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Image credit: Pixabay Many people aspire to sleep just 4-6 hours a day and still be energized and quick-witted
.
For many people, this is indeed a fantasy, but for 1% to 3% of people, this is their real life, and they occasionally complain about waking up too early, but more often they enjoy the familial DNA mutation.
Their sleep advantages, such as mentality, being active, completing their studies faster, and being less prone to dementia
.
Written by | clefable reviewer | Li Shiyuan Few people can always be a "night owl" and an "early bird" at the same time.
In order to get enough rest for the body, most people need 7-8 hours of sleep every day
.
But the remaining 1% to 3% of people will be at the intersection of the two, only need to sleep 4 to 6 hours a day, and do not need a nap
.
Their situation is called Familial Natural Short Sleep.
The time of waking up for this kind of people is 30~60 days longer than normal people in one year, and they can spend about 5~10 days longer than normal people in their lifetime.
years of sobriety - in a sense, they "live" much longer than the average person
.
Genes That Change Sleep In 2009, Leihui Fu, a professor of neurobiology at the University of California, San Francisco, who was elected to the National Academy of Sciences in 2018, received a woman who was troubled by her sleep situation
.
"I wake up at 4 a.
m.
every morning, which is way too early," she complained
.
The professor thought she was an extreme "early bird" and went to bed very early, but she didn't expect that she usually went to bed at midnight
.
Not only her, but some of her family members as well
.
Realizing that the symptom might run in families, Professor Fu and colleagues set out to sequence the genome of the woman and her family, including some who slept normally
.
Fu Yanhui Image source: The official website of the University of California, San Francisco By comparing, they quickly found the differences between the genomes of the family
.
The woman and some of her family have a small mutation in the DEC2 gene (P384R), which may be the key to making them sleep less than people with normal sleep needs
.
Subsequently, Professor Fu et al.
conducted experiments on mice and found that when the mice had a mutation in the DEC2 gene, they slept less, but performed better than normal mice on both physical and cognitive tasks.
.
As more people with similar experiences were included in the study, they also found two other genetic mutations, in the ADRB1 and NPSR1 genes
.
A mutation in the gene ADRB1, which expresses a receptor on neurons, makes people more likely to be awakened by light
.
NPSR1 expresses a neuropeptide S receptor, which is mutated (two sites on the protein have mutations, Y206H and N107I, Y206H has a greater impact), which can make people under strong sleep pressure, Remaining awake, resulting in shorter sleep duration but consolidating memories
.
When these genetic mutations were repeated in mice, they also slept less without adversely affecting their health
.
Later, other researchers found that another gene—GRM1—had similar effects in humans and mice
.
Reasons for not becoming stupid For normal people like us, sleeping only 4-6 hours a day is sleep deprivation.
If we do this for a long time, our brain and body will be seriously damaged, and our faces will look lifeless.
You age faster and you have an increased risk of cardiovascular disease and various types of inflammation
.
According to some studies, we now know that sleep less and more sleep are not good for the brain and may increase the risk of dementia, the most common of which is Alzheimer's disease (AD)
.
Sleep deprivation makes AD-related pathological molecules more likely to appear in the brains of mice, and as AD becomes more severe, the sleep patterns of mice gradually become disordered
.
It's a vicious cycle: poor sleep makes AD worse, and severe AD symptoms make sleep worse
.
A similar situation exists in AD patients
.
However, for high-quality sleepers, this amount of sleep is enough to rejuvenate them
.
Not only do they have more time to wake up, but they are more active in their attitudes and actions, and even perform better than normal people in work and study
.
Despite getting less sleep, some studies have found no increased risk of dementia
.
Could it reduce their sleep genes and help them fight those negative effects? In a study published in iScience, Professor Fu and colleagues uncovered the changes brought about by these genetic mutations, which turned out to actually give some people the advantage of sleeping more efficiently and living Be more active and not get dementia
.
They mainly studied two gene mutations associated with familial natural short sleep: DEC2-P384R (a proline on the gene expressed protein changed to an arginine) and Npsr1-Y206H (a tyrosine changed to an arginine) a histidine)
.
They crossed mice with these two gene mutations and mice prone to AD to test whether these gene mutations could alleviate the development of AD in the mice
.
It needs to be introduced first that Alzheimer's disease is caused by two misfolded proteins: beta-amyloid and hyperphosphorylated tau
.
As AD progresses, these two proteins accumulate in or around neurons and form plaques and tangles, which in turn trigger inflammation, destroy neurons, and cause patients to lose normal cognition, memory, and other abilities
.
