Associated Professional Sleep Societies, June 6-10
The annual meeting of the Associated Professional Sleep Societies (SLEEP 2015) was held from June 6 to 10 in Seattle and attracted approximately 5,000 participants from around the world, including clinicians, academicians, allied health professionals, and others interested in sleep disorders. The conference featured scientific sessions and an exhibition hall focusing solely on sleep medicine and sleep research.
In one study, Akiko Satoh, Ph.D., of the Washington University School of Medicine in Saint Louis, and colleagues found that deletion of the Prdm13 gene, exclusively expressed in a particular portion of the hypothalamus -- the dorsomedial hypothalamus (DMH), promotes sleep fragmentation and strikingly affects sleep quality in mice. In addition, the investigators also found that DMH-specific Prdm13-knockdown mice gradually gain weight, suggesting that sleep fragmentation induced by a deficit in the DMH-enriched gene Prdm13 ultimately causes metabolic complications.
"Our study also pointed to a possibility that Prdm13 in the DMH might play an important role in the regulation of age-associated physiological changes," Satoh said. "We are aware that this might be an overstatement, because the evidence we have is only an association (i.e., expression of Prdm13 in the hypothalamus declines with advanced age, whereas it increased under diet restriction, which is a well-known anti-aging intervention in several organisms. Moreover, long-lived mouse model brain-specific Sirt1-overexpressing transgenic mice (BRASTO) mice display increased Prdm13 expression in the DMH compared with wild-type control mice)."
In another study, Kelly Glazer Baron, Ph.D., M.P.H., of Northwestern University's Feinberg School of Medicine in Chicago, and colleagues evaluated the association between the alignment of the sleep period with the internal biological rhythm. The investigators used a measure called "phase angle," which is the duration between when melatonin goes up and when the individual goes to sleep. The investigators were interested in understanding how this measure of alignment of sleep and the internal circadian rhythm were associated with caloric intake, body mass index, and body fat.
"We found that individuals with a shorter phase angle between melatonin and sleep (i.e., fell asleep close to when melatonin went up) ate more calories per day and had more meals per week. For men, shorter phase angle was associated with higher body fat," Baron said. "Even among healthy non-shift workers, we found that a measure of circadian rhythm alignment was related to dietary behavior, and in men, body fat. Future studies may seek to improve phase alignment as a way to reduce obesity and metabolic disease."
Melissa Chee, M.D., Terry Maratos-Flier, M.D., and Elda Arrigoni, Ph.D., of Harvard Medical School in Boston, found that melanin-concentrating hormone (MCH) neurons have the synaptic machinery to release glutamate. In a brain slice, the investigators used novel optogenetic techniques to selectively turn on only the MCH cells. By doing so, the investigators were able to evoke glutamate release from MCH cells.
"MCH neurons can release glutamate. This is an important finding because it tells us that in a sleep circuit, MCH neurons can directly activate the 'rapid eye movement generator,'" Chee said. "Our findings show that previous models of MCH neurons in neural circuits of sleep must be reconsidered. We and others are continuing to elucidate the neural pathways underlying sleep circuitry. With more detailed understanding of neural circuits controlling sleep and wake, we may enable the development of more refined pharmacological therapies in sleep-wake disorders."