
Poor Sleep: A Contributor to Alzheimer’s Risk
New research from the University of California, Berkeley found compelling evidence that poor sleep may trigger Alzheimer’s disease attacks the brain’s long-term memory.
In particular, scientists found that a deficit of the deep sleep, restorative slumber needed to hit the save button on memories is a channel through which the beta-amyloid protein triggers the onset of the disease. It has long been theorised by many researchers that excessive deposits of beta-amyloid in the brain contributes to the risk of Alzheimer’s, as they cause brain cells to die. Over 40 million people have been diagnosed with this debilitating mental illness, which makes it a serious public health concern.
The discovery offers hope, according to Professor Matthew Walker, senior author of the study. "Sleep could be a novel therapeutic target for fighting back against memory impairment in older adults and even those with dementia." he said.
Walker added that the good news is that poor sleep is potentially treatable and can be enhanced through exercise, behavioural 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.
In the study, 26 older adults who have not been diagnosed with dementia examined their likelihood of developing Alzheimer’s using a powerful combination of brain imaging and other diagnostic tools, researchers looked for the link between bad sleep, poor memory and the toxic accumulation of beta-amyloid proteins.
"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."
"But we don’t yet know which of these two factors - the bad sleep or the bad protein - initially begins this cycle. Which one is the finger that flicks the first domino, triggering the cascade?" That’s a question Walker and his team will be investigating on in the future.
The research was published in the journal Nature Neuroscience.
Source of this article: β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation
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