The Sleeping Brain: Harnessing the Power of the Glymphatic System through Lifestyle Choices
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698404/
Deep sleep takes out the trash
https://www.sciencedaily.com/releases/2 ... 151044.htm
Now for the possible breakthrough.....I searched for similar background articles but found none..
Enhancing deep sleep
https://www.eurekalert.org/news-releases/949098
Might need a bit more research but seems to be on track.
Sleep
Re: Sleep
Hi Greyhound!Greyhound wrote: ↑Sat Apr 09, 2022 6:16 pm The Sleeping Brain: Harnessing the Power of the Glymphatic System through Lifestyle Choices
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698404/
Deep sleep takes out the trash
https://www.sciencedaily.com/releases/2 ... 151044.htm
Now for the possible breakthrough.....I searched for similar background articles but found none..
Enhancing deep sleep
https://www.eurekalert.org/news-releases/949098
Might need a bit more research but seems to be on track.
I liked this quote from the first article:
lifestyle choices such as sleep position, alcohol intake, exercise, omega-3 consumption, intermittent fasting and chronic stress all modulate glymphatic clearance. Lifestyle choices could therefore alter Alzheimer’s disease risk through improved glymphatic clearance, and could be used as a preventative lifestyle intervention for both healthy brain ageing and Alzheimer’s disease.
4/4 and still an optimist!
Re: Sleep
Yes I agree but some of those suggestions may only have minor positive effects.
Sleep position reminds me of a small study where if the head is raised by putting some blocks under the posts so an angle of about 30% will improve drainage of brain fluid and improve sleep. It takes about a few weeks before one gets the benefit. A small book was written by a couple from a Texas university who researched cultural practises of sleep. I wish I could recall title and their names PhD Sidney xxx?? Well they found that hammocks were used by natives and quite good. Anyways the book is a bit corney sounding and amusing in title and it was not universally useful to all reviewers but it seems to link with other research. Its was difficult to find on a search as there is so much already written on sleep.
edit....
Well after sleeping on the recall of the name of the book it came to me while reading the newspaper.
the title is 'Keep it Up"! I did various searches but was unable to find the book. I believe it was self published.
edit # 2 The book is called Get it Up.
read about it here.
edit 2 it should go the amazon books for the link...but I see it does not.
Sleep position reminds me of a small study where if the head is raised by putting some blocks under the posts so an angle of about 30% will improve drainage of brain fluid and improve sleep. It takes about a few weeks before one gets the benefit. A small book was written by a couple from a Texas university who researched cultural practises of sleep. I wish I could recall title and their names PhD Sidney xxx?? Well they found that hammocks were used by natives and quite good. Anyways the book is a bit corney sounding and amusing in title and it was not universally useful to all reviewers but it seems to link with other research. Its was difficult to find on a search as there is so much already written on sleep.
edit....
Well after sleeping on the recall of the name of the book it came to me while reading the newspaper.
the title is 'Keep it Up"! I did various searches but was unable to find the book. I believe it was self published.
edit # 2 The book is called Get it Up.
read about it here.
edit 2 it should go the amazon books for the link...but I see it does not.
Last edited by Greyhound on Sun Apr 17, 2022 8:42 pm, edited 3 times in total.
Re: Sleep
MORE ON SLEEP
Restoring normal sleep reduces amyloid-beta accumulation in mouse model of Alzheimer’s disease
Peer-Reviewed Publication
Baylor College of Medicine
Multiple studies in humans and mouse models indicate that sleep disruptions raise the risk of Alzheimer’s disease (AD) by increasing the accumulation of disease-relevant proteins such as amyloid-beta (A-beta) in the brain. In the current study, a team led by researchers at Baylor College of Medicine discovered that, in an animal model of Alzheimer’s disease, restoring normal sleep by returning to normal the activity of the thalamic reticular nucleus (TRN), a brain region involved in maintaining stable sleep, reduced the accumulation of A-beta plaques in the brain.
Published in the journal Science Translational Medicine, the study suggests that TRN not only may play a previously unsuspected driving role in symptoms associated with Alzheimer’s, but also that restoring its normal activity could be a potential therapeutic approach for this severe condition.
