Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, April 27, 2022

Clearance of protein linked to Alzheimer's controlled by circadian cycle

 But is this better than side sleeping?

A positive side sleeping suggestion here:

Lymphatic vessels cleaning system for the brain and are important for curing Alzheimers, MS, Stroke, TBI May 2017

The latest here:

Clearance of protein linked to Alzheimer's controlled by circadian cycle

Ability of immune system to destroy Alzheimer's-related protein oscillates with daily circadian rhythm

Date:
February 10, 2022
Source:
Rensselaer Polytechnic Institute
Summary:
The brain's ability to clear a protein closely linked to Alzheimer's disease is tied to our circadian cycle, according to new research. The research underscores the importance of healthy sleep habits in preventing the protein Amyloid-Beta 42 (AB42) from forming clumps in the brain, and opens a path to potential Alzheimer's therapies.
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The brain's ability to clear a protein closely linked to Alzheimer's disease is tied to our circadian cycle, according to research published today in PLOS Genetics. The research underscores the importance of healthy sleep habits in preventing the protein Amyloid-Beta 42 (AB42) from forming clumps in the brain, and opens a path to potential Alzheimer's therapies.

"Circadian regulation of immune cells plays a role in the intricate relationship between the circadian clock and Alzheimer's disease," said Jennifer Hurley, an expert in circadian rhythms, and associate professor of biological science at Rensselaer Polytechnic Institute. "This tells us a healthy sleep pattern might be important to alleviate some of the symptoms in Alzheimer's disease, and this beneficial effect might be imparted by an immune cell type called macrophages/microglia."

The research was conducted at the Rensselaer Center for Biotechnology and Interdisciplinary Studies, which has a focus on neurodegenerative disease. Dr. Hurley worked with Rensselaer professors Robert Linhardt, a glycans expert and inventor of synthetic heparin, and Chunyu Wang, whose ongoing research has detailed several mechanisms in the production and spread of proteins implicated in Alzheimer's.

"This insight reveals a new mechanism and path to treatment of neurodegenerative diseases like Alzheimer's through an interdisciplinary approach, and is emblematic of the CBIS strength in research and discovery and provides a new angle to human health and well-being," said Deepak Vashishth, director of the CBIS.

The circadian system is composed of a core set of clock proteins that anticipate the day/night cycle by causing daily oscillations in the levels of enzymes and hormones, ultimately affecting physiological parameters such as body temperature and the immune response. Disruption of the circadian system is increasingly associated with diseases like diabetes, cancer, and Alzheimer's.

A telltale sign of Alzheimer's disease is plaques, extracellular clumps of AB42 in the brain. Macrophages (referred to as microglia when they reside in the brain), which are immune cells that seek and destroy unwanted material, clear AB42 from the brain by ingesting it in a process called phagocytosis. In earlier research, Dr. Hurley and collaborators at the Royal College of Surgeons in Ireland investigated circadian control of macrophages, amassing an exhaustive dataset that made it possible to see which macrophage RNA and proteins oscillate with a circadian rhythm. The researchers noticed oscillations in enzymes that help to make two proteins on the macrophage cell surface -- heparan sulfate proteoglycan and chondroitin sulfate proteoglycan- both of which are known to play a role in regulating clearance of AB42.

Could these cell surface proteoglycans be a link between the circadian system and Alzheimer's? In a series of elegant experiments testing this hypothesis, the team established that the amount of AB42 ingested by healthy macrophages oscillates with a daily circadian rhythm. That pattern did not occur in macrophages without a circadian clock. They also measured daily oscillations in the levels of heparan sulfate proteoglycans and chondroitin sulfate proteoglycans produced on the surface of macrophage cells with healthy circadian cycles. Peak AB42 clearance occurred as production of surface cell proteoglycans was at its lowest level, and removal of these proteoglycans increased ingestion, which suggests that the proteoglycans inhibit AB42 clearance.

"What's clear is that this is all timed by the circadian clock," said Dr. Hurley. "When there's a lot of these cell surface proteoglycans, the macrophages don't ingest the AB42. We're not certain why that would be, but there is definitely a relationship."

That relationship could be used to develop therapies that would encourage greater AB42 clearance, perhaps by boosting the amplitude of daily oscillations, which tend to diminish as we age.

"In theory, if we could boost that rhythm, perhaps we could increase the clearance of AB42 and prevent damage to the brain," said Dr. Hurley.

At Rensselaer, Hurley, Linhardt, and Wang were joined in the research by Gretchen T. Clark, Yanlei Yu, Cooper A. Urban, Fuming Zhang, and Guo Fu, who is now at the Chinese Academy of Sciences. "Circadian Control of Heparan Sulfate Levels Times Phagocytosis of Amyloid Beta Aggregates" was produced with support from the National Institutes of Health, the National Science Foundation, and the Warren Alpert Foundation.


Story Source:

Materials provided by Rensselaer Polytechnic Institute. Original written by Mary L. Martialay. Note: Content may be edited for style and length.


Journal Reference:

  1. Gretchen T. Clark, Yanlei Yu, Cooper A. Urban, Guo Fu, Chunyu Wang, Fuming Zhang, Robert J. Linhardt, Jennifer M. Hurley. Circadian control of heparan sulfate levels times phagocytosis of amyloid beta aggregates. PLOS Genetics, 2022; 18 (2): e1009994 DOI: 10.1371/journal.pgen.1009994
 

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