You are here: Home » Current Affairs » News » Health
Business Standard

Brain-based immune proteins may regulate sleep: Study

The immune proteins are collectively called as inflammasome NLRP3

Press Trust of India  |  Boston 

Image via Shutterstock
Image via Shutterstock

Sleep may be regulated in part by several brain-based immune proteins, according to a new study which may potentially help develop therapies for people with chronic sleep disorders.

The are collectively called as NLRP3, said researchers at Harvard Medical School (HMS) in the US.



The — which works by unleashing a cascade of immune molecules in response to inflammation and infection - emerges as a central promoter of sleep following such events.

Scientists have known for a while that certain immune molecules enhance sleep and are activated by infection, but this is the first study suggesting a common underlying mechanism that regulates sleep and plays a critical role in recuperative sleep responses.

The study, conducted on mice, show that the recruits a sleep-inducing molecule to trigger somnolence following sleep deprivation and exposure to a bacterial toxin.

Animals lacking genes for this protective immune complex showed profound sleep aberrations.

"Our research points, for the first time, to the acting as a universal sensing mechanism that regulates sleep through the release of immune molecules," said from HMS.

The observations suggest that the inflammasome, the constellation of sleep-regulating proteins, may play an evolutionary role as a guardian of and vitality that wards off the effects of sleep deprivation and infection.

"We already know that sleep plays a protective role in resolving infections so our observation of activation following infection suggests this immune mechanism may have a brain-protective role," said Zielinski.

If replicated in other studies, the researchers said the results may become the basis of therapies for people with chronic sleep disorders and sleep disturbances secondary to other diseases.

In a series of experiments, the scientists demonstrated that following sleep deprivation or exposure to bacteria, the activates an inflammatory molecule called interleukin-1 beta, known to induce sleep and promote sleep intensity.

The cells of mice lacking the gene coding for showed a marked absence of this sleep-inducing molecule.

The researchers compared the behaviour, sleep patterns and electrical activity in the brains of mice lacking the gene to those in a group of mice with intact genes.

Mice lacking the gene had abnormal sleep responses following sleep deprivation. On average, such mice slept less and experienced more sleep interruptions than mice with their genes intact.

The study was published in the journal Brain, Behaviour and Immunity.

RECOMMENDED FOR YOU

Brain-based immune proteins may regulate sleep: Study

The immune proteins are collectively called as inflammasome NLRP3

The immune proteins are collectively called as inflammasome NLRP3 Sleep may be regulated in part by several brain-based immune proteins, according to a new study which may potentially help develop therapies for people with chronic sleep disorders.

The are collectively called as NLRP3, said researchers at Harvard Medical School (HMS) in the US.

The — which works by unleashing a cascade of immune molecules in response to inflammation and infection - emerges as a central promoter of sleep following such events.

Scientists have known for a while that certain immune molecules enhance sleep and are activated by infection, but this is the first study suggesting a common underlying mechanism that regulates sleep and plays a critical role in recuperative sleep responses.

The study, conducted on mice, show that the recruits a sleep-inducing molecule to trigger somnolence following sleep deprivation and exposure to a bacterial toxin.

Animals lacking genes for this protective immune complex showed profound sleep aberrations.

"Our research points, for the first time, to the acting as a universal sensing mechanism that regulates sleep through the release of immune molecules," said from HMS.

The observations suggest that the inflammasome, the constellation of sleep-regulating proteins, may play an evolutionary role as a guardian of and vitality that wards off the effects of sleep deprivation and infection.

"We already know that sleep plays a protective role in resolving infections so our observation of activation following infection suggests this immune mechanism may have a brain-protective role," said Zielinski.

If replicated in other studies, the researchers said the results may become the basis of therapies for people with chronic sleep disorders and sleep disturbances secondary to other diseases.

In a series of experiments, the scientists demonstrated that following sleep deprivation or exposure to bacteria, the activates an inflammatory molecule called interleukin-1 beta, known to induce sleep and promote sleep intensity.

The cells of mice lacking the gene coding for showed a marked absence of this sleep-inducing molecule.

The researchers compared the behaviour, sleep patterns and electrical activity in the brains of mice lacking the gene to those in a group of mice with intact genes.

Mice lacking the gene had abnormal sleep responses following sleep deprivation. On average, such mice slept less and experienced more sleep interruptions than mice with their genes intact.

The study was published in the journal Brain, Behaviour and Immunity.
image
Business Standard
177 22

Brain-based immune proteins may regulate sleep: Study

The immune proteins are collectively called as inflammasome NLRP3

Sleep may be regulated in part by several brain-based immune proteins, according to a new study which may potentially help develop therapies for people with chronic sleep disorders.

The are collectively called as NLRP3, said researchers at Harvard Medical School (HMS) in the US.

The — which works by unleashing a cascade of immune molecules in response to inflammation and infection - emerges as a central promoter of sleep following such events.

Scientists have known for a while that certain immune molecules enhance sleep and are activated by infection, but this is the first study suggesting a common underlying mechanism that regulates sleep and plays a critical role in recuperative sleep responses.

The study, conducted on mice, show that the recruits a sleep-inducing molecule to trigger somnolence following sleep deprivation and exposure to a bacterial toxin.

Animals lacking genes for this protective immune complex showed profound sleep aberrations.

"Our research points, for the first time, to the acting as a universal sensing mechanism that regulates sleep through the release of immune molecules," said from HMS.

The observations suggest that the inflammasome, the constellation of sleep-regulating proteins, may play an evolutionary role as a guardian of and vitality that wards off the effects of sleep deprivation and infection.

"We already know that sleep plays a protective role in resolving infections so our observation of activation following infection suggests this immune mechanism may have a brain-protective role," said Zielinski.

If replicated in other studies, the researchers said the results may become the basis of therapies for people with chronic sleep disorders and sleep disturbances secondary to other diseases.

In a series of experiments, the scientists demonstrated that following sleep deprivation or exposure to bacteria, the activates an inflammatory molecule called interleukin-1 beta, known to induce sleep and promote sleep intensity.

The cells of mice lacking the gene coding for showed a marked absence of this sleep-inducing molecule.

The researchers compared the behaviour, sleep patterns and electrical activity in the brains of mice lacking the gene to those in a group of mice with intact genes.

Mice lacking the gene had abnormal sleep responses following sleep deprivation. On average, such mice slept less and experienced more sleep interruptions than mice with their genes intact.

The study was published in the journal Brain, Behaviour and Immunity.

image
Business Standard
177 22