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, February 13, 2017

Growing a Cellular Tree With Healthy Branches

We need this for dendrite outgrowth. What is your doctor doing to followup with the researchers to create a stroke protocol or start human research on this? If nothing is being done you will need to call the hospital president and ask that that incompetent doctor is fired. We have to clear out the dead wood somehow or we will always be stuck at 10% full recovery. I will not be polite in the face of proven incompetency.
http://neurosciencenews.com/dendrites-genetics-axons-4131/

Univ. of Iowa biologists show how brain cells get the message to develop a signaling network.
When you think of a neuron, imagine a tree.
A healthy brain cell indeed looks like a tree with a full canopy. There’s a trunk, which is the cell’s nucleus; there’s a root system, embodied in a single axon; and there are the branches, called dendrites.
Neurons in your brain pass signals from one to another like they’re playing an elaborate, lightning-quick game of telephone, using axons as the transmitters and dendrites as the receivers. Those signals originate in the brain and are passed throughout the body, culminating in simple actions, such as wiggling a toe, to more complex instructions, such as following through on a thought.
Just as you can judge a healthy tree by its canopy, so too can scientists judge a healthy neuron by its dendritic branches. But it had been unclear what causes dendrites to grow, and where those instructions to grow come from.
Biologists at the University of Iowa have determined a group of genes associated with neurons help regulate dendrites’ growth. But there’s a catch: These genes, called gamma-protocadherins, must be an exact match for each neuron for the cells to correctly grow dendrites.
The findings may offer new insight into what causes aggressive or stunted dendrite growth in neurons, which could help explain the biological reasons for some mental-health diseases, as well as help researchers better understand brain development in babies born prematurely.
“Disrupted dendrite arborization is seen in the brains of people with autism and schizophrenia, so processes like the one we have uncovered here may have relevance to human disorders,” says Joshua Weiner, a molecular biologist at the UI and corresponding author on the paper, published online this month in the journal Cell Reports.
Gamma-protocadherins are called “adhesion molecules” because they stick out from a cell’s membrane to bind and hold cells together. The researchers learned about their role by giving a developing brain cell in a mouse the same gamma-protocadherin as in surrounding cells. When they did, the cells grew longer, more complex dendrites. But when the researchers outfitted a mouse neuron with a different gamma-protocadherin than the cells around it, dendritic growth was stunted.
The human brain is filled with neurons. Scientists think adults have 100 billion brain cells, each in close proximity to others and all seeking to make contact through their axons and dendrites. The denser a neuron’s dendritic network, the more apt a cell is to be in touch with another and aid in passing signals.
Gamma-protocadherins act like molecular Velcro, binding neurons together and instructing them to grow their dendrites. Weiner and his team figured out their role when they observed paltry dendritic growth in mouse brain cells where the gamma-protocadherins had been silenced.
The researchers went further in the new study. Using mice, they expressed the same type of gamma-protocadherin (labeled either as A1 or C3) in neurons in the cerebral cortex, a region of the brain that processes language and information. After five weeks, the neurons had sizeable dendritic networks, indicative of a healthy, normally functioning brain. Likewise, when they turned on a gamma-protocadherin gene in a neuron different from the gamma-protocadherin gene with the cells surrounding it, the mice had limited dendrite growth after the same time period.
That’s important because human neurons carry up to six gamma-protocadherins, meaning there are many combinations potentially in play. Yet, it seems the “grow your dendrite” signal only happens when neurons carrying the the same gamma-protocadherin gene pair up.

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