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.

Tuesday, May 21, 2019

Exercise and antioxidants: A winning combination for brain health?

Your doctors and stroke hospital will completely fail at creating EXACT exercise protocols and EXACT antioxidant protocols. You're screwed because they will do nothing to help you navigate the best course of action. You are surrounded by incompetent medical 'professionals'.  Guidelines like this are the lazy version of professionalism. This would never be allowed in the business world, firings would be the result.

Exercise and antioxidants: A winning combination for brain health?

MedicalXpress Breaking News-and-Events | May 20, 2019
An international team of researchers representing several institutions in Japan and the United States has published promising findings that may stand to benefit people living with the specter of Alzheimer's and other neurodegenerative diseases, as well as age-related cognitive decline.
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In their paper published in PNAS, "Leptin in hippocampus mediates benefits of mild exercise by an antioxidant on neurogenesis and memory," Yook and colleagues present results from a series of experiments—murine and in vitro—that elucidate the role of leptin in cognitive function. Leptin is a hormone that is produced in adipose tissue and in the hippocampus, the part of the brain where memory and spatial learning are processed.
The relationship between exercise and improved cognitive function is well established. Likewise, certain dietary supplements, for example, docasahexaenoic acid (DHA) have also shown promise in improving cognition and in slowing or halting cognitive decline. The effect of both exercise and supplementation with an antioxidant on plasticity and cognitive function within the hippocampus has until now been largely unexplored, however. Previous research has demonstrated that leptin in particular is a promising therapeutic target for neurodegenerative diseases such as Alzheimer's.
Yook and colleagues sought to answer the particular question of whether mild exercise (ME) combined with the antioxidant supplement astaxanthin (AX) might confer benefit in terms of cognitive function and neuronal plasticity; and whether or not the two interventions—AX and ME together—could have a synergistic effect beyond the additive effects of either treatment administered separately. The investigators "hypothesized that ME-enhanced hippocampal neurogenesis and memory might be further improved with dietary AX via mediation by a neurotrophic factor such as h-LEP [hippocampal leptin]." To test their hypothesis, they conducted a series of experiments on mice and in vitro using human brain cell lines.
The first experiment examined the performance of four groups of wild-type mice on standard tests used to evaluate murine memory and spatial learning. The mice comprised the following groups: sedentary with placebo (SE+PL); mild exercise with placebo (ME+PL); sedentary with astaxanthin (SE+AX); and mild exercise with astaxanthin (ME+AX). The SE+PL group performed the worst while the ME+PL and SE+AX groups both performed better. The best performers were the mice in the ME+AX group, a finding that supports the enhanced effects of both interventions on memory and spatial learning. The test data were further reinforced by cell counts of Ki67-positive cells and BrdU/NeuN cells, both measures of adult hippocampal neurogenesis (AHN), that showed "a strong additional effect" at work when AX and ME were combined.
To better understand the role of LEP in the changes observed in the mouse brains, the researchers undertook a DNA microarray and gene expression analysis, looking at up- and down-regulated genes in relation to the various groups of mice, and particularly where the genes overlapped between treatment groups. Their results, especially with regard to the antioxidant ABHD3 gene and the LEP gene, confirm the synergistic effect of AX and ME on spatial memory and AHN.
Importantly, the study authors also found after further analysis that circulating plasma leptin levels remained unchanged among treatment groups, a finding which demonstrates that h-LEP—that is, leptin found in the hippocampus—is the specific target molecule responsible for the improvements demonstrated by combined ME+AX therapy. At the protein level, h-LEP and LEPRa (a leptin receptor), were also correlated with improvements in spatial memory, while the AKT/STAT3 signaling pathways were implicated in these improvements as well.
For the in vitro experiment, the investigators used human neuroblastoma cell lines—cells known to endogenously synthesize leptin—to observe the effect of exposing them directly to varying amounts of AX. They noticed a direct dose-dependent response with regard to expressed leptin, as well as up-regulation in the ABHD3 and LEP genes.
Finally, to establish whether or not leptin is required to achieve the synergistic effect seen with the AX+ME mice, Yook and colleagues repeated their earlier mouse experiment on ob/ob knockout mice, using leptin-deficient animals bred for obesity and diabetes research. They found that leptin deficiency did indeed play a role, as these mice performed poorly relative to the wild-type mice, thus confirming leptin as the crucial component of the AX+ME synergy observed in the prior experiment.
To further confirm the mediative effect of leptin in the brain, the scientists injected the ob/ob mice with leptin over the course of 4 weeks, finding that the synergistic effects of AX and ME were restored in these mice. The researchers also observed increased levels of proteins pIGF1R and pP13K in ME+PL and ME+AX groups, independently of whether or not the mice were wild-type or knockout.
The researchers offer further discussion of several details of their study, for example, commenting that "our results of increased leptin and IGF1R support the possibility that the enhancement of AHN and memory function by ME+AX may be due to the interplay of both leptin and IGF1R expression," and also noting a correlation between memory increase and an increase in levels of the hippocampal receptor LEPRa.
While the results shown here in murine models are certainly promising, what might this mean in a clinical context for humans? For one thing, mild exercise for humans has been characterized in this paper as that which is typical of a yoga or tai chi session, which puts it within reach of many people. Another factor is the ready availability of the relatively inexpensive nutritional supplement astaxanthin.
Ultimately, the authors conclude that "our findings advance the notion that ME combined with a dietary antioxidant such as AX, which induces endogenous h-LEP, may be an effective nonpharmacological strategy for preventing or improving cognitive function and brain health, and for slowing cognitive decline. This strategy may be particularly useful in vulnerable individuals, including the elderly."
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