Melatonin a treatment for MS?

Kashani IR, Rajabi Z, Akbari M, Hassanzadeh G, Mohseni A, Eramsadati MK, Rafiee K, Beyer C, Kipp M, Zendedel A. Protective effects of melatonin against mitochondrial injury in a mouse model of multiple sclerosis. Exp Brain Res. 2014 May 6. [Epub ahead of print]

Multiple sclerosis (MS) is the most prevalent inflammatory demyelinating disease of the central nervous system. Besides other pathophysiological mechanisms, mitochondrial injury is crucially involved in the development and progression of this disease. Mitochondria have been identified as targets for the peptide hormone melatonin. In the present study, we sought to evaluate the impact of oxidative stress on mitochondrial density and enzyme transcription during experimentally induced demyelination and the protective influence of melatonin. Adult male mice were fed with cuprizone (a toxin that kills myelin forming cells) for 5 weeks which caused severe demyelination of the corpus callosum (CC. The nerve information highway between the left and right sides of the brain). Animals were simultaneously treated with melatonin by daily intra-peritoneal injections. Melatonin exposure reversed (This means it is demyelination was there and the drug turns back the problem, but as they were treating which demyelinating did it stop the demyelination?) cuprizone-induced demyelination and axon protection. Transmission electron microscopy demonstrated significantly increased mitochondrial (cells energy factories) numbers and slightly increased mitochondrial size within CC axons after cuprizone exposure. Melatonin antagonized (blocked) these effects and, in addition, induced the expression of subunits of the respiratory chain complex over normal control values reflecting a mechanism to compensate cuprizone-mediated down-regulation of these genes. Biochemical analysis showed that oxidative stress (damaging conditions)  induced by cuprizone was regulated by melatonin. The data implicate that melatonin abolishes destructive cuprizone effects in the CC by decreasing oxidative stress, restoring mitochondrial respiratory enzyme activity, used in energy production.

Melatonin is a hormone that is produced when you are in the dark and varies during the day such that it helps in setting the body’s clock and regulates the sleep-wake cycle. In this study using about 500 times more than a human dose, there was an effect on slowing loss of myelin. So this will send people scattering off to the shop for a nutriceutical, freely available in USA. 

There could be good news

Kang JC, Ahn M, Kim YS, Moon C, Lee Y, Wie MB, Lee YJ, Shin T. Melatonin ameliorates autoimmune encephalomyelitis through suppression of intercellular adhesion molecule-1. J Vet Sci. 2001;2(2):85-9.

Melatonin (N-acetyl-5-methoxytryptamine), a pineal neurohormone, is a hydroxyl radical scavenger and antioxidant, and plays an important role in the immune system. We studied the effect of exogenous melatonin on the pathogenesis of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats by immunization with rat spinal cord homogenates. Subsequent oral administration of melatonin at 5 mg/kg significantly reduced the clinical severity of EAE paralysis compared with administration of the vehicle alone (p<0.01). Infiltration of ED1+ macrophages and CD4+ T cells into spinal cords occurred both in the absence and presence of melatonin treatment, but melatonin-treated rats had less spinal cord infiltration of inflammatory cells than did the control group. ICAM-1 immunoreactivity in the blood vessels of EAE lesions was decreased in melatonin-treated rats (chicken or egg) compared to vehicle-treated rats. These findings suggest that exogenous melatonin ameliorates EAE via a mechanism involving reduced expression of ICAM-1 and lymphocyte function associated antigen-1a in autoimmune target organs.

But there could be bad news

Luzindole, a melatonin receptor antagonist, suppresses experimental autoimmune encephalomyelitis.Constantinescu CS, Hilliard B, Ventura E, Rostami A. Pathobiology. 1997;65(4):190-4.
Melatonin has immune-enhancing effects and can exacerbate autoimmunity. Pinealectomy or light exposure, which suppress melatonin, inhibit T cell autoimmunity. To investigate the involvement of melatonin in experimental autoimmune encephalomyelitis (EAE), a T-cell-mediated autoimmune demyelinating disease, we tested the effect of luzindole (blocker of melatonin), a melatonin receptor antagonist, on EAE. Luzindole-treated mice did not develop EAE after immunization with spinal cord homogenate, whereas control mice developed EAE. This study suggests that pharmacological inhibition of the immunoenhancing effects of melatonin may prevent autoimmune demyelination.

EAE is “cure of the week” and be warned about taking things that are unproven, the effects in humans have been pro and anti-inflammatory. There is insufficient evidence to make recommendations until evidence is generated.

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    • It would not stop MS in my view, I doubt any nutriceutical will. Why?

      Because if they were so potent the side effects would be there.You don't get one without the other.

      The question with all such things are do they change the slopes of change

    • You think you got ms bec of melatonin? I have ms and i wanna take it bec of insomnia. My ms isnt progressive tho

    • Lyza, I too have MS, 22+ years now, severe insomnia all my life. Same, not progressive, pain my main symptom, pretty much near normal life. I read that those with auto-immune disorders should not take melatonin, but I want to try it.

  • There is a plethora of research that cites the dopamine function of the brain to MS. Recently, I have been looking into 'brain fog' and time of day. It seems that the majority of people with brain fog are cognitively at their best during the evening. This led me to look at sleep/melatonin etc. Following a hypothesis that 'brain fog' is dopamine/melatonin linked then the following article looks interesting:

    It could be that the two competing theories above are based upon emphasising one over the other, when in fact a more balanced approach of a minimum dosage of melatonin at night followed by Luzindole in the morning might give rise to a regular sleep pattern, loss of 'brain fog' by day and the neuro-protection found in the studies.

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