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, April 3, 2019

Autoimmunity in acute ischemic stroke and the role of blood-brain barrier: the dark side or the light one?

You have described a whole series of problems here. 10 million stroke survivors a year want to know how to prevent these problems. When are you going to deliver solutions?

Or are we waiting for SOMEONE ELSE TO SOLVE THE PROBLEM? 

Like that will ever occur with the current stroke leadership. 

Autoimmunity in acute ischemic stroke and the role of blood-brain barrier: the dark side or the light one?

  • Nikolay V. Tsygan
  • Alexandr P. Trashkov
  • Igor V. Litvinenko
  • Viktoriya A. Yakovleva
  • Alexandr V. Ryabtsev
  • Andrey G. Vasiliev
  • Leonid P. ChurilovEmail author
  • Nikolay V. Tsygan
    • 1
    • 2
  • Alexandr P. Trashkov
    • 1
    • 3
  • Igor V. Litvinenko
    • 2
  • Viktoriya A. Yakovleva
    • 2
  • Alexandr V. Ryabtsev
    • 2
  • Andrey G. Vasiliev
    • 4
  • Leonid P. Churilov
    • 5
    Email author
  1. 1.Department of Molecular and Radiation BiophysicsB.P. Konstantinov Petersburg Nuclear Physics InstituteGatchina, Leningrad RegionRussian Federation
  2. 2.Department of Nervous DiseasesS.M. Kirov Military Medical AcademySaint PetersburgRussian Federation
  3. 3.Department of Experimental PharmacologyI.M. Sechenov Institute of Evolutionary Physiology and BiochemistrySaint PetersburgRussian Federation
  4. 4.Department of Pathological Physiology with the Course of ImmunopathologySaint Petersburg State Pediatric Medical UniversitySaint PetersburgRussian Federation
  5. 5.Department of Pathology, Laboratory of the Mosaic of AutoimmunitySaint Petersburg State UniversitySaint PetersburgRussian Federation
Review

Abstract

This article presents a synopsis of the current data on the mechanisms of blood-brain barrier (BBB) alteration and autoimmune response in acute ischemic stroke. Most researchers confirm the relationship between the severity of immunobiochemical changes and clinical outcome of acute ischemic stroke. Ischemic stroke is accompanied by aseptic inflammation, which alters the brain tissue and exposes the co-stimulatory molecules of the immune system and the neuronal antigens. To date, BBB is not considered the border between the immune system and central nervous system, and the local immune subsystems are found within and behind the BBB. BBB disruption contributes to the leakage of brain autoantigens and induction of secondary autoimmune response to neuronal antigens and long-term inflammation. Glymphatic system function is altered and jeopardized both in hemorrhagic and ischemic stroke types. The receptors of innate immunity (toll-like receptor-2 and toll-like receptor-4) are also involved in acute ischemia-reperfusion injury. Immune response is related to the key processes of blood clotting and fibrinolysis. At the same time, the stroke-induced immune activation may promote reparation phenomena in the brain. Subsequent research on the reduction of the acute ischemic brain injury through the target regulation of the immune response is promising.(And who the fuck is going to do that followup research?)

No comments:

Post a Comment