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, May 1, 2019

Is Memory Decline Associated With Inflammatory Response?

Now is your doctor testing for this or just lazily using Occam's Razor to blame poor memory on stroke and do nothing about it? Ask your doctor that question, you need to know their competency. Does your doctor understand Occam's Razor and the bias it introduces?

 

Is Memory Decline Associated With Inflammatory Response?


First Published November 21, 2017 Research Article
Objective: To examine whether changes in memory over a 10-year period could predict a change in C-reactive protein (CRP) levels.  
Method: A mixed model analysis was first conducted to obtain the estimates for change in memory over the 10-year period using data from the Health and Retirement Study. Then a multivariate regression to determine whether a change in episodic memory could predict subsequent CRP levels was conducted. Furthermore, a general linear model was conducted to determine differences in CRP levels among different rates of change in episodic memory.  
Results: Greater declines in episodic memory were associated with higher levels of subsequent CRP (Estimate = −0.32, SE = 0.12, β = −.03, p = .008). The general linear model revealed that those with greater memory declines were more likely to have higher levels of CRP, F = 26.50, p < .001. Discussion: These results highlight the notion that memory decline and inflammation may be intertwined, and we discuss various avenues that warrant further investigation.

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