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Alzheimer's Disease and Sleep

Alzheimer's Disease is the most common cause of dementia in the world, and epidemiological studies project that by 2050, the number of patients with AD will quadruple (Brookmeyer et al., 2007).  AD is currently incurable, but decades of research into the causes of AD strongly suggest that beta-amyloid is a key player in the development of Alzheimer's disease (Hardy and Selkoe, 2002).  Thus, there is intense interest in identifying factors that modulate beta-amyloid, with the goal of slowing the development or progression of this devastating illness.

PET-PiB images showing increased beta-amyloid burden with reduced sleep duration, from Spira et al. (2013).

Emerging evidence suggests an important and bidirectional relationship between sleep and Alzheimer's disease.  It has long been recognized that patients with Alzheimer's disease have reduced and fragmented sleep at night.  However, more recent data suggests that poor sleep may promote the development of Alzheimer's disease (Ju et al., 2014).  


We have been studying this issue in collaboration with Dr. Adam Spira, who is in the Johns Hopkins Bloomberg School of Public Health and who specializes in sleep and cognition in older adults.  Working with Drs. Susan Resnick, Luigi Ferrucci, and Eleanor Simonsick and the Baltimore Longitudinal Study of Aging cohort, we determined that older adults that report reduced or poor quality sleep have an increased amount of beta-amyloid in their brains, as measured by positron emission tomography (PET) scans (Spira et al., 2013).  In the figure, mean PET PiB images show increased amyloid burden in those subjects who report sleeping less than 6 hours nightly (Spira et al., 2013).


Despite its importance and prevalence, research into the mechanisms and potential therapies for Alzheimer's Disease remains underfunded.  In addition to our basic science research on Sleep and Alzheimer's disease, we are continually working with other investigators at Johns Hopkins to exploit our understanding of how sleep and neural excitability impact Alzheimer's disease, in order to develop novel treatment approaches for this incurable disease.


To join the Johns Hopkins Department of Neurology in the fight against Alzheimer's Disease, please click here.


If you are interested in supporting our research on Alzheimer's Disease, please click here and specify "Lab of Mark Wu".

We have also examined the relationship between sleep and beta-amyloid using a Drosophila model of AD, and our data support a bidirectional relationship between sleep and AD (Tabuchi et al., 2015).  These studies have uncovered a crucial role for neuronal excitability in mediating the increase in beta-amyloid caused by reduced sleep.  By exploiting the power of fly genetics and the wide array of molecular tools available, we hope to uncover the mechanisms by which poor sleep can worsen the progression of AD.  Ultimately, if sleep is an important modulator of beta-amyloid, this would have significant clinical implications, as pharmacological and behavioral therapies exist to improve sleep.

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