By Yasmin Anwar, UC Berkeley News
Poor sleep, more common in old age, is linked to the protein implicated in Alzheimer’s disease.
Sleep may be a missing piece in the Alzheimer’s disease puzzle.
UC Berkeley scientists have found compelling evidence that poor sleep — particularly a deficit of the deep, restorative slumber needed to hit the save button on memories — is a channel through which the beta-amyloid protein believed to trigger Alzheimer’s disease attacks the brain’s long-term memory.
“Our findings reveal a new pathway through which Alzheimer’s disease may cause memory decline later in life,” said UC Berkeley neuroscience professor Matthew Walker, senior author of the study published today in the journal Nature Neuroscience.
Excessive deposits of beta-amyloid are key suspects in the pathology of Alzheimer’s disease, a virulent form of dementia caused by the gradual death of brain cells. An unprecedented wave of aging baby boomers is expected to make Alzheimer’s disease, which has been diagnosed in more than 40 million people, one of the world’s fastest-growing and most debilitating public health concerns.
The good news about the findings, Walker said, is that poor sleep is potentially treatable and can be enhanced through 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.
“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 was co-led by UC Berkeley neuroscientists Bryce Mander and William Jagust, a leading expert on Alzheimer’s disease. The team has received a major National Institutes of Health grant to conduct a longitudinal study to test their hypothesis that sleep is an early warning sign or biomarker of Alzheimer’s disease.
Heavy deposits of the toxic protein, beta-amyloid, shown in red in the brain on the right, are linked to poor sleep and may be paving the way for Alzheimer’s disease. A brain benefiting from deep sleep brain waves and an absence of beta-amyloid is shown on the left. (Photo courtesy of Bryce Mander and Matthew Walker)
While most research in this area has depended on animal subjects, this latest study has the advantage of human subjects recruited by Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory.
“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.”
Using a powerful combination of brain imaging and other diagnostic tools on 26 older adults who have not been diagnosed with dementia, researchers looked for the link between bad sleep, poor memory and the toxic accumulation of beta-amyloid proteins.
“The data we’ve collected are very suggestive that there’s a causal link,” said Mander, lead author of the study and a postdoctoral researcher in the Sleep and Neuroimaging Laboratory directed by Walker. “If we intervene to improve sleep, perhaps we can break that causal chain.”