Immune Cells That Clear Alzheimer's Disease Proteins Are Controlled By Circadian Rhythms

According to a study published in the journal PLOS Genetics, the brain's ability to clear proteins closely associated with Alzheimer's disease is linked to our circadian rhythms. This study highlights the importance of healthy sleep habits in preventing beta-amyloid 42 (Aβ42) from forming clumps in the brain and opens the way for a potential Alzheimer's treatment.

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The study was published in the journal "PLOS Genetics" (latest impact factor: 5.917) on February 10, 2022 "Circadian regulation of immune cells plays a role in the intricate relationship between the circadian clock and Alzheimer's disease," said circadian rhythm expert Jennifer Hurley, associate professor of biological sciences at Rensselaer Polytechnic Institute. This tells us that healthy sleep patterns may be important in relieving some of the symptoms of Alzheimer's disease and that this beneficial effect may be provided by a type of immune cell called macrophage/microglia."

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The research was conducted by Rensselaer Polytechnic Institute's Center for Biotechnology and Interdisciplinary Studies (CBIS), which focuses on neurodegenerative diseases. Dr. Hurley collaborated with Rensselaer Polytechnic Institute professor Robert Linhardt, a glycan expert, and inventor of synthetic heparin. Chunyu Wang's ongoing research details the production and spread mechanisms of several proteins involved in Alzheimer's disease.

The circadian system consists of a core set of clock proteins that predict circadian rhythms by causing daily fluctuations in enzyme and hormone levels, ultimately affecting physiological parameters such as body temperature and immune responses. Disturbances in the circadian rhythm system are increasingly linked to diseases such as diabetes, cancer, and Alzheimer's disease.

One sign of Alzheimer's disease is plaques, extracellular clumps of Aβ42 in the brain. Macrophages (called microglia in the brain) are immune cells that seek out and destroy unwanted substances and remove Aβ42 from the brain through phagocytosis. In earlier research, Dr. Hurley and her collaborators at the Royal College of Surgeons In Ireland (RCSI) investigated circadian control in macrophages, collecting exhaustive datasets that made it possible to see to which macrophage RNAs and proteins fluctuate with circadian rhythms. The researchers noticed fluctuations in the enzymes on the surface of macrophages that produce two proteins—heparan sulfate proteoglycan and chondroitin sulfate proteoglycan—both of which are It is thought to play a role in regulating the clearance of Aβ42.

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Are these cell surface proteoglycans related to the circadian system and Alzheimer's disease? In a series of experiments, the team demonstrated that the amount of Aβ42 taken up by healthy macrophages fluctuates with the daily circadian rhythm. In macrophages without a circadian clock, this pattern does not occur. They also measured daily fluctuations in the levels of heparan sulfate proteoglycans and chondroitin sulfate proteoglycans produced on the surface of macrophages with healthy circadian rhythms. The peak of Aβ42 clearance occurs when surface cell proteoglycan production is lowest, and removal of these proteoglycans increases uptake, suggesting that proteoglycans inhibit Aβ42 clearance.

"Clearly, it's all timed by the circadian clock," said Dr. Hurley. "When there's a lot of this cell-surface proteoglycan, macrophages don't take up Aβ42. We're not sure why that's the case, but it's definitely related. ."

This relationship could be used to develop a therapy that promotes more Aβ42 clearance by increasing the magnitude of daily fluctuations that tend to diminish as we age.

"Theoretically, if we could elevate this rhythm, maybe we could increase Aβ42 clearance, preventing damage to the brain," said Dr. Hurley.

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