Having problems while sleeping is an early indicator of Alzheimer’s disease. Patients with Alzheimer’s face a lack of sleep, trouble while sleeping, and cognitive symptoms such as memory loss and confusion. Alzheimer’s disease causes brain changes that interrupt sleeping patterns and poor sleep.

According to a recent study, people who take sleeping pill before bed experience a drop in Alzheimer’s proteins which is a good sign as the higher level of Alzheimer’s protein worsens the disease.  It has been found that a sleeping aid known as suvorexant which is already approved by the Food and Drug Administration (FDA) for insomnia has the potential of sleep medications to slow or stop the development of Alzheimer’s disease.

The sleeping medication Suvorexant is also used to treat insomnia known as dual orexin receptor antagonists. Orexin is a natural biomolecule that promotes wakefulness and when it is blocked, people fall asleep.

The disease of Alzheimer’s starts developing when plaques of the protein amyloid beta start building up in the brain. After the accumulation of amyloid, a second brain protein, tau starts to form tangles that are toxic to neurons. People with Alzheimer’s disease experience cognitive symptoms such as memory loss around the time tau tangles become detectable.

The study involved 38 participants of aged 45-65 with no cognitive impairments to undergo a two-night sleep study. A number of 13 participants were given a lower dose of suvorexant while 12 people were given a higher dose of suvorexant or a placebo to 13 people at 9 p.m. Researchers withdrew a small amount of cerebrospinal fluid via spinal tap every two hours for 36 hours, starting one hour before the sleeping aid or placebo was administered, to measure how amyloid and tau levels changed over the next day and a half.

As a result, Amyloid levels dropped 10% to 20% in the cerebrospinal fluid of people who had received the high dose of suvorexant compared to people who had received placebo, and the levels of a key form of tau known as hyperphosphorylated tau dropped 10% to 15%, compared to people who had received placebo. Both differences are statistically significant. There was not a significant difference between the people who received a low dose of suvorexant and those who received the placebo.

Moreover, the accumulation of amyloid plaques in the brain will decrease over time and hyperphosphorylated tau is very important in the development of Alzheimer’s disease, as it is associated with forming tau tangles that kill neurons. Reducing tau phosphorylation, potentially would lead to less tangle formation and less neuronal death.

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