Deans' stroke musings: atheroprogression

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.

Showing posts with label atheroprogression. Show all posts

Wednesday, March 14, 2018

Brain-released alarmins and stress response synergize in accelerating atherosclerosis progression after stroke

You don't want more atherosclerosis after your stroke, so DEMAND your doctor come up with a solution. Not doing anything at all should be grounds for firing. Dead wood needs to be removed and we have to start someplace, your stroke hospital is not cleaning house of incompetent staff.
http://stm.sciencemag.org/content/10/432/eaao1313?utm_campaign=toc_stm_2018-03-14&et_rid=33952789&et_cid=1907187

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An alarmin(g) consequence of stroke

Patients surviving a stroke are at an increased risk for subsequent cardiovascular events. Preclinical models have shown accelerated atherosclerosis after stroke; however, the mechanisms underlying this enhanced plaque formation and inflammation in arteries have not been investigated. Now, Roth et al. have discovered that stroke-induced alarmin high-mobility group box 1 (HMGB1) release and sympathetic stress response activation exert a synergistic effect, resulting in exacerbation of atherosclerotic plaques in mice. The authors suggest that interfering with these processes after stroke might reduce the risk of secondary cardiovascular events.

Abstract

Stroke induces a multiphasic systemic immune response, but the consequences of this response on atherosclerosis—a major source of recurrent vascular events—have not been thoroughly investigated. We show that stroke exacerbates atheroprogression via alarmin-mediated propagation of vascular inflammation. The prototypic brain-released alarmin high-mobility group box 1 protein induced monocyte and endothelial activation via the receptor for advanced glycation end products (RAGE)–signaling cascade and increased plaque load and vulnerability. Recruitment of activated monocytes via the CC-chemokine ligand 2–CC-chemokine receptor type 2 pathway was critical in stroke-induced vascular inflammation. Neutralization of circulating alarmins or knockdown of RAGE attenuated atheroprogression. Blockage of β3-adrenoreceptors attenuated the egress of myeloid monocytes after stroke, whereas neutralization of circulating alarmins was required to reduce systemic monocyte activation and aortic invasion. Our findings identify a synergistic effect of the sympathetic stress response and alarmin-driven inflammation via RAGE as a critical mechanism of exacerbated atheroprogression after stroke.

http://www.sciencemag.org/about/science-licenses-journal-article-reuse

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