profiles of Anti- and Pro-apoptotic Actions of Dopamine, R-Apomorphine, Green Tea Polyphenol (-)-Epigallocatechine-3-gallate, and Melatonin

ORLY WEINREB, SILVIA MANDEL AND MOUSSA B.H. YOUDIM

Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research and Department of Pharmacology, Rappaport Family Research Institute, Technion-Faculty of Medicine, Haifa, Israel


Significant evidence has been provided to support the hypothesis that oxidant stress may be responsible for degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease.

Dopamine (DA), R-apomorphine (R-APO), green tea polyphenol (-)-epigallocatechine-3-gallate (EGCG), and melatonin are neuroprotective and radical scavenger compounds. The aim of this study was to establish the mechanism of the concentration-dependent neuroprotective and pro-apoptotic action of these drugs via gene expression and protein determination.

cDNA microarrays provide new prospects to study and identify various mechanisms of drug action. We employed this technique for the study reported in this paper. Total RNA was extracted from SH-SY5Y cells exposed to low neuroprotective and high toxic concentrations of the drugs, followed by synthesis of cDNA, and hybridization to a microarray membrane related to apoptosis, survival, and cell cycle pathways.

We demonstrated a concentration and time-dependent correlation between R-APO, DA, EGCG, and melatonin in modulation of cell survival/cell death-related gene pathways.

The results were confirmed by quantitative real-time PCR and protein profiles. Unlike the effects of low concentrations (1-10 µM), where an antiapoptotic response was manifest, a proapoptotic pattern of gene expression was observed at high toxic concentrations (50-500 µM) of the antioxidants (e.g., increase in caspases, fas, and gadd45).

Our results have provided novel insights into the gene mechanisms involved in both the neuroprotective and proapoptotic activities of neuroprotective drugs. We have shown that DA, R-APO, EGCG, and melatonin exhibit similar gene expression and protein profiles.