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, February 21, 2012

Antidepressant-like effects of Ginsenoside Rg1 produced by activation of BDNF signaling pathway and neurogenesis in the hippocampus

It wasn't clear to me exactly what they are trying to say, if only I had access to complete articles.
http://onlinelibrary.wiley.com/doi/10.1111/j.1476-5381.2012.01902.x/full

Summary

Background and purpose. Background and purpose: Ginsenoside Rg1 (Rg1) is one of the major bioactive ingredients of Panax Ginseng with little toxicity and has been shown to have neuroprotective effects. In this study, we investigated the antidepressant-like effect of Rg1 in models of depression in mice.

Experimental approach. Experimental approach: The effects of Rg1 were assessed in the forced swim test (FST) and tail suspension test (TST) in mice. Rg1 was also investigated in the chronic mild stress (CMS) mouse model of depression with imipramine being a positive control. Changes in hippocampal neurogenesis and spine density, the brain derived neurotrophic factor (BDNF) signaling pathway, and serum corticosterone level after chronic stress and Rg1 treatment were then investigated. The tryptophan hydroxylase inhibitor and the tyrosine kinase B (TrkB) inhibitor were also used in determining the antidepressive mechanism of Rg1.

Key Results. Key results: Ginsenoside Rg1 exhibited antidepressant-like activity in the FST and TST in mice without affecting locomotor activity. It was also effective in the CMS mice model of depression. Furthermore, Rg1 up-regulated the BDNF signaling pathway in the hippocampus and down-regulated serum corticosterone level during CMS procedure. In addition, Rg1 was able to reverse the decrease in dendritic spine density and hippocampal neurogenesis caused by CMS. However, Rg1 has no discernable effect on the monoaminergic system.

Conclusions and Implications. Conclusions and Implications: In conclusion, our results provide the first evidence that Rg1 has antidepressant activity via activation of BDNF signaling pathway and up-regulation of hippocampal neurogenesis.

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