Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, February 22, 2018

Liquefaction of the brain following stroke shares a similar molecular and morphological profile with atherosclerosis and mediates secondary neurodegeneration in an osteopontin dependent mechanism

Well shit, another area needing followup, which will likely not occur until your grandchildren need it.  Do we need to aspirate this liquid from our brain? 
https://www.biorxiv.org/content/early/2018/02/16/264275
Amanda Chung, Jennifer Frye, Jacob C. Zbesko, Eleni Constantopoulos, Megan I. Hayes, Anna G. Figueroa, W. Antony Day, John P. Konhilas, Brian S. McKay, Thuy-Vi V. Nguyen, Kristian P. Doyle

Abstract

The response to ischemic injury in the brain is different to the response to ischemic injury in other organs and tissues. Almost exclusive to the brain, and for unknown reasons, dead tissue liquefies in response to ischemia by the process of liquefactive necrosis. However, the data we present here indicate that at the macroscopic, microscopic, and molecular level, liquefactive necrosis strongly resembles atherosclerosis. We show that chronic stroke infarcts contain foamy macrophages, cholesterol crystals, high levels of osteopontin and matrix metalloproteinases, and a similar cytokine profile to atherosclerosis. Excessive cholesterol loading of macrophages is a principal driver of atherosclerosis. Therefore, because cholesterol is an important structural component of myelin, liquefactive necrosis in response to stroke may be caused by an inflammatory response to myelin debris that is prolonged by the formation of cholesterol crystals within macrophages. We propose that this results in the chronic production of high levels of proteases, which in a partially osteopontin dependent mechanism, causes secondary neurodegeneration and encephalomalacia of the surrounding tissue. In support of this, we show that genetically ablating osteopontin substantially reduces the production of degradative enzymes following stroke, reduces secondary neurodegeneration, and improves recovery. These findings suggest that treatments that prevent atherosclerosis or target the regression of atherosclerosis may also be useful for mitigating the harmful effects of liquefactive necrosis following stroke.

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