Why You Should Sleep Well: Loss of Sleep Causes Dementia?
A 43-year-old businessman arrives at the sleep clinic for his first
appointment. He tells the physician that he falls asleep easily -- in
fact, he's out before his wife can turn off the light -- however, he
feels that his sleep is restless, and he often wakes up unrefreshed. He
pushes through the day and struggles to stay awake during meetings. Most
concerning of all is the decline he's noticed in his memory and ability
to concentrate. Simple tasks require a renewed focus to complete, and
his friends have commented on his inability to remember certain details
from their conversations. He describes a sensation of sleepwalking
through his waking state, as if he's living in a constant fog.
The association between sleep deprivation and cognitive impairment is nothing new. In fact, it is something we have all experienced. It only takes one poor night's sleep for us to notice that our reaction time slows, concentration requires more effort, and our ability to form new memories is impaired. For those of us in the medical profession, we can all relate to long nights of hospital call and the feeling at 3 a.m. or 4 a.m. as if we were wading through a form of intellectual molasses. Fortunately, new work-hour requirements have limited this practice in medical training, as they have in the aviation and transportation industry.
The association between sleep deprivation and cognitive impairment is nothing new. In fact, it is something we have all experienced. It only takes one poor night's sleep for us to notice that our reaction time slows, concentration requires more effort, and our ability to form new memories is impaired. For those of us in the medical profession, we can all relate to long nights of hospital call and the feeling at 3 a.m. or 4 a.m. as if we were wading through a form of intellectual molasses. Fortunately, new work-hour requirements have limited this practice in medical training, as they have in the aviation and transportation industry.
It has been well established by now that sleep is
integral to memory formation. Researchers have demonstrated that
sleep-deprived students perform poorly on memory-specific tasks (1).
More interestingly, they have also shown that students allowed to nap
after learning new material have greater recall than students who
followed healthy, non-sleep restricted patterns but did not nap.
Functional MRI during sleep in all subjects demonstrated increased blood
flow in the same areas of the brain that were active while awake, when
the subjects were learning the new material. This indicates that our
brains continue to process new information while we sleep, and that
sleep likely helps facilitate the memory encoding process.
We
also know that sleep architecture, or the progression we make through
various stages of sleep every night, changes significantly as we age.
Our sleep becomes more fragmented, we are more easily awakened, and our
slow wave sleep, sometimes referred to as "deep sleep," progressively
diminishes. Older adults generally sleep less than younger adults do
and, interestingly, are better equipped to handle the effects of sleep
deprivation. Perhaps because we are so used to it.
So what does
this have to do with memory? If it's been well established that
short-term sleep deprivation can produce transient cognitive impairment,
what about chronic sleep deprivation? Can this eventually lead to
permanent memory loss? Does fragmented sleep lead to dementia, such as
that of Alzheimer's disease? There have been several recent studies that
have attempted to better answer this important question.
In a
multisite cohort of community-dwelling women aged 65 years or older
(mean age of 82), researchers analyzed the effect of both sleep
fragmentation from any cause and sleep fragmentation from sleep apnea on
the risk of cognitive impairment, as measured approximately five years
later with neuropsychological cognitive testing (2). They found that the
presence of sleep apnea was associated with a 1.8-fold increased risk
of developing cognitive impairment and dementia. This was after
adjusting for several variables including age, race, weight, education,
smoking, diabetes, and medication use.
Interestingly, this risk
was not associated with sleep fragmentation from any cause. They found
no significant association between cognitive impairment and sleep
fragmentation measures such as the arousal index, wake after sleep onset
(total time spent awake after initially falling asleep), or total sleep
time. Furthermore, the risk of cognitive impairment seen in sleep apnea
patients was very much correlated with the degree of oxygen
desaturations throughout the night, indicating that it was not the
increased arousal threshold but rather the low oxygen levels from the
apneas themselves that contributed to the patients' cognitive decline.
This
same group of researchers presented new data recently at the 66th
annual meeting of the American Academy of Neurology, in which they
demonstrated, in a cohort of younger patients (age 37-52) that those who
slept less than seven hours a night and reported more sleep
fragmentation had a greater amount white matter changes on brain MRI
(3). White matter changes, while nonspecific, can serve as an imaging
marker of small vessel disease, a hardening of the small arteries in the
brain, similar to what happens inside the small arteries of the heart
in patients with coronary artery disease. In severe cases this can cause
stroke, as well as dementia, and has been termed "vascular dementia" or
"muli-infarct dementia" in the neurology literature.
In data
also presented at the AAN meeting, another group of researchers
demonstrated that sleep might serve to clear certain "toxic" protein
products that have been linked to the development of Alzheimer disease.
Amyloid
A-Beta peptide (AB) is protein cleavage product that can accumulate to
form so-called "senile plaques." These conglomerations of protein can
then deposit in areas of the brain that are crucial to memory, language,
and spatial awareness and can contribute to the some of the impairments
we often see in patients with Alzheimer's disease.
When mice
were sleep deprived, they developed significantly more AB deposition. In
addition, when the animals were allowed to eventually sleep, they
cleared much of the AB from their brains. This lead the researchers to
hypothesize that sleep deprivation or fragmentation could potentially
lead to excessive AB release, thus leading to excessive amyloid
deposition. In addition, stress and other environmental factors may also
regulate AB levels.
So does sleep deprivation lead to permanent
cognitive impairment or dementia, as that seen in Alzheimer's disease?
The results so far are mixed, and far from conclusive. One thing is for
sure though -- as we age, and our natural sleep architecture becomes
increasingly fragmented, we should all be doing what we can to try and
get a good night's sleep. Most importantly, if any signs of sleep apnea
are present -- such as snoring, breath holding, gasping or choking,
excessive sweating, restless sleep, or early morning headaches, to name
but a few -- your brain may be at risk, and you should ask your doctor
about being evaluated by a sleep specialist.
Source: Huff Posts
Category: Health Matters
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