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 Dr. Matthew Walker, UC Berkeley neuroscience professor and senior author of the study published in June 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, Dr. 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.
The study was co-led by UC Berkeley neuroscientists Dr. Bryce Mander and Dr. William Jagust, a leading expert on Alzheimer’s disease. While most research in this area has depended on animal subjects, this latest study has the advantage of human subjects recruited by Dr. Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the UC Berkeley School of Public Health, and Lawrence Berkeley National Laboratory. 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.
“Over the past few years, the links between sleep, beta-amyloid, memory, and Alzheimer’s disease have been growing stronger,” Dr. 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 Dr. Mander, 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.”