Recent quotes:

Melatonin in Synaptic Impairments of Alzheimer's Disease. - PubMed - NCBI

It is reported that both the melatonin deficit and synaptic impairments are present in the very early stage of AD and strongly contribute to the progress of AD. In the mammalian brains, the effects of melatonin are mainly relayed by two of its receptors, melatonin receptor type 1a (MT1) and 1b (MT2). To have a clear idea on the roles of melatonin in synaptic impairments of AD, this review discussed the actions of melatonin and its receptors in the stabilization of synapses, modulation of long-term potentiation, as well as their contributions in the transmissions of glutamatergic, GABAergic and dopaminergic synapses, which are the three main types of synapses relevant to the synaptic strength. The synaptic protective roles of melatonin in AD treatment were also summarized. Regarding its protective roles against amyloid-β neurotoxicity, tau hyperphosphorylation, oxygenation, inflammation as well as synaptic dysfunctions, melatonin may be an ideal therapeutic agent against AD at early stage.

New findings explain how melatonin promotes sleep: Discovery may lead to new therapy for insomnia -- ScienceDaily

The experiments singled out one receptor, MT1, as the mechanism via which melatonin acts to inhibit the specific orexin neurons that wake you up. This discovery could help lead to medications that target only the MT1 receptor instead of multiple receptors, which could lead to fewer side effects for those who take sleep-promoting drugs. "Melatonin has been used as a sleep drug for many years, but people didn't know how it worked," Thakkar said. "Our research suggests that if you target the melatonin MT1 receptor, you will get the most sleep with minimal side effects."

Effects of night-time light on internal body clock -- ScienceDaily

Melatonin suppression and circadian phase resetting are often correlated such that high levels of melatonin suppression can be associated with large shifts of the body clock. This association between the two responses has often been assumed to represent a functional relationship, resulting in the acceptance that one could be used as a proxy measure for the other. Circadian phase resetting is more difficult to measure than melatonin suppression, meaning the latter has often been used to assess disruption to the body clock caused by light exposure at night. However, this research has found that the magnitude of the shift in internal body clock is functionally independent from melatonin suppression. This casts doubt on the use of melatonin suppression as a proxy for circadian phase resetting. This knowledge may shape future research designed to improve treatments for depression and shift work sleep disorder.