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.

Saturday, February 9, 2019

Circulating antioxidants and Alzheimer disease prevention: A Mendelian randomization study

While this one failed, this type of research is EXACTLY what we need to know. Which circulating micronutients will prevent dementia and what ARE THE EXACTS AMOUNTS TO CONSUME to get to those levels. Guidelines are worthless, fire anyone who suggests guidelines, we can't have such lazy people stay in the stroke field.

Circulating antioxidants and Alzheimer disease prevention: A Mendelian randomization study


American Journal of Clinical NutritionWilliams DM, et al. | February 04, 2019
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In this study, researchers determined if long-term circulating antioxidant exposure plays a role in Alzheimer disease (AD) etiology by testing the premise that AD risk would be lower in individuals with lifelong, genetically predicted increases in concentrations of four circulating antioxidants that are modifiable by diet. To that end, they performed two-sample Mendelian randomization analyses, and investigated single-nucleotide polymorphisms (SNPs) that determine variation in circulating ascorbate (vitamin C), β-carotene, retinol (vitamin A), and urate by analyzing published genetic-association studies. Using data of a genome-wide association study of late-onset AD cases and controls (n=17,008 and 37,154, respectively), they extracted statistics for genotype associations with AD risk for each set of SNP data. According to findings, no lowered risk of AD was observed in association with higher exposure to ascorbate, β-carotene, retinol, or urate. Replication Mendelian randomization studies could assess this further, providing larger AD case-control samples and, ideally, using additional variants to instrument each exposure.
Read the full article on American Journal of Clinical Nutrition

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