Poor sleep quality has been linked to cognitive decline, neuro-degeneration and Alzheimer’s disease in seniors—but it may be possible to counteract certain risks.
A new study shows that specific sleep brain waves provide protection against the harmful effects of a brain chemical associated with wakefulness, sleep transition, and narcolepsy.
Concordia University-led researchers examined levels of the neurotransmitter orexin in the cerebral spinal fluid of 60 adults with mild to moderate Alzheimer’s Disease over a three-year period.
They found that individuals with elevated levels of orexin, which is vital to sleep and appetite regulation, were more likely to exhibit symptoms of cognitive decline, including poorer memory and thinking, more severe behavioral and psychiatric symptoms and had higher levels of biological markers associated with neurodegenerative disease and inflammation.
However, that relationship was found to be mitigated by specific brainwaves during sleep. Individuals who produced stronger sleep spindles and sleep oscillations — types of brainwaves associated with memory support and preservation — during non-rapid eye movement (NREM) sleep had less cognitive decline over time than those with weaker ones.
This sleep activity appears to provide neural resilience against the negative effects of higher levels of orexin on their cognition and mental health.
“This study shows that there is a direct association between orexin levels in the brain and biomarkers of Alzheimer’s disease,” says study co-author Thanh Dang-vu, a neurologist and professor in the Department of Health, Kinesiology and Applied Physiology.
Clear pathways to treatment
The study’s data, published in the journal Neurology, was collected by researchers at Lleida University in Catalonia, Spain. The 60 participants spent a night in a sleep laboratory where researchers recorded their brain activity using overnight poly-somnography. The following morning, cerebrospinal fluid samples were collected to measure orexin and other established Alzheimer’s biomarkers.
Participants also completed a series of cognitive and neuropsychiatric assessments at regular intervals over the next three years, allowing researchers to examine how sleep, brain chemistry and cognitive decline changed together over time.
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“Having this longitudinal data is important, because Alzheimer’s disease is a moving target,” says the study’s co-first author Arsenio Paez, a neuroscience lecturer in the Sleep, Cognition and Neuroimaging Lab.
“With this data, we can see how the course of people’s Alzheimer’s disease changes over time. Alzheimer’s is a very long process, so this gives us a better picture of how conditions can change over time and we might intervene at different stages of the disorder.”
The researchers note that orexin-blocking drugs are already being used to treat insomnia and narcolepsy, and are being explored as possible therapies for Alzheimer’s disease.
This study suggests that monitoring sleep spindles, slow oscillations and orexin levels could help measure disease progression and to identify which patients would benefit from specialized treatment.
“This study shows us that there are new ways to potentially act on sleep to slow the progression of Alzheimer’s disease, and opens the door for further studies moving forward,” says Dang-vu.
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