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.

Monday, October 10, 2022

Flavonoids from Stems and Leaves of Scutellaria baicalensis Georgi Improve Composited Aβ-induced Alzheimer's Disease Model Rats' Memory and Neuroplasticity Disorders

 

WHOM will be doing the human testing? And then get the protocol rolled out to all stroke hospitals? With NO stroke leadership I'm afraid nothing will be done, other promising animal research never seems to get to human testing and protocols.  

With your elevated risk of Alzheimers/dementia you'll want your doctor following this carefully.  Is your doctor ensuring further studies occur?

Or is your doctor incompetently WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM? 

Your risk of dementia, has your doctor told you of this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

What is your doctor's EXACT PROTOCOL TO PREVENT DEMENTIA?

The latest here:

Flavonoids from Stems and Leaves of Scutellaria baicalensis Georgi Improve Composited Aβ-induced Alzheimer's Disease Model Rats' Memory and Neuroplasticity Disorders 

Hui Zhang  1 , Liu Qian-Qian  1 , Ding Sheng-Kai  1 , Hong Li  2 , Ya-Zhen Shang  1
Affiliations

Abstract

Aim: To investigate the effects and mechanism of flavonoids from stems and leaves of Scutellaria baicalensis Georgi (SSF) on the disorders in learning and memory and neuroplasticity induced by beta amyloid 25-35 (Aβ25-35) combined with aluminum trichloride (AlCl3) and human recombinant transfer factor-β1 (RHTGF-β1) (composited Aβ) in rats.

Methods: A rat Alzheimer's disease (AD) model was established by intracerebroventricular injection of Aβ25-35 combined with AlCl3 and RHTGF-β1. The successful AD model of rats was screened with Morris water maze. The successful model rats were randomly divided into a model group and three doses of SSF treated group. The Morris water maze was used to detect the rats' learning and memory abilities. The real-time fluorescence quantitative (qPCR) was applied to assay the mRNA expressions of CaM, CamkIV and Ferritin, as well as the neuroplasticity factors of HuB, HuC and HuD. The Western blotting was used to measure the protein expressions of CaM, CamkIV, HuB/D, HuC+HuD and Ferritin in CaM-CamkIV-CREB signal pathway.

Results: Compared with sham group, the abilities of learning and memory in the model group were significantly impaired (P<0.01), and the mRNA or protein expressions of CaM, CamkIV, HuB, HuC, HuD, HuB/D, HuC+HuD and Ferritin in CaM-CamkIV-CREB signal pathway were abnormal changed in model group. However, the three doses of SSF can differently ameliorated the impaired learning and memory and regulate the abnormal expressions of mRNA or protein in rats' CaM, CamkIV, HuB, HuC, HuD, HuB/D, HuC+HuD and Ferritin induced by composited Aβ.

Conclusion: The improvement of SSF on the learning and memory disorder induced by composited Aβ is primarily derived from the positive regulation in CaM-CamkIV-CREB signal pathway and activation in neuroplasticity.

Keywords: Alzheimer's disease; CaM-CamkIV-CREB signal pathway; Flavonoids from stems and leaves of Scutellaria baicalensis Georgi; learning and memory; neuroplasticity.

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