Something to sleep on
This article was co-written by Smita Patel, DO, FAASM, and Anne Marie Fosnacht, MPH, CPT
The rate of Alzheimer’s disease (AD) continues to soar due, in part, to the successful aging of the largest generation ever to walk the earth.
Limited by a dearth of successful pharmacological agents, more and more physicians are shifting from a treatment paradigm to one of prevention.
Here at the NorthShore Center for Brain Health we believe that getting enough sleep--7 or more hours nightly--is a way to help prevent AD.
Prevention necessitates intervening on modifiable risk factors. Evidence is mounting that lifestyle factors, such as diet, daily activity, education, and social engagement--combined with non-modifiable factors such as family history and genetics--play a significant role in the ontogeny of Alzheimer’s disease in patients over time.
Recent clinical trials in Spain and Finland have shown that eating a Mediterranean diet, or receiving healthy-eating counseling and assistance are associated with improvement in cognitive function.
Exercise training has been shown to increase the size of the hippocampus, the memory center of the brain, and to improve memory.
Epidemiologic studies suggest that people with more years of education can tolerate changes associated with neurodegeneration longer than those with less education, effectively delaying onset of cognitive dysfunction.
Cohort studies have found that social engagement is associated with larger brain volume.
Non-modifiable risk factors include a family history of dementia and having a certain variant (APOE4) of the apolipoprotein allele, which is responsible for cholesterol transport and mediation in the brain. Individuals with 1 copy of APOE4 have a 2- to 4-fold increased risk of AD while those who have inherited 2 copies have 10-fold increased risk.
While disturbances in the sleep cycle and altered circadian rhythms are common symptoms of dementia and Alzheimer’s disease, sleep quality throughout one’s lifetime is gaining momentum as a possible factor associated with eventual development of AD.
Helping patients achieve better sleep may help reduce their risk of developing the disease.
While experimental studies in humans are rare, there are animal models of sleep-related causation. The results of these studies are compelling.
In 2009, Kang and colleagues reported that beta amyloid dynamics were found to be regulated by the sleep-wake cycle in mice.
In 2013, Xie and colleagues reported that in mice sleep was associated with naturally-occurring flushing/removal of exogenous AB from the brain by cerebrospinal fluid.
Others have found that deprivation of sleep exacerbates neuronal injury and tau phosphorylation.
Recently, key cross-sectional studies have shown an association between Alzheimer’s and sleep variables in humans.
Spira and colleagues found that self-reported short sleep duration and poor sleep quality were associated with increased AB burden as seen in PET amyloid imaging. Similarly Ju and colleagues reported that greater amyloid burden was associated with poor sleep efficiency and wakefulness episodes.
Observational studies also offer compelling data linking sleep to Alzheimer’s risk. Virta et al. report that among 2,300 middle age Finnish twins, self reports of too much (>8 hrs) sleep was associated with 1.8 times higher odds of developing AD. Hahn and colleagues found that self reports of decrease in depth of sleep were associated with 70 to 100% greater odds of having AD 9 years later.
While the exact mechanisms by which sleep duration and quality affect development of Alzheimer’s and dementia are still enigmatic, more and more research show they are firmly associated.
Educating patients on the impact of sleep on their brain health and helping patients achieve high quality sleep can be important steps in mitigating the risk of neurodegeneration.
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