Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Tuesday, January 10, 2017

Parkin functionally interacts with PGC-1α to preserve mitochondria and protect dopaminergic neurons

Would Parkin be useful is saving mitochondia from this in the first 5 minutes of the stroke?

Brain cell powerhouses appear good treatment target for stroke, TBI recovery

Possible help here:

 Parkin functionally interacts with PGC-1α to preserve mitochondria and protect dopaminergic neurons

  1. Bernard L. Schneider1,*
+ Author Affiliations
  1. 1 Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland
  2. 2 Laboratory of Integrative and Systems Physiology, EPFL, 1015 Lausanne, Switzerland
  3. 3 Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, 49503, USA
  4. 4 Centre of Interdisciplinary Electron Microscopy, EPFL, 1015 Lausanne, Switzerland
  1. *Corresponding author: Bernard Schneider, EPFL-SV-BMI-LEN, Station 19, 1015 Lausanne, Switzerland, Phone: +41 21 693 95 05, Fax: +41 21 693 95 20, Email:
  • Received August 13, 2016.
  • Revision received December 1, 2016.
  • Accepted December 2, 2016.


To understand the cause of Parkinson’s disease (PD), it is important to determine the functional interactions between factors linked to the disease. Parkin is associated to autosomal recessive early-onset PD, and controls the transcription of PGC-1α, a master regulator of mitochondrial biogenesis. These two factors functionally interact to regulate the turnover and quality of mitochondria, by increasing both mitophagic activity and mitochondria biogenesis. In cortical neurons, co-expressing PGC-1α and Parkin increases the number of mitochondria, enhances maximal respiration, and accelerates the recovery of the mitochondrial membrane potential following mitochondrial uncoupling. PGC-1α enhances Mfn2 transcription, but also leads to increased degradation of the Mfn2 protein, a key ubiquitylation target of Parkin on mitochondria. In vivo, Parkin has significant protective effects on the survival and function of nigral dopaminergic neurons in which the chronic expression of PGC-1α is induced. Ultrastructural analysis shows that these two factors together control the density of mitochondria and their interaction with the endoplasmic reticulum. These results highlight the combined effects of Parkin and PGC-1α in the maintenance of mitochondrial homeostasis in dopaminergic neurons. These two factors synergistically control the quality and function of mitochondria, which is important for the survival of neurons in Parkinson’s disease.

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