The accelerated aging hypothesis of Parkinson's disease is not supported by the pattern of circadian melatonin secretion.

Hypotheses pertaining to the etiology of Parkinson's disease (PD) have suggested that the disease reflects an accelerated form of the normal aging process. Aging is associated with progressive failure of the pineal gland associated with a gradual decline in nighttime plasma melatonin secretion. The decline in melatonin secretion with age, at an average rate of 10-15% per decade, is considered a marker of brain aging in humans and estimations of plasma melatonin levels could be used to distinguish the processes of normal aging from pathological age-related changes. The accelerated aging hypothesis of PD is not supported by studies which have examined nocturnal melatonin secretion in drug naive Parkinsonian patients compared to age matched normal control subjects. Specifically, these studies have revealed no significant differences in the melatonin rhythms (i.e., peak nocturnal melatonin level and 24-hour melatonin output) between PD patients and normal age matched controls. On the other hand, melatonin secretion is significantly lower in Alzheimer's patients compared to age matched normal subjects. Collectively, it is suggested, on the basis of melatonin circadian rhythms, that Alzheimer's disease rather than PD is related to an accelerated aging process, a hypothesis which is supported by pathological and neurochemical studies.