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We’ve long known that people with Alzheimer’s disease often experience problems with their sleep. But according to a new study from the University of California, Berkeley, poor shut-eye in older adults may play a role in the development of the disease in the first place.
Scientists researching the potential connections between deep, restorative sleep and the protein fragment beta-amyloid recently found that poor sleep not only hinders the brain’s ability to save new memories, but also creates a channel through which this Alzheimer’s-triggering protein is able to travel and attack long-term memory storage.
“Over the past few years, the links between sleep, beta-amyloid, memory, and Alzheimer’s disease have been growing stronger,” William Jagust, a UC Berkeley neuroscientist, Alzheimer’s disease expert and co-leader of the study said in a statement. “Our study shows that this beta-amyloid deposition may lead to a vicious cycle in which sleep is further disturbed and memory impaired.”
This study is also one of the first of its kind to use human subjects, thanks to Jagust. He recruited 26 adult participants between the ages of 65 to 81 who had not yet been diagnosed with any form of dementia, or neurodegenerative, sleep or psychiatric disorders. They each received a PET scan to measure the accumulation of beta-amyloid in their brains, and were subsequently given 120 word pairs to memorize.
Each participant then slept for eight hours while an electroencephalographic test measured their brain waves. When they awoke the following morning, they received functional MRI scans to measure the activity occurring in the brain as they attempted to recall the word pairs from the night before. The results revealed that those with the highest levels of beta-amyloid residing in the medial frontal cortex not only had the poorest quality of sleep, but also performed the worst on the memory test. Some forgot more than half of the information they had consumed the previous day.
“The data we’ve collected are very suggestive that there’s a causal link,” said study co-leader Bryce Mander in a statement. “If we intervene to improve sleep, perhaps we can break that causal chain.”
Previous research has implicated the deposits of beta-amyloid in the development of Alzheimer’s disease, because it begins destroying synapses before clumping them into plaques in the brain that lead to the death of important nerve cells. But this new study suggests that, while poor sleep creates the pathway for this nerve damage to occur, it is an entirely treatable issue. According to Matthew Walker, a UC Berkeley neuroscience professor and senior author of this study, exercise, behavioral therapy and electrical stimulation of brain waves during sleep are all viable ways for young adults to increase their overnight memory — and protect against the build-up of beta-amyloid proteins.
“Sleep is helping wash away toxic proteins at night, preventing them from building up and from potentially destroying brain cells,” Walker said in a statement. “It’s providing a power cleanse for the brain.”
The aging of the baby boomer generation is expected to make Alzheimer’s disease one of the world’s fastest-growing and most debilitating public health issues, so this discovery offers a sense of hope. Sleep won’t just leave people feeling well rested — it may help them fight future memory loss, and even limit the degradation that is already occurring in those with dementia.
The study was published in the journal Nature Neuroscience earlier this week.
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