Alzheimer’s–Sleep Link? New Research Suggests Poor Sleep Increases Risk Of The Disease

New research released Monday at the Alzheimer’s Association International Conference suggests there could be a link between sleep — or lack thereof — and Alzheimer’s Disease.

It has long been understood that there is a correlation between lack of sleep and poor memory function. Memory consolidation — the process in which memories are transferred from the short-term to long-term memory bank — for example, happens during the deepest stage of non-rapid eye movement (NREM) slow-wave activity (SWA) sleep. Sleep disorders such as sleep apnea inhibit memory consolidation, which is why people who lack sleep, or have trouble sleeping throughout the night, have a harder time remembering things in the short term.

Dr. Matthew Walker paired this knowledge with the animals studies done by Dr. David Holtzman of Washington University in St. Louis on beta-amyloid production in sleep deprived mice. Beta-amyloid is a protein that presents itself as a gunky build-up in the brain that collects in larger quantities in those at risk for Alzheimer’s Disease. Dr. Holtzman’s research found that the more sleep deprived the mice were, the more the toxic protein built up in their brains. Even more interesting in the animal study was that once the deposits of amyloid began, the longer the mice stayed awake on their own.

In Dr. Walker’s link between sleep and Alzheimer’s, he found that sleep deprivation and beta-amyloid buildup starts damaging the brain as much as 20 years before major lapses in memory occur. It also gives researchers a new place to begin the development of a potential treatment.

“It’s very clear that sleep disruption is an underappreciated factor. It’s a new player on the scene that increases risk of Alzheimer’s disease. Sleep is a modifiable factor. It’s a new treatment target.”

Dr. Walker also explained at the conference that the more amyloid buildup there was in a particular region of the brain, the less deep sleep people got, which, in turn, led to more production of the harmful protein.

“It may be a vicious cycle,” says Dr. Miroslaw Mackiewicz of the National Institute on Aging.

During their Alzheimer’s research, Dr. Walker and his team studied 26 volunteers, between the ages of 65 and 81, who had never been diagnosed with Alzheimer’s, dementia, neurodegenerative, or sleep disorders. The team gave the volunteers PET scans in order to measure the amount of the protein in their brains, and then gave them words to memorize before and after an eight hour sleep cycle. What they found was that the individuals with higher amounts of amyloid had a more disruptive sleep than those with less of the protein, and thus they performed worse in the memory test the following day.

This finding gives rise to the possibility that treating sleep disorders — before the onset of Alzheimer’s — could potentially stave off the disease in later life, explained Dr. Walker.

“Data from a study of patients with sleep apnea supports this idea. If you have sleep apnea, you develop Alzheimer’s at a younger age, but if you treat the sleep apnea, this earlier onset can be averted. This suggests that treating a sleep disorder can causally break the self-perpetuating cycle. Improving sleep may therefore be able to enhance clearance of excess beta-amyloid, and enhance sleep-dependent memory functions at the same time.”

Though this link between sleep and Alzheimer’s disease is not the only factor that leads to the development of cognitive impairments in later life, this new research gives hope that a treatment, and perhaps a cure, could one day become a reality.

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