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Multiple Sclerosis, Melatonin, and Neurobehavioral Diseases

R. Wurtman

Published 2017 in Frontiers in Endocrinology

ABSTRACT

Numerous neurobehavioral diseases typically exhibit annual rhythms in the frequency with which they cause flare-ups. A prime example is the seasonal affective disorder syndrome (SADS), in which symptoms usually start to appear in November and disappear in the late winter, after which many patients remain asymptomatic until the following fall (1, 2). Smaller seasonal variations in mood and behavior are also sometimes noted among patients with Depression, per se, but less so among normal control subjects (3, 4). Multiple sclerosis (MS), an inflammatory neuroimmune disease which typically first affects women in their 20s, also often displays seasonality in the incidence of flare-ups: symptoms are more likely to occur in spring/summer than in fall/winter (5–7), and are more frequent in northern than in southern climates. The disease causes microglial activation, perhaps mediated by myelinreactive T cells and specific IgG antibodies, which ultimately affects oligodendrocytes and their myelin product. The loss of myelin can lead to chronic neurodegeneration. The basic etiology of MS remains unknown; the disease has a genetic component (8) and has not been shown to involve viruses. It should be noted that MS has recently become partly treatable with new drugs which, besides diminishing flare-ups, may modify its natural history: a large, recent (2017) 60-year population-based Norwegian study found that whereas median life expectancy of MS patients was significantly shortened (by about 7 years) among patients in the study’s initial time blocks, an effect on longevity was no longer observed in the last time block examined (1997–2012) (9), perhaps because partially effective treatments had started to become available.

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