Death of neurons
Decreased melatonin Metabolic disruption
Losing sleep Alzheimer’s disease
disrupts sleep. And disrupted sleep itself
might encourage Alzheimer’s by allowing
buildup of amyloid-beta, or A-beta, which
is thought to lead to the death of neurons.
This cycle of sleep deprivation can also
affect levels of the hormone melatonin,
which helps the body to sleep, and can
interfere with metabolism, a disruption
that is also a risk factor for Alzheimer’s.
SOURCE: Y. SAEED AND S. M. ABBOT T/CURREN T
NEUROLOGY AND NEUROSCIENCE REPORTS 2017
disease, such as the presence of amyloid-beta,
a protein fragment that can clump into sticky
plaques in the brain. Those plaques are a hallmark of Alzheimer’s, the most common form of
Each person also fills out lengthy questionnaires about their lives in the hopes that one day
the information will offer clues to the disease.
Among the inquiries: How tired are you?
Some answers to the sleep questions have been
eye-opening. Bendlin and her colleagues identified 98 people from the registry who recorded
their sleep quality and had brain scans. Those who
slept badly — measured by such things as being
tired during the day — tended to have more A-beta
plaques visible on brain imaging, the researchers
reported in 2015 in Neurobiology of Aging.
In a different subgroup of 101 people willing
to have a spinal tap, poor sleep was associated
with biological markers of Alzheimer’s in the
spinal fluid, Bendlin’s team reported last year in
Neurology. The markers included some related to
A-beta plaques, as well as inflammation and the
protein tau, which appears in higher levels in the
brains of people with Alzheimer’s.
Bendlin’s studies are part of a modest but growing
body of research suggesting that a sleep-deprived
brain might be more vulnerable to Alzheimer’s disease. In animal studies, levels of plaque-forming
A-beta plummet during sleep. Other research suggests that a snoozing brain runs the “clean cycle”
to remove the day’s metabolic debris— notably
A-beta—an action that might protect against
the disease. Even one sleepless night appears to
leave behind an excess of the troublesome protein
fragment (SN Online: 7/10/17).
But while the new research is compelling,
plenty of gaps remain. There’s not enough evidence yet to know the degree to which sleep might
make a difference in the disease, and study results
are not consistent.
A 2017 analysis combined results of 27 studies
that looked at the relationship between sleep
and cognitive problems, including Alzheimer’s.
Overall, poor sleepers appeared to have about a
68 percent higher risk of these disorders than
those who were rested, researchers reported
last year in Sleep. That said, most studies have a
chicken-and-egg problem. Alzheimer’s is known
to cause difficulty sleeping. If Alzheimer’s both
affects sleep and is affected by it, which comes
For now, the direction and the strength of
the cause-and-effect arrow remain unclear. But
approximately one-third of U.S. adults are con-
sidered sleep deprived (getting less than seven
hours of sleep a night) and Alzheimer’s is expected
to strike almost 14 million U.S. adults by 2050
( 5. 7 million have the disease today). The research
has the potential to make a big difference.
It would be easier to understand sleep deprivation if scientists had a better handle on sleep itself.
The brain appears to use sleep to consolidate and
process memories (SN: 6/11/16, p. 15) and to catalog thoughts from the day. But that can’t be all.
Even the simplest animals need to sleep. Flies and
But mammals appear to be particularly dependent on sleep — even if some, like elephants and
giraffes, hardly nod off at all (SN: 4/1/17, p. 10). If
rats are forced to stay awake, they die in about a
month, sometimes within days.
And the bodies and brains of mice change
when they are kept awake, says neurologist David
Holtzman of Washington University School of
Medicine in St. Louis. In one landmark experiment, Holtzman toyed with mice’s sleep right