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, September 12, 2016

Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus After Ischemic Stroke

I have never been able to find any research proof that myelin is damaged in stroke but this research remarks on repairing myelin damage. So ask your doctor what stroke protocol is being used to repair your myelin.  You are on your own trying to translate the amount of exercise from gerbils to yourself, so get cracking on those calculations. Something our fucking failures of stroke associations should be doing but aren't. I bet there will be no followup in humans.
Maybe this:

Brain Equation: Subtract Protein, Generate Myelin-making Cells

Or maybe you need to look at the Myelin Repair Foundation


 

 

Long-Term Exercise Improves Memory Deficits via Restoration of Myelin and Microvessel Damage, and Enhancement of Neurogenesis in the Aged Gerbil Hippocampus After Ischemic Stroke

  1. Ji Hyeon Ahn, PhD1
  2. Jung Hoon Choi, DVM, PhD2
  3. Joon Ha Park, PhD2
  4. In Hye Kim, PhD2
  5. Jeong-Hwi Cho, MS2
  6. Jae-Chul Lee, PhD2
  7. Hyun-Mo Koo, PhD3
  8. Gak Hwangbo, PhD4
  9. Ki-Yeon Yoo, PhD5
  10. Choong Hyun Lee, DVM, PhD6
  11. In Koo Hwang, DVM, PhD7
  12. Jun Hwi Cho, MD, PhD2
  13. Soo Young Choi, PhD1
  14. Young-Guen Kwon, PhD8
  15. Young-Myeong Kim, PhD2
  16. Il-Jun Kang, PhD1
  17. Moo-Ho Won, DVM, PhD2⇑
  1. 1Hallym University, Chuncheon, South Korea
  2. 2Kangwon National University, Chuncheon, South Korea
  3. 3Kyungsung University, Busan, South Korea
  4. 4Daegu University, Gyeongsan, South Korea
  5. 5Gangneung-Wonju National University, Gangneung, South Korea
  6. 6Dankook University, Cheonan, South Korea
  7. 7Seoul National University, Seoul, South Korea
  8. 8Yonsei University, Seoul, South Korea
  1. Moo-Ho Won, DVM, PhD, Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, South Korea. Email: mhwon@kangwon.ac.kr
  2. Il-Jun Kang, PhD, Department of Food Science and Nutrition, Hallym University, Chuncheon 24252, South Korea. Email: ijkang@hallym.ac.kr

Abstract

Background. The positive correlation between therapeutic exercise and memory recovery in cases of ischemia has been extensively studied; however, long-term exercise begun after ischemic neuronal death as a chronic neurorestorative strategy has not yet been thoroughly examined.  
The purpose of this study is to investigate possible mechanisms by which exercise ameliorates ischemia-induced memory impairment in the aged gerbil hippocampus after transient cerebral ischemia. 
Methods. Treadmill exercise was begun 5 days after ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks. The animals were sacrificed 31 days after the induction of ischemia. Changes in short-term memory, as well as the hippocampal expression of markers of cell proliferation, neuroblast differentiation, neurogenesis, myelin and microvessel repair, and growth factors were examined by immunohistochemistry and/or western blots.  
Results. Four weeks of exercise facilitated memory recovery despite neuronal damage in the stratum pyramidale (SP) of the hippocampal CA1 region and in the polymorphic layer (PoL) of the dentate gyrus (DG) after I-R. Long-term exercise enhanced cell proliferation and neuroblast differentiation in a time-dependent manner, and newly generated mature cells were found in the granule cell layer of the DG, but not in the SP of the CA1 region or in the PoL of the DG. In addition, long-term exercise ameliorated ischemia-induced damage of myelin and microvessels, which was correlated with increased BDNF expression in the CA1 region and the DG.  
Conclusions. These results suggest that long-term treadmill exercise after I-R can restore memory function through replacement of multiple damaged structures in the ischemic aged hippocampus.
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