A new study has revealed that poor sleep is linked to toxic buildup of Alzheimer's protein and memory loss.
Scientists at the University of California, Berkeley, 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.
UC Berkeley's Matthew Walker said that the findings reveal a new pathway through which Alzheimer's disease may cause memory decline later in life.
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, he said, sleep could be a novel therapeutic target for fighting back against memory impairment in older adults and even those with dementia.
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Bryce Mander, who co-led UC Berkeley neuroscientists, said that this is a new pathway linking Alzheimer's disease to memory loss and it's an important one because they can do something about it.
The study appears in the journal Nature Neuroscience.