Although mice are susceptible to Alzheimer's disease, gene mutations related to FNSS can reduce amyloid plaques in the brains of mice.
Picture from research paper 1 For mice prone to AD, they 3 At the age of one month, the symptoms of AD will appear initially, and after 6 months, there will be obvious beta-amyloid plaques in the brain, and cognitive decline will be more obvious
.
If AD-prone mice also carried the DEC2-P384R mutation, at 3 months of age they were no different from AD-prone mice without the mutation, but at 6 months of age their There are significantly fewer beta-amyloid plaques in the cerebral cortex and hippocampus, making them less prone to AD and other dementias
.
The same is true for tau proteins
.
In addition, AD-prone mice with Npsr1-Y206H also had significantly lower levels of tau protein hyperphosphorylation in the cerebral cortex and hippocampus at 6 months of age than in AD-prone mice without this mutation.
mice
.
In general, the hyperphosphorylated tau protein (also known as T-tau) loses its normal function, triggering AD, and in these mutant mice, this is suppressed
.
In the brains of AD-prone mice with DEC2-P384R or Npsr1-Y206H, there seems to be a game between these genes
.
By the time these mice were 3 months old, they already had a lot of tau and phosphorylated tau in their brains, and the hyperphosphorylated proteins were already present in their brains compared to mice that did not carry the mutation but were prone to AD.
The enzymes are also expressed normally, but the chances of these tau proteins being hyperphosphorylated are low
.
That is to say, these proteins can already go "bad" at this point, but they have not actually changed
.
The researchers believe that DEC2-P384R and Npsr1-Y206H are preventing them from becoming "bad," possibly by inhibiting their continued phosphorylation
.
PS19 mice are more prone to Alzheimer's disease, and their brains have many hyperphosphorylated tau proteins, and the Npsr1-Y206H mutation reduces these toxic proteins in the mouse brains
.
The picture comes from the paper.
Another explanation is that the glial lymphatic system in the brain can speed up the removal of harmful plaques
.
During sleep, the cerebrospinal fluid in the brain helps remove these harmful metabolites before they damage the brain
.
The researchers found that the amount of phosphorylated tau protein in the waste products excreted in the cerebrospinal fluid of DEC2-P384R-carrying mice did increase at 3 months of age, and by 6 months of age, the levels had increased significantly
.
Enhanced excretion undoubtedly reduces the likelihood of plaque buildup in the brain, damaging neurons
.
On the other hand, the Npsr1-Y206H mutation actually makes the NPSR1 receptor it expresses more active, which theoretically results in more tau protein outside the cell, and can cause synaptic damage and more scarring in the brain, but In reality these processes do not take place
.
This is because Npsr1-Y206H also increases the ability of some cells in the brain to phagocytose and degrade tau protein, reducing synaptic damage and brain scarring, making mice less susceptible to AD
.
Familial sleep characteristics After understanding such a useful and anti-dementia gene, you may have begun to envy people who have familial natural short sleep
.
Undoubtedly, this group of people is lucky because there are others who have other familial sleep problems, but they often have some bad or even painful experiences
.
For example, people with familial advanced sleep-wake phase syndrome will feel sleepy at 4-5 pm and need to sleep, and usually wake up at 1-2 am.
A very lonely moment, sober they can only do some things by themselves
.
This symptom is more likely to appear in middle-aged and elderly people
.
Others have Familial Natural Long Sleep, which requires more than 8 hours of sleep a day to restore energy
.
In addition, there is a very serious genetic disease, fatal familial insomnia (FFI), in which patients suffer from insomnia, hallucinations, memory impairment, and abnormal bodily functions
.
As the disease worsened, their insomnia symptoms would get worse
.
Patients usually die within a few months to several years after becoming ill
.
This is because they have abnormalities in the common prion proteins in their brains, which are endogenous prions, causing more prion proteins to misfold and pile up, causing these severe symptoms
.
It is gratifying that the first clinical trial for human prion diseases such as FFI has achieved relatively satisfactory results
.
Some patients in the trial showed signs of improvement after receiving antibodies against the prion protein
.
Previously, 70% of patients died within a year of diagnosis
.
In the face of this ferocious disease, mankind has taken another giant step forward
.
Reference link: https:// (original paper) https://en.
wikipedia.
org/wiki/Familial_sleep_traitshttps:// nih-research-matters/lack-sleep-middle-age-may-increase-dementia-riskhttps:// ucsf.
edu/news/2019/08/415261/after-10-year-search-scientists-find-second-short-sleep-gene https:// Click on the picture or read the original text when the new issue of "Universal Science" is on sale in March.
