SLEEP AND NEUROLOGICAL DISORDERS (JL DEWOLFE, SECTION EDITOR)
Sleep and Dementia
Okeanis E. Vaou
Shih Hao Lin
Published online: 21 May 2018
Springer International Publishing AG, part of Springer Nature 2018
Purpose of Review In this review, we seek to analyze the most novel findings recently published in the literature on sleep and
Recent Findings The degeneration of suprachiasmatic nucleus and prefrontal cortex in dementia disrupts sleep-wake rhythmicity
and contributes to cognitive deterioration in Alzheimer’s Dementia (AD), respectively. Sleep deprivation increases amyloid-β
production and decreases its clearance. Short and long duration of sleep increase risk of cognitive disorders. Studies suggest that
obstructive sleep apnea accelerates amyloid deposition though intermittent hypoxia. Effect of CPAP on cognition is controversial.
Subjects with severe daytime sleepiness or sleep-related movement disorder have a higher risk for vascular dementia.
Summary These findings highlight the impact of sleep on dementia. Thus, the bi-directional link of sleep and neurodegenerative
disease may influence each other in many ways that have important implications for the diagnosis and treatment of AD.
Obstructive sleep apnea
REM behavior disorder
Dementia is usually caused by neurodegenerative diseases
such as Alzheimer’s disease (AD), Lewy body disease
(LBD), Parkinson’s disease (PD), frontotemporal disease
(FTD), or Creutzfeldt-Jacob disease. With an aging popula-
tion, the incidence of dementia increases. It is estimated that
47 million people live with dementia, and this number is ex-
pected to double by year 2030. AD is the most common neu-
rodegenerative disorder and accounts for 75% of most com-
mon types of dementias. As a consequence, most of this re-
view will focus on issues of sleep related to AD. When
appropriate, additional references will be made to the other
types of dementias.
Dementia is characterized by progressive loss of cognition,
memory, emotions, and behavior . The prevalence of AD
increases exponentially with age, from 1.5% of the general pop-
ulation aged 60–69 years to 40% among those aged 90–99 years.
The economic burden of dementia is also rising, and it is cur-
rently estimated to be 1% of the gross domestic product .
Each dementia type is characterized by a particular pheno-
type and a specific pathology. FTD is somewhat unusual be-
cause it may have varied phenotypes (behavioral v. language)
and varied pathologies. AD is characterized by extracellular
amyloid β (Aβ) plaques and intracellular neurofibrillary tan-
gles comprised of hyperphosphorylated tau protein. The dis-
ease involves widespread synaptic loss in the neocortex and
the hippocampus . In the earliest stage of AD, soluble Aβ
becomes insoluble and aggregates into amyloid plaques.
Amyloid β is considered to be neurotoxic, driving the pro-
gression of neuronal damage and resulting in neurodegenera-
tion by promoting neuroinflammation and disrupting
neurogenesis, glial (microglial and astrocytic) related inflam-
matory response, and tau hyperphosphorylation .
Early in the disease, patients present with sleep distur-
bances such as circadian rhythm disorders and agitation close
to bedtime. On average, 25–60% of all AD patients report
sleep disorders  such as insomnia, hypersomnia with phase
reversal of their sleep, frequent nighttime awakenings, and
This article is part of the Topical Collection on Sleep and Neurological
* Okeanis E. Vaou
Shih Hao Lin
Boston Medical Center, 725 Albany St 7th Floor, Suite 7B,
Boston, MA 02118, USA
Current Sleep Medicine Reports (2018) 4:134–142