A novel therapeutic target for recovery after stroke

Shit this just sounds like the combination of three already known theories of the

neuronal cascade of death.

Or maybe you want to read about this research way back in September 1999?

The Role of Diaschisis in Stroke Recovery March 2018

 

Now we just need our non-existent stroke leadership to get research going to solve these neuron killer processes. That will never occur. WE HAVE NO STROKE LEADERSHIP!

1. Capillaries that don't open due to pericytes  

2. glutamate poisoning
 

3. excitotoxicity

The latest here:

A novel therapeutic target for recovery after stroke

by Institute for Basic Science

Stroke affects not only the brain areas where the blood supply is interrupted or reduced (infarct), but also other distal areas (diaschisis). The researchers studied mouse brains and found that diaschisis is due to the excessive production of the neurotransmitter GABA and that the administration of KDS2010 combined with rehabilitation can improve motor function after stroke. Credit: IBS

Researchers at the Center for Cognition and Sociality, within the Institute for Basic Science (IBS), Gwangju Institute of Science and Technology (GIST), and Korea Institute of Science and Technology (KIST) have discovered a new mechanism to explain the effects of subcortical strokes and a new possible therapeutic approach.

Every year, 15 million people worldwide suffer from stroke according to the World Health Organization. Five million of those die and another five million are permanently disabled. Stroke is one of the most commonly reported causes of death and greatly impacts patients' quality of life. However, despite its prevalence and negative impact, there are no direct medical treatments for recovery after stroke and patients rely on rehabilitation.
A stroke occurs when the blood supply is interrupted or reduced due to bleeding or occlusion of blood vessels in some part of the brain. Brain cells subsequently begin to die within minutes, causing a regional brain damage. In addition, the stroke leads to a loss of function, called diaschisis, in other brain regions connected to the damaged area. Proposed 115 years ago, diaschisis worsens symptoms and prognosis of stroke patients. However, despite broad clinical interest, diaschisis' molecular and cellular mechanisms are still unknown.
In this study, the researchers reported that diaschisis in the cortex of the mouse brain with subcortical stroke is caused by the decline of neuronal activity, due to the reduction in neuronal glucose uptake. They showed that this is dependent on pathological changes of astrocytes, the most abundant cell type in the brain. "Astrocytes respond to the presence of any chemical disregulation, caused by stroke. They become reactive, proliferate and increase in size," says C. Justin Lee, Director of the Cognitive Glioscience Group, at the IBS Center for Cognition and Sociality and co-corresponding author of this research. The researchers discovered that reactive astrocytes synthesize and release an excessive amount of GABA, an inhibitory neurotransmitter, that affects the activity of neighboring motor neurons.