Friday January 24, 2020

Poor Sleep May Signal The Risk of Alzheimer’s in Elderly

For the study, the team studied 119 people aged 60 or older among which almost 80 per cent were cognitively normal and the remainder were very mildly impaired

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Poor sleep can predict Alzheimer's Risk in elderly. Pixabay

Poor sleep quality may signal the risk of Alzheimer’s disease in older adults, a study suggests.

People with Alzheimer’s tend to wake up tired and their nights become even less refreshing as memory loss and other symptoms worsen.

However, the reason was not fully understood.

The study, led by the Washington University in St. Louis found that older adults who sleep poorly or have less slow-wave sleep — deep sleep needed to consolidate memories and wake up feeling refreshed — have higher levels of tau — a toxic brain protein.

Tau has also been linked to brain damage and cognitive decline.

“Measuring how people sleep may be a non-invasive way to screen for Alzheimer’s disease before or just as people begin to develop problems with memory and thinking,” said lead author Brendan Lucey, Assistant Professor from the varsity.

"The question for us now is not how to eliminate cholesterol from the brain, but about how to control cholesterol's role in Alzheimer's disease through the regulation of its interaction with amyloid-beta," Vendruscolo said.
In Alzheimer’s disease, patients start losing memory, Pixabay

Moreover, the findings, published in the journal Science Translational Medicine, showed that it was not the total amount of sleep that was linked to tau, but the slow-wave sleep, which reflects quality of sleep.

The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep.

“What’s interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired,” Lucey added.

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For the study, the team studied 119 people aged 60 or older among which almost 80 per cent were cognitively normal and the remainder were very mildly impaired.

Up to two decades before Alzheimer’s symptoms of memory loss and confusion appear, amyloid beta protein begins to collect into plaques in the brain. Tangles of tau appear later, followed by decline of key brain areas. Only then do people start showing unmistakable signs of cognitive decline.

The challenge is finding people on track to develop Alzheimer’s before such brain changes undermine their ability to think clearly. For that, sleep may be a handy marker, the researchers said. (IANS)

Next Story

This Protein in the Human Brain Can Protect Against Alzheimer’s disease

Brain protein that could protect against Alzheimer's disease

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Immune cells in the brain, called microglia, play a critical role in Alzheimer's disease. Pixabay

Researchers have found that a protein that regulates white blood cells in the human brain could protect against Alzheimer’s disease.

The results published in the journal Communications Biology suggest that this protein, called CD33, could have important implications in the fight against Alzheimer’s disease.

“Immune cells in the brain, called microglia, play a critical role in Alzheimer’s disease,” explained study co-author Matthew Macauley, Assistant Professor at University of Alberta in Edmonton, Canada.

“They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease,” Macauley added.

Scientists have identified the CD33 protein as a factor that may decrease a person’s likelihood of Alzheimer’s disease.

Brain
CD33 protein in the brain plays a crucial role in modulating the function of microglia. Pixabay

Now, Macauley’s research has shown that the most common type of CD33 protein plays a crucial role in modulating the function of microglia.

“The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer’s disease under the right circumstances,” said Abhishek Bhattacherjee, first author and postdoctoral fellow in the Macauley lab.

Alzheimer’s disease affects more than 44 million people around the world.

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“These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer’s Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease – by targeting CD33,” said Macauley.

“Microglia have the potential to ‘clean up’ the neurodegenerative plaques, through a process called phagocytosis — so a therapy to harness this ability to slow down or reverse Alzheimer’s disease can be envisioned,” Macauley said. (IANS)