Alzheimer’s is quite a deadly disease. There are apparently various factors within our body only which may be responsible in causing the disease. Now a new research from Washington University School of Medicine in St. Louis claims that chronic sleep deprivation in a mouse model of Alzheimer’s disease could make Alzheimer’s brain plaques emerge in advance and more frequently.
It was also found out that orexin, a protein that may assist in regulating the sleep cycle, apparently seemed to be directly involved in the increase. Neuro-degenerative disorders such as Alzheimer’s disease and Parkinson’s disease could frequently disturb sleep. These latest results are claimed to be some of the first signs that sleep loss could play a function in the origin of such disorders.
“Orexin or compounds it interacts with may become new drug targets for treatment of Alzheimer’s disease. The results also suggest that we may need to prioritize treating sleep disorders not only for their many acute effects but also for potential long-term impacts on brain health,” commented Senior author David M. Holtzman, M.D., the Andrew and Gretchen Jones Professor and chair of the Department of Neurology at the School of Medicine and neurologist-in-chief at Barnes-Jewish Hospital,
A method called as vivo microdialysis is used by Holtzman’s laboratory, so as to observe levels of amyloid beta in the brains of mice which was apparently genetically engineered as a model of Alzheimer’s disease. Amyloid beta is claimed to be a protein fragment that may be the major constituent of Alzheimer’s plaques.
It was observed by Jae-Eun Kang, Ph.D., a post-doctoral fellow in Holtzman’s lab that brain amyloid beta levels in mice may rise and fall in connection with sleep and wakefulness, apparently rising in the night, when mice are said to be typically awake, and supposedly declining during the day, when they are believed to be generally asleep.
A different research of amyloid beta levels in human cerebrospinal fluid which was headed by Randall Bateman, M.D., assistant professor of neurology and a neurologist at Barnes-Jewish Hospital, apparently also illustrated that amyloid beta levels were claimed to be usually higher when participants were awake and lower when they slept.
To substantiate the relation, Kang supposedly learned to utilize electroencephalography (EEG) on the mice at the Sleep and Circadian Neurobiology Laboratory at Stanford University with researchers Seiji Nishino, M.D., Ph.D., and Nobuhiro Fujiki, M.D., Ph.D. The EEG readings facilitated the researchers to supposedly find out when the mice were asleep or awake and apparently corroborated the connection i.e. mice that apparently remained awake longer supposedly had higher amyloid beta levels.
Not allowing the mice to sleep apparently was the reason for an approximate 25 percent increase in amyloid beta levels. Levels were said to be lower when mice were permitted to sleep. Obstructing a hormone formerly associated with stress and amyloid beta production supposedly did not have any effect on these changes, alleging that they weren’t caused by the stress of sleep deprivation. This was the opinion of Hotzman.
Researchers, in a different place, had supposedly related mutations in orexin to narcolepsy, a disorder that may be illustrated by undue daytime sleepiness. The brain is believed to have two types of receptors for orexin, which is also said to be allied with regulation of feeding behavior.
When Holtzman’s group apparently inserted orexin into the brains of the mice, they supposedly remained awake for a longer time, and amyloid beta levels were believed to increase. When researchers made use of a drug known as almorexant to obstruct both orexin receptors, amyloid beta levels appeared to be considerably lower and animals were apparently not awake for much time.
Miranda M. Lim, M.D., Ph.D., a neurology resident and post-doctoral researcher in Holtzman’s lab, supposedly conducted long-term behavioral experiments with the mice. It was discovered that about three weeks of constant sleep deprivation apparently increased the speed of amyloid plaque deposition within the brain. In contrast, when mice received almorexant for around two months, plaque deposition appeared to notably reduce, apparently falling by more than 80 percent in some brain areas.
Holtzman observes that not only does the possibility of Alzheimer’s apparently boost with age, the sleep/wake cycle supposedly also begins to break down, with older adults gradually receiving less and less sleep. Holtzman also wants to learn more of the molecular details of how orexin apparently influence amyloid beta.
Further researches may deal with the questions of whether increased amyloid beta during wakefulness may be associated with increased synaptic activity and whether a few facets of sleep may lower amyloid beta levels independent of synaptic activity.
The findings were published in Science Express.