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, December 21, 2019

Hydrogen sulfide improves spatial memory impairment via increases of BDNF expression and hippocampal neurogenesis following early postnatal alcohol exposure

Hydrogen sulfide research back to 2013 proved helpful for survivors and you do want BDNF. 8 posts on it here.  But shit once again nothing seems to have been done that might actually help stroke survivors. I blame our fucking failures of stroke associations, great at doing nothing for survivors. WHAT IS YOUR DOCTOR'S PROTOCOL FOR PROMOTING BDNF?

Hydrogen sulfide improves spatial memory impairment via increases of BDNF expression and hippocampal neurogenesis following early postnatal alcohol exposure






Highlights

Hydrogen sulfide improve spatial memory impairment in a model of fetal alcohol spectrum disorders.
Hydrogen sulfide reduced apoptotic cell death in model of fetal alcohol spectrum disorders
Hydrogen sulfide increased neurogenesis in model of fetal alcohol spectrum disorders
Hydrogen sulfide increased of BDNF expression in model of fetal alcohol spectrum disorders

Abstract

According to experimental and clinical findings, fetal brain development may be interrupted by maternal alcohol consumption during pregnancy. Adult hippocampal neurogenesis is thought to play a role in cognition function (i.e. learning and memory). Recent evidence suggests that ethanol administration causes major apoptotic neurodegeneration in many regions of the rats’ developing brain during the synaptogenesis period. Based on the recent studies, H2S improve learning and memory via increased neurogenesis and antiapoptotic mechanisms in different animal models. In this study, we aimed to evaluate the protective effects of hydrogen sulfide on alcohol-induced memory impairment, hippocampus neurogenesis and neuronal apoptosis in rat pups with postnatal ethanol exposure.
Administration of ethanol to male rat pups was performed through intragastric intubation on postnatal days 2-10. The pups were administered 1 mg/kg of NaHS (H2S donor) on postnatal days 2-10. For examining the spatial memory, Morris water maze test was carried out 36 days after birth. Following the behavioral test, immunohistochemical staining was performed to evaluate the expression levels of BrdU, BDNF and Apoptotic cell death was detected by TUNEL staining.
Hydrogen sulfide (H2S) treatment could significantly improve spatial memory impairment (P< 0.05) and significantly increase the expression of BrdU and BDNF in dentate gyrus area (P< 0.05). It also decreased positive TUNEL cells, compared with the ethanol group (P< 0.01).
Based on the findings, H2S makes significant neuroprotective effects on Ethanol neurotoxicity due to its neurogenesis and anti-apoptotic activity.

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