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December 18, 2020 03:30 am

Biomarker of Alzheimer's Found To Be Regulated By Sleep Cycles

Following a 2018 study demonstrating how disrupted sleep can accelerate the buildup of toxic plaques associated with the disease, scientists from Washington University School of Medicine (WUSM) in St. Louis have now identified a protein implicated in the progression of the disease that appears highly regulated by the circadian rhythm, helping them join the dots and providing a potential new therapeutic target. New Atlas reports: In their previous research, the WUSM team set out to explore how disruptions to our natural sleep cycles, or circadian rhythm, may accelerate the accumulation of amyloid plaques in the brain, which are strongly linked to Alzheimer's disease. Through studies on humans and in mice, the team was able to show a strong correlation between the two, and now through follow up work, the team has identified a brain protein that appears to play a role in this relationship. The brain protein in question is called YKL-40 and for years has served as a biomarker for Alzheimer's, as high levels of it have been found in the cerebrospinal fluid of those suffering from the disease and these levels rise as the disease progresses. The researchers were screening for genes that are regulated by the circadian rhythm, and were intrigued to see the gene for this brain protein pop up. From there, the team investigated this connection between YKL-40 and Alzheimer's, which is characterized by chronic inflammation, by exploring how much of the protein is made under inflammatory conditions both with and without a key circadian gene. Indeed, this demonstrated that the circadian rhythm controls how much YKL-40 is produced. Next up, the team worked with mice prone to developing amyloid plaques, and genetically modified one group of them to be lacking the gene for YKL-40. As the mice reached old age, the team analyzed their brains and found that those without the YKL-40 protein exhibited around half the amyloid plaques of the control group. Digging deeper into the reasons why, the team found that the mice lacking the YKL-40 gene featured more microglia, which are immune cells that surround amyloid plaques and prevent them from spreading. Essentially, this meant that those mice had more hungry immune cells prepared to gobble up the amyloid. [...] The team also examined this idea in human subjects, drawing on genetic data on 778 subjects from aging and dementia studies and finding only a quarter of them featured a genetic variant that lowers levels of YKL-40, and that cognitive function declined 16 percent more slowly in that group. The research was published in the journal Science Translational Medicine.

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