Dr. Matthew Walker, in his book Why We Sleep, explained to us that our sleep is controlled by a center in the pre-frontal cortex right above your nose. This center atrophies as we age even faster than the rest of the brain, which causes insomnia in us older adults. And so we have more and more trouble with insomnia. In Alzheimer's disease, this atrophy is even worse, and people with Alzheimer's have even bigger problems with insomnia. Ask anyone who works in memory care.
And as we explained in Beating the Dementia Monster, deep sleep is incredibly important in preventing and controlling Alzheimer's disease. A record of poor and interrupted sleep is strongly associated with the development of Alzheimer's disease. Our sleep repeats a 90-minute cycle throughout the night, and the most important part of that cycle for Alzheimer's disease is deep sleep.
But there's a lot more to sleep than what the prefrontal cortex does. Another actor in the brain is the thalamus. According to Dr. Walker, the thalamus acts as a gate to keep distracting thoughts out of your brain and let you get to sleep. And that gate is more than a metaphor. Certain proteins can punch physical holes in the gate, and disruptive thoughts can then enter and contribute to insomnia.
Within the thalamus is a structure called the thalamic reticular nucleus (TRN). While there is debate about what the TRN does and how it does it, scientists believe that it plays a role specifically in the regulation of deep sleep. In fact, mice experience insomnia when activity of the TRN is low.
So what if we could stimulate the TRN in a way that would promote deep sleep? Recent research suggests that we can. Dr. Jeannie Chin at the Baylor College of Medicine found they can stimulate the TRN leading to restored sleep maintenance and reduced amyloid plaque load in both the cortex and the hippocampus -- of mice.
These were mice that had had their genes edited to produce the human amyloid precursor protein that we discuss in Beating the Dementia Monster. Enzymes cutting the protein produce the amyloids that accumulate in plaques on neurons in Alzheimer's disease. So we can associate sleep problems with the generation of beta amyloid and their plaques in these mice.
Of course, we've talked before about how great an idea seems to be when working with mice, but it falls apart when we try to apply what we learned to humans. Sometimes it's helpful, but research with mice can lead to disappointment.
So what did Dr. Chin and her team do? They injected the mice with a virus that would carry a special receptor to the TRN. They then injected a chemical that would be received by the receptors and stimulate the TRN to do a better job controlling deep sleep. And that seemed to work.
Are they ready to try this out on people? Well, hold on. People are not mice, and what worked with mice isn't necessarily expected to work with people. So they're mapping the TRN to figure out a receptor system that could do something similar. But this whole idea is in early stages. It'll be a while, but we'll watch for news.
Meanwhile, I still have a heck of a time getting a good night's sleep.
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