disturbances are commonly reported in people with dementia ,
whether this is a cause or a consequence of the disease is unclear.
Evidence is mounting that alterations to normal sleep patterns affect
disease progression, promoting the appearance of β-amyloid (Aβ) and
tau aggregates that are progressively deposited in the brains of
patients with Alzheimer's disease (AD). Human and mouse studies
support a role for sleep in curbing the accumulation of Aβ ;
however, tau aggregates are more closely associated with synaptic
degeneration and clinical symptoms of AD .
Holth et al. in a new report provide direct evidence that disrupting sleep, or stimulating excitatory neurons in brain nuclei that control wakefulness and arousal, promotes the release and spread of damaging tau aggregates across the brains of mice, and that sleep deprivation leads to increased extracellular Aβ and tau in people.