The TRN is quiet in AD
“Our interest in studying the TRN in the context of Alzheimer’s disease began when we observed in an animal model that TRN activity was generally reduced when compared to the TRN activity of animals without the condition,” said corresponding author Dr. Jeannie Chin, associate professor of neuroscience at Baylor.
When we sleep, the TRN is in general more active than when we are awake, Chin explained. This increased TRN activity reduces the perception of peripheral sensory information. Consequently, when we sleep, we typically are not aware of sounds, lights and other sensations, which helps us get a good night sleep.
“Observing that the TRN in our animal model was less active than in animals without the condition, we investigated the possibility that a quiet TRN could be a reason for the sleep interruptions that are common in people with Alzheimer’s disease,” said first author Dr. Rohan Jagirdar, an instructor in the Chin lab.
The researchers began by determining whether their Alzheimer’s disease mice would wake up more often than mice without the disease during normal sleeping hours. Using a wireless system to record the animals’ brain activity, the researchers discovered that, indeed, the Alzheimer’s mice woke up 50% more times than non-Alzheimer’s mice. Moreover, the Alzheimer’s mice got less than the normal amount of slow wave sleep, the deep restorative sleep during which waste products and metabolites are cleared from the brain. This was observed in the early stages of disease progression, before the animals developed memory deficits.
“This finding is relevant to the human condition, as research has shown that sleep fragmentation and other sleep disturbances in cognitively normal people are associated with increased Alzheimer’s disease risk,” Chin said. “When AD mice got older, reaching about three to five months, their sleep continued to be disrupted and they also presented with memory deficits.”
Quiet TRN linked to A-beta plaque load
In the AD animal model, measurable levels of A-beta began to appear in the brain when the mice reached about one month of age and began to deposit into plaques by approximately six months of age.
“We assessed whether the sleep fragmentation and reduction of slow wave sleep that we observed in our AD mouse model might be associated with the accumulation of A-beta at later stages, by examining mice at six to seven months of age,” Jagirdar said. “We found that the magnitude of sleep fragmentation was directly related to plaque load in the brains of six-month-old AD mice.”
Taken together, these findings show that AD mice present disruptions in sleep that could influence the accumulation of proteins involved in disease progression.
In addition, Chin, Jagirdar and their colleagues analyzed postmortem tissues from patients who had either Alzheimer’s disease, mild cognitive impairment or none of those conditions. They discovered that, as they had found in the mouse model, neurons in the TRN of Alzheimer’s patients showed signs of having been less active when compared to the controls. Also, the brains of AD patients with the least active TRN had the highest A-beta plaque deposition. These findings support the possibility of a relationship between reduced TRN activity and increased accumulation of disease-causing proteins in AD.
Could reactivating TRN improve the condition?
Using a chemogenetic system, a technology that allows one to chemically activate specific cells, the team activated TRN neurons in the animal model. After a single round of chemogenetic activation of the TRN, the AD-mice woke up less often and spent more time in slow wave sleep, signs of improved sleep activity.
“It was exciting to see that, after receiving chemogenetic activation of the TRN daily for a month, the AD mice showed sustained activation of TRN neurons, consistent improvements in sleep and, remarkably, reduced accumulation of A-beta,” Chin said.
The researchers point out that, although this approach seems to improve sleep disruption and A-beta deposition in this mouse model of Alzheimer’s disease, not all sleep disturbances involve TRN.
“Sleep disturbances are associated with a number of disorders and arise from diverse causes,” Jagirdar explained. “Targeting the TRN may not be as effective if the sleep disturbance is due to unrelated causes, such as obstructive sleep apnea or restless leg syndrome.”
“Our findings support that selective activation of the TRN is a promising therapeutic intervention to improve sleep disturbances and slow the accumulation of A-beta in AD,” Chin said.
https://www.eurekalert.org/news-releases/933728
Restoring normal sleep reduces amyloid-beta accumulation in mouse model of Alzheimer’s disease
Peer-Reviewed Publication
Baylor College of Medicine
Multiple studies in humans and mouse models indicate that sleep disruptions raise the risk of Alzheimer’s disease (AD) by increasing the accumulation of disease-relevant proteins such as amyloid-beta (A-beta) in the brain. In the current study, a team led by researchers at Baylor College of Medicine discovered that, in an animal model of Alzheimer’s disease, restoring normal sleep by returning to normal the activity of the thalamic reticular nucleus (TRN), a brain region involved in maintaining stable sleep, reduced the accumulation of A-beta plaques in the brain.