Click [Watching] to receive our content updates in a timely manner.
.
For many people, this is indeed a fantasy, but for 1% to 3% of people, this is their real life, and they occasionally complain about waking up too early, but more often they enjoy the familial DNA mutation.
Their sleep advantages, such as mentality, being active, completing their studies faster, and being less prone to dementia
.
Written by | clefable reviewer | Li Shiyuan Few people can always be a "night owl" and an "early bird" at the same time.
In order to get enough rest for the body, most people need 7-8 hours of sleep every day
.
But the remaining 1% to 3% of people will be at the intersection of the two, only need to sleep 4 to 6 hours a day, and do not need a nap
.
Their situation is called Familial Natural Short Sleep.
The time of waking up for this kind of people is 30~60 days longer than normal people in one year, and they can spend about 5~10 days longer than normal people in their lifetime.
years of sobriety - in a sense, they "live" much longer than the average person
.
Genes That Change Sleep In 2009, Leihui Fu, a professor of neurobiology at the University of California, San Francisco, who was elected to the National Academy of Sciences in 2018, received a woman who was troubled by her sleep situation
.
"I wake up at 4 a.
m.
every morning, which is way too early," she complained
.
The professor thought she was an extreme "early bird" and went to bed very early, but she didn't expect that she usually went to bed at midnight
.
Not only her, but some of her family members as well
.
Realizing that the symptom might run in families, Professor Fu and colleagues set out to sequence the genome of the woman and her family, including some who slept normally
.
Fu Yanhui Image source: The official website of the University of California, San Francisco By comparing, they quickly found the differences between the genomes of the family
.
The woman and some of her family have a small mutation in the DEC2 gene (P384R), which may be the key to making them sleep less than people with normal sleep needs
.
Subsequently, Professor Fu et al.
conducted experiments on mice and found that when the mice had a mutation in the DEC2 gene, they slept less, but performed better than normal mice on both physical and cognitive tasks.
.
As more people with similar experiences were included in the study, they also found two other genetic mutations, in the ADRB1 and NPSR1 genes
.
A mutation in the gene ADRB1, which expresses a receptor on neurons, makes people more likely to be awakened by light
.
NPSR1 expresses a neuropeptide S receptor, which is mutated (two sites on the protein have mutations, Y206H and N107I, Y206H has a greater impact), which can make people under strong sleep pressure, Remaining awake, resulting in shorter sleep duration but consolidating memories
.
When these genetic mutations were repeated in mice, they also slept less without adversely affecting their health
.
Later, other researchers found that another gene—GRM1—had similar effects in humans and mice
.
Reasons for not becoming stupid For normal people like us, sleeping only 4-6 hours a day is sleep deprivation.
If we do this for a long time, our brain and body will be seriously damaged, and our faces will look lifeless.
You age faster and you have an increased risk of cardiovascular disease and various types of inflammation
.
According to some studies, we now know that sleep less and more sleep are not good for the brain and may increase the risk of dementia, the most common of which is Alzheimer's disease (AD)
.
Sleep deprivation makes AD-related pathological molecules more likely to appear in the brains of mice, and as AD becomes more severe, the sleep patterns of mice gradually become disordered
.
It's a vicious cycle: poor sleep makes AD worse, and severe AD symptoms make sleep worse
.
A similar situation exists in AD patients
.
However, for high-quality sleepers, this amount of sleep is enough to rejuvenate them
.
Not only do they have more time to wake up, but they are more active in their attitudes and actions, and even perform better than normal people in work and study
.
Despite getting less sleep, some studies have found no increased risk of dementia
.
Could it reduce their sleep genes and help them fight those negative effects? In a study published in iScience, Professor Fu and colleagues uncovered the changes brought about by these genetic mutations, which turned out to actually give some people the advantage of sleeping more efficiently and living Be more active and not get dementia
.
They mainly studied two gene mutations associated with familial natural short sleep: DEC2-P384R (a proline on the gene expressed protein changed to an arginine) and Npsr1-Y206H (a tyrosine changed to an arginine) a histidine)
.
They crossed mice with these two gene mutations and mice prone to AD to test whether these gene mutations could alleviate the development of AD in the mice
.
It needs to be introduced first that Alzheimer's disease is caused by two misfolded proteins: beta-amyloid and hyperphosphorylated tau
.
As AD progresses, these two proteins accumulate in or around neurons and form plaques and tangles, which in turn trigger inflammation, destroy neurons, and cause patients to lose normal cognition, memory, and other abilities
.
Although mice are susceptible to Alzheimer's disease, gene mutations related to FNSS can reduce amyloid plaques in the brains of mice.
