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.

Saturday, December 23, 2017

Effects of Scopolamine and Melatonin Cotreatment on Cognition, Neuronal Damage, and Neurogenesis in the Mouse Dentate Gyrus

Mouse, not human, so of course followup is needed. Save your pennies so you can hire your own researchers on this, it is the only way followup will get done.  Or GoFundMe.
https://link.springer.com/article/10.1007/s11064-017-2455-x

  • Bai Hui Chen
  • Ji Hyeon Ahn
  • Joon Ha Park
  • Soo Young Choi
  • Yun Lyul Lee
  • Il Jun Kang
  • In Koo Hwang
  • Tae-Kyeong Lee
  • Bich-Na Shin
  • Jae-Chul Lee
  • Seongkweon Hong
  • Yong Hwan Jeon
  • Myoung Cheol Shin
  • Jun Hwi Cho
  • Moo-Ho Won
  • Young Joo Lee
  • Bai Hui Chen
    • 1
  • Ji Hyeon Ahn
    • 2
  • Joon Ha Park
    • 2
  • Soo Young Choi
    • 2
  • Yun Lyul Lee
    • 3
  • Il Jun Kang
    • 4
  • In Koo Hwang
    • 5
  • Tae-Kyeong Lee
    • 6
  • Bich-Na Shin
    • 6
  • Jae-Chul Lee
    • 6
  • Seongkweon Hong
    • 7
  • Yong Hwan Jeon
    • 8
  • Myoung Cheol Shin
    • 9
  • Jun Hwi Cho
    • 9
  • Moo-Ho Won
    • 6
  • Young Joo Lee
    • 10
  1. 1.Department of Histology and Embryology, Institute of NeuroscienceWenzhou Medical UniversityWenzhouPeople’s Republic of China
  2. 2.Department of Biomedical Science and Research Institute for Bioscience and BiotechnologyHallym UniversityChuncheonSouth Korea
  3. 3.Department of Physiology, College of Medicine, and Institute of Neurodegeneration and NeuroregenerationHallym UniversityChuncheonSouth Korea
  4. 4.Department of Food Science and NutritionHallym UniversityChuncheonSouth Korea
  5. 5.Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary ScienceSeoul National UniversitySeoulSouth Korea
  6. 6.Department of Neurobiology, School of MedicineKangwon National UniversityChuncheonSouth Korea
  7. 7.Department of Surgery, School of MedicineKangwon National UniversityChuncheonSouth Korea
  8. 8.Department of Radiology, School of MedicineKangwon National University, Kangwon National University HospitalChuncheonSouth Korea
  9. 9.Department of Emergency Medicine, and Institute of Medical Sciences, Kangwon National University Hospital, School of MedicineKangwon National UniversityChuncheonSouth Korea
  10. 10.Department of Emergency Medicine, Seoul Hospital, College of MedicineSooncheonhyang UniversitySeoulSouth Korea
Original Paper
  • 13 Downloads

Abstract

It has been demonstrated that melatonin plays important roles in memory improvement and promotes neurogenesis in experimental animals. We examined effects of melatonin on cognitive deficits, neuronal damage, cell proliferation, neuroblast differentiation and neuronal maturation in the mouse dentate gyrus after cotreatment of scopolamine (anticholinergic agent) and melatonin. Scopolamine (1 mg/kg) and melatonin (10 mg/kg) were intraperitoneally injected for 2 and/or 4 weeks to 8-week-old mice. Scopolamine treatment induced significant cognitive deficits 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly improved spatial learning and short-term memory impairments. Two and 4 weeks after scopolamine treatment, neurons were not damaged/dead in the dentate gyrus, in addition, no neuronal damage/death was shown after cotreatment of scopolamine and melatonin. Ki67 (a marker for cell proliferation)- and doublecortin (a marker for neuroblast differentiation)-positive cells were significantly decreased in the dentate gyrus 2 and 4 weeks after scopolamine treatment, however, cotreatment of scopolamine and melatonin significantly increased Ki67- and doublecortin-positive cells compared with scopolamine-treated group. However, double immunofluorescence for NeuN/BrdU, which indicates newly-generated mature neurons, did not show double-labeled cells (adult neurogenesis) in the dentate gyrus 2 and 4 weeks after cotreatment of scopolamine and melatonin. Our results suggest that melatonin treatment recovers scopolamine-induced spatial learning and short-term memory impairments and restores or increases scopolamine-induced decrease of cell proliferation and neuroblast differentiation, but does not lead to adult neurogenesis (maturation of neurons) in the mouse dentate gyrus following scopolamine treatment.

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