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.

Wednesday, February 13, 2019

The cytoskeleton of neurons found to play role in Alzheimer's disease

You will need to know this. What EXACTLY  is your doctor doing to followup and use protocols that prevent you from getting Alzheimers?

YOUR DOCTORS' RESPONSIBILITY!

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.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

 

The cytoskeleton of neurons found to play role in Alzheimer's disease

A researcher at the UPV/EHU-University of the Basque Country has participated in the study into the impairment of the dynamics of spines that receive information from other neurons
A researcher at the UPV/EHU has participated in a study describing what it is during the early stages of Alzheimer's that triggers the loss of dynamics and subsequent impairment of the dendritic spines, the compartments of the neurons responsible for receiving nerve impulses from other neurons. The role played by the actin cytoskeleton of these compartments and how it responds in the presence of beta-amyloid peptides, the component most commonly associated with Alzheimer's, have been described.
José Martínez-Hernández, an Ikerbasque researcher in the Neuronal Ubiquitin Pathways group in the Department of Biochemistry and Molecular Biology of the UPV/EHU's Faculty of Science and Technology, has participated in a study by the Grenoble Institut des Neurosciences which describes the relationship existing between the presence of beta amyloid peptides, known to be the components of the plaques that build up in the brains of people affected by Alzheimer's, and the rapid fall in the dynamism of the actin cytoskeleton of the dendritic spines, the neural area responsible for receiving information coming from other neurons by means of nerve impulses. This reduced dynamics prevents information from being transmitted as it should, and this ultimately triggers the loss of spines and, therefore, the synaptic capacity of the neurons.
The cytoskeleton is a three-dimensional network of proteins that provides cells with internal support, organizes their structures and intervenes in processes such as intracellular transport or traffic. One of the components of the cytoskeleton are the actin filaments which, as Dr Martínez describes, "are anchored but are constantly moving as if they were an escalator; a protein known as cofilin 1 undertakes to sever the filaments and separate the actin units, a task that keeps the dynamics active".
However, if the cofilin 1 has become phosphorylated, in other words, if a phosphorous atom is added to it, this protein moves into an inactive state, it ceases to carry out its function and at the same time prevents neural activity from taking place correctly. "In our study we analyzed samples from human brains with Alzheimer's as well as animal models of this disease, and in them we saw that the inactive form of cofilin 1 is present in higher quantities than in healthy neurons."

Relationship between beta amyloid peptides, phosphorylated cofilin 1 and the ROCK enzyme

In neuronal cultures they saw that exposure to beta amyloid peptides, the main component of the plaques or deposits that build up in the brains of individuals with Alzheimer's, leads to an increase in phosphorylated cofilin 1, and therefore causes the actin filaments to become too stabilized; the latter lose dynamism and alter the functioning of the dendritic spines. "What is more, the beta amyloid peptides lead to fewer spines in the long term; when they cease to be functional, they are gradually lost over time," highlighted the researcher.
One of the pathways of cofilin 1 phosphorylation is a kinase known as ROCK, a kind of enzyme that modifies other molecules by means of phosphorylation, sometimes activating them and other times deactivating them. In the study they wanted to see whether  ROCK enzyme, a drug used in clinical practice, the function of which is to inhibit the action of the ROCK enzyme, reversed the effect observed in the actin filaments and "we saw that it did. We have not come up with an action mechanism, but we confirmed that the inhibition of the phosphorylation pathway of cofilin 1 prevents exposure to beta amyloid peptides from causing the deactivation of the protein, and the consequent effect on the cytoskeleton of the dendritic spines," said Martínez.
"Our results support the idea that the damage caused by the beta amyloid peptides on the level of the dendritic spines during the early stages of the disease may be prevented by modulating ROCK and cofilin 1, and that, therefore, research needs to be conducted into medications that specifically stop that phosphorylation of cof1 in neurons, so that future medical treatments to combat Alzheimer's disease can be produced," concluded Dr Martínez. ­

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