Picture from research paper 1 For mice prone to AD, they 3 At the age of one month, the symptoms of AD will appear initially, and after 6 months, there will be obvious beta-amyloid plaques in the brain, and cognitive decline will be more obvious
.
If AD-prone mice also carried the DEC2-P384R mutation, at 3 months of age they were no different from AD-prone mice without the mutation, but at 6 months of age their There are significantly fewer beta-amyloid plaques in the cerebral cortex and hippocampus, making them less prone to AD and other dementias
.
The same is true for tau proteins
.
In addition, AD-prone mice with Npsr1-Y206H also had significantly lower levels of tau protein hyperphosphorylation in the cerebral cortex and hippocampus at 6 months of age than in AD-prone mice without this mutation.
mice
.
In general, the hyperphosphorylated tau protein (also known as T-tau) loses its normal function, triggering AD, and in these mutant mice, this is suppressed
.
In the brains of AD-prone mice with DEC2-P384R or Npsr1-Y206H, there seems to be a game between these genes
.
By the time these mice were 3 months old, they already had a lot of tau and phosphorylated tau in their brains, and the hyperphosphorylated proteins were already present in their brains compared to mice that did not carry the mutation but were prone to AD.
The enzymes are also expressed normally, but the chances of these tau proteins being hyperphosphorylated are low
.
That is to say, these proteins can already go "bad" at this point, but they have not actually changed
.
The researchers believe that DEC2-P384R and Npsr1-Y206H are preventing them from becoming "bad," possibly by inhibiting their continued phosphorylation
.
PS19 mice are more prone to Alzheimer's disease, and their brains have many hyperphosphorylated tau proteins, and the Npsr1-Y206H mutation reduces these toxic proteins in the mouse brains
.
The picture comes from the paper.
Another explanation is that the glial lymphatic system in the brain can speed up the removal of harmful plaques
.
During sleep, the cerebrospinal fluid in the brain helps remove these harmful metabolites before they damage the brain
.
The researchers found that the amount of phosphorylated tau protein in the waste products excreted in the cerebrospinal fluid of DEC2-P384R-carrying mice did increase at 3 months of age, and by 6 months of age, the levels had increased significantly
.
Enhanced excretion undoubtedly reduces the likelihood of plaque buildup in the brain, damaging neurons
.
On the other hand, the Npsr1-Y206H mutation actually makes the NPSR1 receptor it expresses more active, which theoretically results in more tau protein outside the cell, and can cause synaptic damage and more scarring in the brain, but In reality these processes do not take place
.
This is because Npsr1-Y206H also increases the ability of some cells in the brain to phagocytose and degrade tau protein, reducing synaptic damage and brain scarring, making mice less susceptible to AD
.
Familial sleep characteristics After understanding such a useful and anti-dementia gene, you may have begun to envy people who have familial natural short sleep
.
Undoubtedly, this group of people is lucky because there are others who have other familial sleep problems, but they often have some bad or even painful experiences
.
For example, people with familial advanced sleep-wake phase syndrome will feel sleepy at 4-5 pm and need to sleep, and usually wake up at 1-2 am.
A very lonely moment, sober they can only do some things by themselves
.
This symptom is more likely to appear in middle-aged and elderly people
.
Others have Familial Natural Long Sleep, which requires more than 8 hours of sleep a day to restore energy
.
In addition, there is a very serious genetic disease, fatal familial insomnia (FFI), in which patients suffer from insomnia, hallucinations, memory impairment, and abnormal bodily functions
.
As the disease worsened, their insomnia symptoms would get worse
.
Patients usually die within a few months to several years after becoming ill
.
This is because they have abnormalities in the common prion proteins in their brains, which are endogenous prions, causing more prion proteins to misfold and pile up, causing these severe symptoms
.
It is gratifying that the first clinical trial for human prion diseases such as FFI has achieved relatively satisfactory results
.
Some patients in the trial showed signs of improvement after receiving antibodies against the prion protein
.
Previously, 70% of patients died within a year of diagnosis
.
In the face of this ferocious disease, mankind has taken another giant step forward
.
Reference link: https:// (original paper) https://en.
wikipedia.
org/wiki/Familial_sleep_traitshttps:// nih-research-matters/lack-sleep-middle-age-may-increase-dementia-riskhttps:// ucsf.
edu/news/2019/08/415261/after-10-year-search-scientists-find-second-short-sleep-gene https:// Click on the picture or read the original text when the new issue of "Universal Science" is on sale in March.
Click [Watching] to receive our content updates in a timely manner.
