Poor sleep may cause an increase in brain protein linked to Alzheimer’s

It’s enough to make you think about getting any extra sleep when you can.
It’s enough to make you think about getting any extra sleep when you can.
Image: Reuters/Supri
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A new study shows that sleep deprivation is linked to higher levels of a protein called beta-amyloid—a notorious precursor to Alzheimer’s disease.

The study, published (paywall) April 9 in the Proceedings of the National Academy of Sciences, involved a somewhat unpleasant setup. Researchers had 20 participants sleep for a night at the clinical testing center at the National Institutes of Health in Bethesda, Maryland. The next day, they received positron emission tomography, or PET, scans, to monitor proteins in their brains.

About two weeks later, each person came back to spend a night at the center—but this time, a nurse woke them up every hour. Afterward, they endured a PET scan 31 hours into their sleep deprivation, with strict instructions to stay awake.

The results: Nineteen out of 20 participants, whose ages ranged from 22 to 72, had higher beta-amyloid in their brains after their night of exhaustion compared to their well-rested baselines. Although none of these levels were clinically significant for Alzheimer’s disease, the study suggests a possible connection between sleep habits and the ultimately fatal form of dementia.

Doctors diagnose Alzheimer’s in part by detecting thick plaques of beta-amyloid through PET scans. But as of now, they still aren’t sure what initially causes these buildups.

All of us produce beta-amyloid in our brains at low levels as precursors to other proteins. Scientists know that healthy brains clean out beta-amyloid regularly, and have hypothesized that sleep somehow scrubs the brain of beta-amyloid and other undesirable waste. Sleepy mice, for example, have been found to have higher levels of the same protein than their well-rested friends, and exhausted fruit flies have developed more beta-amyloid in laboratory models (paywall) of Alzheimer’s disease.

The new study was conducted by scientists from the NIH, Yale, and Piramal Pharma, a company in Boston that manufactures some of the radioactive molecules used in PET and provided some funding for the study. While small, it was the first of its kind to use human beings in a controlled setting. Human studies so far have relied on self-reported sleep patterns, which are less reliable because it’s hard for anyone to know exactly how much shut-eye they got on any given night. Participants in this case were closely monitored, and were also asked how many hours of sleep they got on average. Sure enough, people who got less sleep had slightly higher baseline levels of beta-amyloid, although it’s impossible to say if this is because of their sleep habits specifically.

Researchers don’t know if higher levels of beta-amyloid showed up because sleep deprivation stopped the brain’s routine cleaning process, or because the brain produced more of this protein as a result of being awake for so long. Perhaps higher levels of beta-amyloid even lead to trouble sleeping! But the relationship suggests that more studies on sleep itself could lead to other therapies for Alzheimer’s disease.