Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Monday, October 3, 2016

Caffeine Based Compounds Show Promise Against Parkinson’s

I've only written 107 posts on coffee and 49 on caffeine which means your doctor has missed writing the article; 'Coffee-based compounds show promise against stroke'. But then we already know your doctor and stroke hospital are totally incompetent against stroke.
http://neurosciencenews.com/caffeine-parkinsons-dopamine-5167/
Summary: Researchers have developed two caffeine based compounds that show promise in the fight against Parkinson’s disease.
Source: University of Saskatchewan.
A team of researchers from the University of Saskatchewan has developed two caffeine-based chemical compounds that show promise in preventing the ravages of Parkinson’s disease.
Parkinson’s disease attacks the nervous system, causing uncontrolled shakes, muscle stiffness, and slow, imprecise movement, chiefly in middle-aged and elderly people. It is caused by the loss of brain cells (neurons) that produce dopamine, an essential neurotransmitter that allows neurons to “talk” to each other.
The team focused on a protein called α-synuclein (AS), which is involved in dopamine regulation.
In Parkinson’s sufferers, AS gets misfolded into a compact structure associated with the death of dopamine-producing neurons. Worse, AS appears to act like a prion disease (for example, variant Creutzfeldt-Jacob or “mad cow”). In prion diseases, one mis-folded protein triggers mis-folding in others, spreading like falling dominos.
Jeremy Lee, a biochemist from the U of S College of Medicine, and Ed Krol from the College of Pharmacy and Nutrition led the team, which included researchers Troy Harkness and Joe Kakish from the U of S College of Medicine, as well as Kevin Allen from the Drug Discovery and Research Group in the College of Pharmacy and Nutrition.
“Many of the current therapeutic compounds focus on boosting the dopamine output of surviving cells, but this is effective only as long as there are still enough cells to do the job,” Lee said. “Our approach aims to protect dopamine-producing cells by preventing α-synuclein from mis-folding in the first place.”

In Parkinson’s sufferers, AS gets misfolded into a compact structure associated with the death of dopamine-producing neurons. Worse, AS appears to act like a prion disease (for example, variant Creutzfeldt-Jacob or “mad cow”). In prion diseases, one mis-folded protein triggers mis-folding in others, spreading like falling dominos. NeuroscienceNews.com image is for illustrative purposes only.
Although the chemistry was challenging, Lee explained the team synthesized 30 different “bifunctional dimer” drugs, that is, molecules that link two different substances known to have an effect on dopamine-producing cells. They started with a caffeine “scaffold,” guided by literature that shows the stimulant has a protective effect against Parkinson’s. From this base, they added other compounds with known effects: nicotine, the diabetes drug metformin, and aminoindan, a research chemical similar to the Parkinson’s drug rasagiline.
Using a yeast model of Parkinson’s disease, Lee and his team discovered two of the compounds prevented the AS protein from clumping, effectively allowing the cells to grow normally.
“Our results suggest these novel bifunctional dimers show promise in preventing the progression of Parkinson’s disease,” Lee said.
About this Parkinson’s disease research article
Funding: Funding for the research was provided through the Saskatchewan Health Research Foundation and the Natural Sciences and Engineering Research Council of Canada. The U of S Industry Liaison Office provided initial funding through its Proof of Concept Fund and has prepared a summary of the technology, inviting potential charitable funding and commercial partnerships to help develop it further.
Source: Jennifer Thoma – University of Saskatchewan

Original Research: Abstract for “Novel Dimer Compounds That Bind α-Synuclein Can Rescue Cell Growth in a Yeast Model Overexpressing α-Synuclein. A Possible Prevention Strategy for Parkinson’s Disease” by Joe Kakish, Kevin J.H. Allen, Troy A. Harkness, Edward Stanley Krol, and Jeremy Stuart Lee in ACS Chemical Neuroscience. Published online September 27 2016 doi:10.1021/acschemneuro.6b00209

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