Poor Sleep May Contribute to Build-Up of Alzheimer's Amyloid

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Sleeping poorly may be connected to higher levels of memory-robbing Amyloid protein.
Sleeping poorly may be connected to higher levels of memory-robbing Amyloid protein.

HealthDay News — Poor sleep in old age may be linked to the brain-clogging plaques thought to contribute to Alzheimer's disease, new research suggests.

“Sleep appears to be a missing piece in the Alzheimer's puzzle, and enhancing sleep may lessen the cognitive burden that Alzheimer's disease imparts,” said study author Bryce Mander, PhD, a postdoctoral fellow at the University of California, Berkeley.

It's not clear how sleep and memory affect — or are affected by — the accumulation of beta amyloid plaques, believed to interfere with mental functioning. Still, the study findings hint at a major message regarding Alzheimer's, said Mander, who works at the university's Sleep and Neuroimaging Laboratory.

For the new study, published in the journal Nature Neuroscience, Mander and colleagues recruited 26 mentally healthy adults ages 70 to 79. They underwent brain imaging to assess plaque buildup, and were asked to remember pairs of words before and after a night's sleep. Overnight, researchers measured their brain waves, and the next day they conducted MRI scans during the memory testing.

Those patients with the highest levels of amyloid plaques in one part of the brain — the medial prefrontal cortex — had lighter sleep and higher levels of memory problems, the researchers found.

The study suggests — but does not prove — that insufficient deep sleep contributes to “a reduced ability to cement memories in the brain over the long-term, resulting in greater memory loss,” he noted.

However, he added, it's not known for sure “whether this link between sleep and Alzheimer's disease can explain memory loss in older adults” with higher levels of the plaques.

Reference

Mander B. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation. Nat Neurosci. 2015; doi:10.1038/nn.4035

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