Published in the journal Science Translational Medicine, the study suggests that TRN not only may play a previously unsuspected driving role in symptoms associated with Alzheimer’s, but also that restoring its normal activity could be a potential therapeutic approach for this severe condition.
The TRN is quiet in AD
“Our interest in studying the TRN in the context of Alzheimer’s disease began when we observed in an animal model that TRN activity was generally reduced when compared to the TRN activity of animals without the condition,” said corresponding author Dr. Jeannie Chin, associate professor of neuroscience at Baylor.
When we sleep, the TRN is in general more active than when we are awake, Chin explained. This increased TRN activity reduces the perception of peripheral sensory information. Consequently, when we sleep, we typically are not aware of sounds, lights and other sensations, which helps us get a good night sleep.
“Observing that the TRN in our animal model was less active than in animals without the condition, we investigated the possibility that a quiet TRN could be a reason for the sleep interruptions that are common in people with Alzheimer’s disease,” said first author Dr. Rohan Jagirdar, an instructor in the Chin lab.
The researchers began by determining whether their Alzheimer’s disease mice would wake up more often than mice without the disease during normal sleeping hours. Using a wireless system to record the animals’ brain activity, the researchers discovered that, indeed, the Alzheimer’s mice woke up 50% more times than non-Alzheimer’s mice. Moreover, the Alzheimer’s mice got less than the normal amount of slow wave sleep, the deep restorative sleep during which waste products and metabolites are cleared from the brain. This was observed in the early stages of disease progression, before the animals developed memory deficits.
“This finding is relevant to the human condition, as research has shown that sleep fragmentation and other sleep disturbances in cognitively normal people are associated with increased Alzheimer’s disease risk,” Chin said. “When AD mice got older, reaching about three to five months, their sleep continued to be disrupted and they also presented with memory deficits.”
Quiet TRN linked to A-beta plaque load
In the AD animal model, measurable levels of A-beta began to appear in the brain when the mice reached about one month of age and began to deposit into plaques by approximately six months of age.
“We assessed whether the sleep fragmentation and reduction of slow wave sleep that we observed in our AD mouse model might be associated with the accumulation of A-beta at later stages, by examining mice at six to seven months of age,” Jagirdar said. “We found that the magnitude of sleep fragmentation was directly related to plaque load in the brains of six-month-old AD mice.”
Taken together, these findings show that AD mice present disruptions in sleep that could influence the accumulation of proteins involved in disease progression.
In addition, Chin, Jagirdar and their colleagues analyzed postmortem tissues from patients who had either Alzheimer’s disease, mild cognitive impairment or none of those conditions. They discovered that, as they had found in the mouse model, neurons in the TRN of Alzheimer’s patients showed signs of having been less active when compared to the controls. Also, the brains of AD patients with the least active TRN had the highest A-beta plaque deposition. These findings support the possibility of a relationship between reduced TRN activity and increased accumulation of disease-causing proteins in AD.
Could reactivating TRN improve the condition?
Using a chemogenetic system, a technology that allows one to chemically activate specific cells, the team activated TRN neurons in the animal model. After a single round of chemogenetic activation of the TRN, the AD-mice woke up less often and spent more time in slow wave sleep, signs of improved sleep activity.
“It was exciting to see that, after receiving chemogenetic activation of the TRN daily for a month, the AD mice showed sustained activation of TRN neurons, consistent improvements in sleep and, remarkably, reduced accumulation of A-beta,” Chin said.
The researchers point out that, although this approach seems to improve sleep disruption and A-beta deposition in this mouse model of Alzheimer’s disease, not all sleep disturbances involve TRN.
“Sleep disturbances are associated with a number of disorders and arise from diverse causes,” Jagirdar explained. “Targeting the TRN may not be as effective if the sleep disturbance is due to unrelated causes, such as obstructive sleep apnea or restless leg syndrome.”
“Our findings support that selective activation of the TRN is a promising therapeutic intervention to improve sleep disturbances and slow the accumulation of A-beta in AD,” Chin said.
https://www.eurekalert.org/news-releases/933728
