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

Tuesday, February 27, 2018

Study describes new protection mechanisms to fight neurodegeneration in Parkinson's and Alzheimer's

You'll want your doctor to follow this research because of your likely Alzheimer and Parkinsons risks.

Your chances of getting dementia.

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.
 
Your Parkinsons risk:

Study describes new protection mechanisms to fight neurodegeneration in Parkinson's and Alzheimer's

A new research study reveals RAC1 protein could be a new therapeutic target to study the molecular mechanisms related to the neurodegenerative processes in Parkinson's disease.
The study, published in the online edition of the journal Molecular Neurobiology, is led by Antonella Consiglio, researcher at the Faculty of Medicine and Health Sciences of the University of Barcelona, the Institute of Biomedicine of the UB (IBUB) and the Bellvitge Biomedical Research Institute (IDIBELL), and Esther Dalfo, from the Univesitat Autònoma de Barcelona and Universitat de Vic - Universitat Central de Catalunya.
The study describes new protection mechanisms to fight neurodegeneration which is common in neurodegenerative diseases -such as Parkinson's and Alzheimer's-, which usually display a protein accumulation. The study shows that RAC1 protein -which takes part in the assembly of the active protein, one of the elements in the skeletal substance- could be an important regulatory factor in in Parkinson's disease's neurodegeneration process.
From Caenorhabditis elegans model to patients suffering from Parkinson
In the first stages of the study, the experts proved there was a decrease in the activity of RAC1 protein in the Caenorhabditis elegans nematode -an animal model in biology and genomics- speeded up dopaminergic neuronal death and degeneration -the first ones affected by Parkinson's disease. This process caused an accumulation of α-Synuclein, the main protein that piles up in several neurodegenerative diseases (Parkinson's, Lewy body disease, etc.).
Moreover, the use of transcriptomics techniques -the study of RNA- in cells of patients with Parkinson's showed that those genes that code proteins of the family of RAC1 were at lower levels compared to cells from those healthy individuals.
With these data, the scientific team studied a population of dopaminergic neurons from patients with Parkinson's disease, which present a higher accumulation of α-Synuclein, a block in autophagy -the recycling machinery for cell compounds- and neuronal death.
Objective: boosting RAC1 protein's function
These dopaminergic neurons, obtained from pluripotent cells from patients' skin, "proved an increase of RAC1's activity which produces an improvement in the markers of the previously described pathology", says one of the first authors of the study, researcher Carles Catalayud, member of the IBUB, IDIBELL and the Center of Regenerative Medicine in Barcelona (CMRB). These results point out that boosting the function of RAC1 protein could balance the effects related to Parkinson's disease, with a benefiting result for those patients.

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