It was a revelation for Alzheimer’s experts. “That
showed experimentally for the first time that there
was an effect of sleep deprivation on Alzheimer’s dis-
ease pathology,” says Spira. “That’s what really flipped
everything on its head.” In 2013, to test whether the
same effect occurred in people, Spira studied brain
scans of 70 healthy adults with an average age of
- Indeed, the scans of those who reported less or
compromised sleep showed higher levels of amyloid
plaques than the scans of those who slept better.
A year later, a biological explanation for why
poor sleep might be linked to Alzheimer’s emerged.
Dr. Maiken Nedergaard, co-director of the Center
for Translational Neuromedicine at the University
of Rochester, identified a previously ignored army
of cells that is called to duty during sleep in the
brains of mice and acts as a massive pump for slosh-
ing fluid into and out of the brain. This plumbing
system, which she dubbed the “glymphatic system”
(it works in parallel to the lymph system that drains
fluid from other tissues in the body), seemed to per-
form a neural rinsing of the brain, swishing out the
toxic proteins generated by active neurons (including
those amyloid fragments) and clearing the way for an-
other busy daily cycle of connecting and networking.
Taken together with Spira’s discovery that levels
of amyloid spiked during the day and dropped
during sleep, Nedergaard’s findings gave further
credence to the theory that sleep might perform
a housekeeping function critical for warding off
diseases like Alzheimer’s. “These results very much
support the notion that one of the roles of sleep is
to actually accelerate the clearance of beta amyloid
from the brain,” says Nora Volkow, director of the
U.S. National Institute on Drug Abuse.
Late Last year, Laura Lewis, assistant professor
of biomedical engineering at Boston University, built
on Nedergaard’s work by matching up the ebb and
flow of cerebro spinal fluid in the brain with brain-
wave activity, which indicates different stages of
sleep. She showed that in healthy adults, during the
day when the brain is active, there is less fluid bath-
ing neurons and tissues in the organ. During sleep—
and especially during deeper sleep—this solution
saturates the brain in a cleansing flood. The finding
reinforced Nedergaard’s theory that sleeping may
help clear the brain of toxic proteins that can even-
tually cause disease.
Still, while all these discoveries are strongly sug-
gestive, they are not what scientists would call defini-
tive. For that, researchers need two additional pieces
of evidence: first, a clear correlation between dis-
rupted sleep patterns and a higher risk for Alzheim-
er’s; and second, evidence that if these high-risk peo-
ple improve their sleep, that risk falls.
They are currently working to build those data
sets, and already the results are promising. For
example , Volkow measured baseline amyloid levels
in the brains of 20 healthy people ages 22 to 72 years,
then scanned their brains again after each had a good
night’s sleep and yet again after each was kept awake
for about 31 hours straight. After a loss of sleep, levels
of amyloid were 5% more than after adequate sleep;
the spikes were concentrated in parts of the brain
involved in memory and higher thinking, which are
typically affected in Alzheimer’s.
But seeing levels of amyloid change with more
or less sleep doesn’t necessarily mean sleep habits
are contributing to Alzheimer’s. To make that case,
researchers are studying people with disorders like
sleep apnea, or those who work night shifts or keep
irregular working hours, such as first responders,
pilots and flight attendants. Studies already sug-
gest that all of these groups are more vulnerable to
Alz heimer’s. The next step is to see if treatment, or
changes in sleep habits, matters. For people with
sleep apnea, for example, doctors can prescribe de-
vices to wear during sleep to keep oxygen flowing
more consistently to the brain so they don’t wake up.
In shift workers, researchers want to test the impact
of resetting their biological clocks to a standard day-
night schedule. If these efforts lower their likelihood
of developing Alzheimer’s, that would make a strong
case for a connection between lifelong sleep patterns
and risk of dementia.
Researchers also need to better understand how
sleep medications and treatments like melatonin
affect the dementia process. While some sleep aids
promote the deeper sleep that seems to be protec-
tive against brain decline, it’s not clear yet whether
long-term dependence on such medications can
maintain the benefit.
Even while these studies are being done, many
experts believe the data are already strong enough to
start educating at least older people, especially those
at higher risk of developing Alzheimer’s, about im-
proving their sleep habits. Yaffe, for one, already does
that with her patients. “Even practical sleep-hygiene
tips, where we teach people best practices like avoid-
ing caffeine in the evening and darkening their room
and staying off their phones, could help them sleep
better,” she says. “I would love to see whether this
low-cost and pragmatic approach could improve cog-
nition or prevent decline in Alzheimer’s patients.”
She and others don’t believe sleep alone can fully
prevent Alzheimer’s or halt its progression. But to-
gether with other therapies that could emerge to treat
the disease, sleep may be a powerful way to help peo-
ple lower their risk even further. It’s even possible
that sleep could play an important role in keeping our
brains healthy in other ways: by controlling metabo-
lism and other cellular functions behind diseases like
diabetes, hypertension and even cancer. As the latest
research shows, a good night’s sleep isn’t a luxury—
it’s critical for keeping the brain healthy. The system
seemed to
perform
a neural
rinsing of
the brain,
swishing
out toxic
proteins86 Time August 17/August 24, 2020
Sleep