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.

Sunday, September 20, 2020

Graphene-Based Nanoparticles as Potential Treatment Options for Parkinson’s Disease: A Molecular Dynamics Study

You might very well need this, so have your doctor and hospital follow this closely and create protocols for this.  Of course your doctors already know about graphene from this in February 2016, sorry there is no sarcasm marker that I can use for that last statement.

Graphene Shows Promise For Brain Implants February, 2016

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

Graphene-Based Nanoparticles as Potential Treatment Options for Parkinson’s Disease: A Molecular Dynamics Study

Authors Alimohammadi E, Khedri M, Miri Jahromi A, Maleki R, Rezaian M

Received 1 June 2020

Accepted for publication 8 September 2020

Published 18 September 2020 Volume 2020:15 Pages 6887—6903

DOI https://doi.org/10.2147/IJN.S265140

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Anderson Oliveira Lobo


Ehsan Alimohammadi1 *,* Mohammad Khedri2 *,* Ahmad Miri Jahromi,3 Reza Maleki,4 Milad Rezaian5

1Neurosurgery Department, Kermanshah University of Medical Sciences, Kermanshah, Iran; 2Department of Chemical Engineering, Amirkabir University of Technology (Tehran Polytechnic), Tehran 1591634311, Iran; 3Department of Petroleum Engineering, Amirkabir University of Technology (Tehran Polytechnic), Tehran 1591634311, Iran; 4Department of Chemical Engineering, Sharif University of Technology, Tehran, Iran; 5Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran 19839-63113, Iran

*These authors contributed equally to this work

Correspondence: Reza Maleki
Department of Chemical Engineering, Sharif University of Technology, Tehran, Iran
Email Rezamaleki96@gmail.com

Introduction: The study of abnormal aggregation of proteins in different tissues of the body has recently earned great attention from researchers in various fields of science. Concerning neurological diseases, for instance, the accumulation of amyloid fibrils can contribute to Parkinson’s disease, a progressively severe neurodegenerative disorder. The most prominent features of this disease are the degeneration of neurons in the substantia nigra and accumulation of α-synuclein aggregates, especially in the brainstem, spinal cord, and cortical areas. Dopamine replacement therapies and other medications have reduced motor impairment and had positive consequences on patients’ quality of life. However, if these medications are stopped, symptoms of the disease will recur even more severely. Therefore, the improvement of therapies targeting more basic mechanisms like prevention of amyloid formation seems to be critical. It has been shown that the interactions between monolayers like graphene and amyloids could prevent their fibrillation.
Methods: For the first time, the impact of four types of last-generation graphene-based nanostructures on the prevention of α-synuclein amyloid fibrillation was investigated in this study by using molecular dynamics simulation tools.
Results: Although all monolayers were shown to prevent amyloid fibrillation, nitrogen-doped graphene (N-Graphene) caused the most instability in the secondary structure of α-synuclein amyloids. Moreover, among the four monolayers, N-Graphene was shown to present the highest absolute value of interaction energy, the lowest contact level of amyloid particles, the highest number of hydrogen bonds between water and amyloid molecules, the highest instability caused in α-synuclein particles, and the most significant decrease in the compactness of α-synuclein protein.
Discussion: Ultimately, it was concluded that N-Graphene could be the most effective monolayer to disrupt amyloid fibrillation, and consequently, prevent the progression of Parkinson’s disease.

Keywords: α-synuclein, amyloid, graphene, Parkinson’s disease, molecular dynamics

  This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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