Disruptive sleep, daytime sleepiness, and other indications in an individual's circadian rhythm are typical complaints of individuals who have Alzheimer's disease, and the problems only worsen as the disease develops.
However, the reason for this association between Alzheimer's and circadian disorder is not clearly understood. In new research, the study authors discovered that a hint might lie in the brain protein, also known as YKL-40.
According to Knowridge Science Report, the researchers discovered that YKL-40 is both controlled by clock genes and engaged in clearing away, possibly the toxic accumulation of "Alzheimer's proteins in the brain."
More so, people with Alzheimer's carrying a genetic variant that decreases YKL-40 levels retain their cognitive faculties longer than those who do not have the variant.
Possible Link
The study findings propose that the said protein is a possible link between circadian rhythm dysfunction and Alzheimer's disease. Treatments that target the said protein may slow the illness's progression.
Research conducted at Washington University School of Medicine in St. Louis. A master clock sets one's daily rhythms in the brain driven by both the night and day cycle.
Each cell is also retaining its own internal clock, attached to the master clock. An astonishingly extensive range of biological procedure, from absorption of sugar to body temperature, to immune and inflammation responses, differ by time of day.
In addition, even though circadian dysfunction impacts a lot of aspects of health and illness, it is most simply detected as sleep disruption like difficulty falling asleep or "staying asleep at night and increased sleepiness during the day."
Typical in Alzheimer's Patients
Such problems are typical in Alzheimer's patients, even the people in the disease's earliest stage when amyloid plaques have started to form, but cognitive symptoms have not yet appeared.
Past studies had found that higher YKL-40 levels in cerebrospinal food are an indication of Alzheimer's disease.
Succeeding research showed that YKL-40 levels increase with normal aging and as Alzheimer's develops. In this research, the researchers used "Alzheimer's mouse models prone to developing amyloid plaques and crossed them with genetically modified mice" that do not have the gene for YKL-40 protein or with unchanged mice to compare.
The moment the mice turned eight months old, the elderly, based on mouse standards, the study authors analyzed the brains of the mice.
Research Finding
The amyloid-prone mice that did not have YKL-40 were about 50 percent more amyloid than those with the gene.
Usually, amyloid plaques are surrounded by immune cells, also known as microglia, that contribute to the stoppage of the spread of plaques.
Furthermore, in the mice that did not have YKL-40, the microglia were more abundant, not to mention more primed to consume and eliminate amyloid.
Such a finding jibes with data from investigations in people. In connection to this, the group examined genetic data from over 770 people.
Out of this number, roughly one-fourth or 26 percent had a genetic variant that lowers the YKL-40 levels. Also, cognitive skills dropped 16 percent more slowly in individuals who had the variant.
Results of the study propose that Alzheimer's disease is bad. Those with less of it fare better. If researchers could develop a treatment for the lowering YKL-40, it might help microglia eliminate more amyloid and probably, slow the disease's progression.
One of the study authors is neurology associate professor Erik Musiek, MD, Ph.D. It was the Science Translational Medicine that published this same research.
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