Scientists from the University of Columbia, Berkeley believe that sleeplessness leads to memory loss as a deficit of the deep, restorative slumber needed to hit the save button on memories in turn leads to the beta-amyloid protein to trigger Alzheimer’s disease.
“Our findings reveal a new pathway through which Alzheimer’s disease may cause memory decline later in life,” said UCB’s neuroscience professor Matthew Walker, in a paper published in the journal Nature Neuroscience.
Excess beta-amyloid is suspected to be behind the Alzheimer’s disease, or extreme form of dementia due to death of brain cells. Alzheimer’s is one of the world’s fastest-growing disease with 40 million people, mostly elders and aged people, afflicted by it.
Walker is however, confident that good sleep is the answer to delay the Alzheimer’s disease. Besides good sleep, exercise, behavioral therapy and even electrical stimulation that amplifies brain waves during sleep, a technology that has been used successfully in young adults to increase their overnight memory can be used to treat the disease, he said.
“This discovery offers hope,” Walker said. “Sleep could be a novel therapeutic target for fighting back against memory impairment in older adults and even those with dementia.”
The study, led by other UC Berkeley neuroscientists Bryce Mander and William Jagust, tried to test their hypothesis that sleep is an early warning sign or biomarker of Alzheimer’s disease and a human trial taken up by Jagust proved successful in finding that the results were positive.
“Over the past few years, the links between sleep, beta-amyloid, memory, and Alzheimer’s disease have been growing stronger,” Jagust said. “Our study shows that this beta-amyloid deposition may lead to a vicious cycle in which sleep is further disturbed and memory impaired.”
With brain MRI and other diagnostic tools on 26 older adults aged between the ages of 65 and 81 with dementia, researchers looked for the link between bad sleep, poor memory and the toxic accumulation of beta-amyloid proteins.
Confirming that the data collected is “very suggestive that there’s a causal link,” Mander, lead author of the study and a postdoctoral researcher in the Sleep and Neuroimaging Laboratory of Walker, said: “If we intervene to improve sleep, perhaps we can break that causal chain.”
A buildup of beta-amyloid has been found in Alzheimer’s patients and, independently, in people reporting sleep disorders. Moreover, a 2013 University of Rochester study found that the brain cells of mice would shrink during non-rapid-eye-movement (non-REM) sleep to make space for cerebrospinal fluids to wash out toxic metabolites such as beta-amyloid.
Sleep washes off toxic proteins at night, preventing them from building up and from potentially destroying brain cells, explains Walker. “It’s providing a power cleanse for the brain.”
In their previous study, Mander, Jagust and Walker found that that the powerful brain waves generated during non-REM sleep play a key role in transferring memories from the hippocampus in the frontal cortex. In elderly people, deterioration of this frontal region of the brain has been linked to poor sleep.
“The more you remember following a good night of sleep, the less you depend on the hippocampus and the more you use the cortex,” Walker said. “It’s the equivalent of retrieving files from the safe storage site of your computer’s hard drive, rather than the temporary storage of a USB stick.”
The less deep sleep you have, the less effective you are at clearing out this bad protein. It’s a vicious cycle, Walker said.