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, August 25, 2015

Icariin decreases both APP and Aβ levels and increases neurogenesis in the brain of Tg2576 mice

Don't assume that because this TCM worked in mice that you should be doing this.
https://cld.pt/dl/download/5cf0dc5f-72b0-4b05-953e-484f624b49f6/MyPapers/l984jnf_95.pdf



Abstract
Icariin is a major component derived from the traditional Chinese herb
Epimedium brevicornum Maxim. Our previous studies have shown that icariin protects neurons from the neurotoxicity and ischemia-conditions. In
this study, we investigated the effect of icariin on the expression of amyloid precursor protein (APP) and the level of amyloid-β peptide (Aβ), as well as neurogenesis in the brain of Tg2576 mice, an animal model of Alzheimer’s disease (AD). Tg2576 mice and wild type littermates (WT) were randomly assigned to three groups: Tg2576, Tg2576+icariin and WT groups. At 9 months old, all mice were treated with icariin (60 mg/kg/d) or distilled
water for 3 months. The results showed that administration with icariin for 3 months improved the spatial working memory of Tg2576 mice as examined in Y-maze task. Furthermore, icariin treatment reduced the level of
insoluble Aβ1-40 (69%) and Aβ1-42
(50%) in the cortex and hippocampus as determined by ELISA. Western blot analysis indicated the down-regulation of the APP expression, and double staining showed the elevation of BrdU/NeuN double-positive cells in the dentate gyrus region of hippocampus compared with Tg2576 mice. The current study demonstrated that icariin improved memory function, decreased the levels of Aβ and APP in the brain and increased the neurogenesis in the hippocampus of Tg2576 mice. Taken together,
these results suggest that icariin could be a potential drug candidate for AD treatment.

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