Did you know that if you’re not getting enough sleep each night, you may not be clearing out dementia-related toxins? While mitigating insulin resistance will help, there’s an even cheaper and easier way to ward off Alzheimer’s: SLEEP.
Mathew Walker, PhD, founder and director of the Center for Human Sleep Science at the University of California, Berkeley, has been studying this connection. They’ve found that “there’s a strong relationship … between insufficientand the mechanisms of Alzheimer’s disease.” Additionally, they discovered that short sleep predicts a shorter life, and is both casually and significantly linked to every fatal disease. Surprisingly, short sleep is defined as just six hours or less every night.
Misfolded proteins like beta amyloid and tau tangles are the hallmark of Alzheimer’s disease. It turns out that sleep is very important inof your brain each night.
Just as the body has a lymphatic system that excretes toxins, the brain also has its own sewage system. This system kicks into high gear during deep sleep, clearing out “all of the metabolic waste that’s been building up throughout the day,” Walker explains. “One of the toxic byproducts that it actually removes at night is a sticky protein called beta amyloid, which is one of the leading causes that we believe [is] underlying Alzheimer’s disease.”
In addition to beta amyloid,with a lack of sleep. “We saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired,” says Brendan Lucey, MD, an assistant professor of neurology and director of the Washington University Sleep Medicine Center. Elevated tau is a sign of Alzheimer’s disease, linked to cognitive decline and brain damage.
Another potential treatment besides sleep?. Alzheimer’s-affected brains have receptors, suggesting that cannabis can be used therapeutically. THC to help clear plaques of beta amyloid in the brain, but a claims it’s “the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells.”
engineered to have symptoms of Alzheimer’s, those treated with synthetic THC for six weeks performed just as well as normal mice and had less amyloid clumps. However, normal mice treated with THC had problems learning, suggesting it may not be a prevention mechanism.
This research points to the hopeful possibility that midlife intervention could prevent Alzheimer’s from progressing. “It certainly argues that treatingduring midlife as well as getting appropriate levels of sleep is likely to decrease risk for Alzheimer’s disease,” says David Holtzman, a neurologist and neuroscientist at Washington University School of Medicine in St. Louis.
Combined with further cannabis research, a possible Alzheimer’s treatment is looking more attainable than ever.