Deans' stroke musings: Reversible recovery of neuronal structures depends on the degree of neuronal damage after global cerebral ischemia in mice

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.

Tuesday, December 13, 2016

Reversible recovery of neuronal structures depends on the degree of neuronal damage after global cerebral ischemia in mice

So are we finally getting a time limit on when the neuronal cascade of death starts? When will followup in humans occur? Greater than three hours would mean that direct action to stop

the 5 causes of the neuronal cascade of death

is needed.

http://www.sciencedirect.com/science/article/pii/S0014488616304022

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http://dx.doi.org/10.1016/j.expneurol.2016.12.002

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Highlights

•: Recovery of neuronal structures is critically dependent on the duration of ischemia.
•: Ischemic damage progressively spreads to deeper dendritic shafts.
•: The timeframe for recovery of dendritic structures is within 3–6 h after stroke onset.
•: Reversible recovery of neurons may determine the therapeutic time window for stroke.

Abstract

It has been observed by in vivo imaging that damaged neuronal structures can be reversibly restored after ischemic insults with the application of timely therapeutic interventions. However, what degree of neuronal damage can be restored and the time frame for reversible recovery of neuronal structures remain unclear. Here, transcranial two-photon imaging, histological staining and electron microscopy were used to investigate the reversible recovery of neuronal structures from dendrites to soma after different durations of global cerebral ischemia in mice. Intravital imaging revealed that the damage to dendritic structures was reversible when ischemia time was < 1 h, but they became difficult to restore after > 3 h of ischemia. Data from fixed YFP brain slice and Golgi staining indicated that the damage of dendritic structures progressively extended to deeper dendritic shafts with the extension of ischemia time. Furthermore, longer duration of ischemia caused an increasing number of degenerating neurons. Importantly, significant chromatin margination and karyopyknosis of neuron were observed after 6 h of ischemia. These data suggested that neuronal structures could be reversibly restored when ischemia time was < 1 h, but irreversible and progressive damage to neurons occurred with longer duration of ischemia. Consistently, behavioral performance of post-ischemic animals experienced an ischemia time-dependent recovery. Taken together, our data suggested that recovery of neuronal structures following ischemia was dependent on the duration of ischemia, and prevention of neuronal loss is a key target for therapeutic interventions in ischemic stroke.