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, September 16, 2015

BDNF Reduces Toxic Extrasynaptic NMDA Receptor Signaling via Synaptic NMDA Receptors and Nuclear-Calcium-Induced Transcription of inhba/Activin A

Your doctor should be jumping for joy on this because it seems to address one of the causes of the neuronal cascade of death. But I bet not a single neurologist in the world will create a stroke protocol out of this to help stroke survivors. I welcome any and all neurologists to explain why you aren't doing anything about this. Saying it is not completely proven by research is not a valid excuse because YOU should be doing the research to prove it then.
http://www.cell.com/cell-reports/abstract/S2211-1247%2815%2900798-6?
David Lau
,
C. Peter Bengtson
,
Bettina Buchthal
,
Hilmar Badingcorrespondence
Open Access
DOI: http://dx.doi.org/10.1016/j.celrep.2015.07.038
|
Open access funded by the Author(s)
Figure thumbnail fx1

Highlights

  • •BDNF-induced neuroprotection requires synaptic NMDA receptors and nuclear calcium
  • •BDNF-nuclear calcium signaling induces transcription of inhba/activin A
  • •Activin A reduces toxic extrasynaptic NMDA receptor signaling, shielding mitochondria
  • •Activin A protects against excitotoxic cell death in cultured neurons and in vivo

Summary

The health of neurons is critically dependent on the relative signaling intensities of survival-promoting synaptic and death-inducing extrasynaptic NMDA receptors. Here, we show that BDNF is a regulator of this balance and promotes neuroprotection by reducing toxic NMDA receptor signaling. BDNF acts by initiating synaptic NMDA-receptor/nuclear-calcium-driven adaptogenomics, leading to increased expression of inhibin β-A (inhba). Inhibin β-A (its homodimer is known as activin A) in turn reduces neurotoxic extrasynaptic NMDA-receptor-mediated calcium influx, thereby shielding neurons against mitochondrial dysfunction, a major cause of excitotoxicity. Thus, BDNF induces acquired neuroprotection by enhancing synaptic activity and lowering extrasynaptic NMDA receptor death signaling through a nuclear calcium-inhibin β-A pathway. This process, which confers protection against ischemic brain damage in a mouse stroke model, may be compromised in Huntington’s disease, Alzheimer’s disease, or aging-related neurodegenerative conditions that are associated with reduced BDNF levels and/or enhanced extrasynaptic NMDA receptor signaling.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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