Tuesday, June 9, 2015. The results of a double-blind trial reported in the journal Clinical Interventions in Aging indicate a benefit for prolonged-release melatonin in cognitive function and sleep in men and women with mild to moderate Alzheimer's disease.
Melatonin, a hormone released by the brain's pineal gland, initiates sleep in addition to being associated with other health benefits. "Sleep has an important role in memory consolidation," note Alan G. Wade and colleagues in the introduction to their article. "Emerging evidence links poor sleep to increased Alzheimer's disease risk and memory loss. However, to prove causality, it is important to show that improvement in sleep can ameliorate the disease."
Seventy-three patients receiving standard Alzheimer's disease drug therapy were randomized to receive two milligrams of prolonged-release melatonin or a placebo nightly for 24 weeks. Alzheimer's Disease Assessment Scale-Cognition, Instrumental Activities of Daily Living, Mini–Mental State Examination and Pittsburgh Sleep Quality Index assessments were administered at the beginning of the study and at 12 and 24 weeks, and a sleep diary documented midsleep awakenings.
After 24 weeks, those who received melatonin had significantly better cognitive performance, as indicated by two of three test results, compared to the placebo group. Improved sleep efficiency was also observed in the melatonin-treated group in comparison with baseline. Among a subgroup of 13 patients who had insomnia at the beginning of the trial, melatonin significantly improved all test results.
"A plausible mechanism for prolonged-release melatonin effects in Alzheimer's disease could be that the improved sleep efficiency leads to lower risk of accumulation of beta amyloid deposition and/or increase in beta amyloid clearance from the brain, which can ultimately result in the attenuation of Alzheimer's disease progression," the authors write. "If so, patients with good sleep quality can potentially also benefit from the neuroprotective effects of the hormone."
On December 22, 2014, the Proceedings of the National Academy of Science published findings by researchers at Boston's Brigham and Women's Hospital of a suppressive effect for evening use of light-emitting electronic devices on sleep and melatonin secretion.
"Electronic devices emit light that is short-wavelength-enriched light, which has a higher concentration of blue light — with a peak around 450 nm — than natural light," explained lead author Anne-Marie Chang. "This is different from natural light in composition, having a greater impact on sleep and circadian rhythms."
Twelve healthy adults were randomized to read a light-emitting eBook or a printed book in dim room light approximately four hours before bedtime for five evenings. At the end of the five day period, participants switched their assignments. Blood samples collected during portions of the study were analyzed for melatonin levels. Sleep latency, time and efficiency were assessed via polysomnography.
eBook reading was associated with more time needed to fall asleep and less rapid eye movement sleep in comparison with reading a printed book. Evening melatonin levels were suppressed by an average of 55.12% in eBook readers while those who read printed books had no suppression. Compared to printed book reading, the onset of melatonin release in response to dim light occurred 1 ½ hours later the day following reading of an eBook.
"Our most surprising finding was that individuals using the e-reader would be more tired and take longer to become alert the next morning," Dr Chang reported. "This has real consequences for daytime functioning, and these effects might be worse in the real world as opposed to the controlled environment we used."
"We live in a sleep-restricted society, in general," she added. "It is important to further study the effects of using light-emitting devices, especially before bed, as they may have longer term health consequences than we previously considered."
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A number of processes are believed to contribute to the cognitive decline observed in Alzheimer's disease. Brain deterioration in Alzheimer's disease is thought to begin decades before symptoms become evident.
Oxidative stress is a process in which highly reactive molecules called free radicals damage cellular structures. Free radicals are byproducts of normal metabolism, but during states of metabolic abnormality such as mitochondrial dysfunction, they are created more rapidly and in greater quantity. In the case of Alzheimer's disease, oxidative stress both facilitates some of the damage caused by amyloid beta and spurs its formation (Dong-gyu 2010; Hampel 2011).
Oxidative stress propagates Alzheimer's disease via another route as well. As neurons become damaged, free iron accumulates on their surfaces and within nearby cells called microglia. Free iron causes radical formation and drives oxidative stress (Mandel 2006).
Endogenous melatonin not only helps regulate the sleep-wake cycle, but is also a strong antioxidant (Bubenik 2011). Melatonin secretion within the brain declines with age, and lower levels are associated with a higher degree of cognitive impairment (Magri 2004). Melatonin concentration is lower in Alzheimer's patients than in healthy people of the same age (Cardinali 2011). In animal studies, melatonin improved cognitive function and reduced oxidative injury and deposition of amyloid beta (Cheng 2006). Additional studies have confirmed that melatonin protects brain cells from amyloid beta toxicity by impairing amyloid beta generation and slowing the formation of plaque deposits (Wang 2006a). Melatonin has also been shown to reduce tau tangles and amyloid beta toxicity (Srinivasan 2006).
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