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.

Friday, June 5, 2020

Sleep loss disrupts pericyte-brain endothelial cell interactions impairing blood-brain barrier function

You'll need your doctor you give you a sleep protocol because one of the 5 causes

of the neuronal cascade of death is these and that is already causing you brain blood barrier problems. 

Blood-Brain Barrier Integrity Suffers Days After Ischemic Stroke Leading To Serious Complications
 

Lysosomal Membrane Permeabilization as a Key Player in Brain Ischemic Cell Death: a “Lysosomocentric” Hypothesis for Ischemic Brain Damage

The latest here:

Sleep loss disrupts pericyte-brain endothelial cell interactions impairing blood-brain barrier function

GabrielaHurtado-AlvaradoaArturoContis-Montes de OcacStefaniePaola López-CervantesbdMinaKonigsbergdMaria A.DeliefBeatrizGómez-Gonzáleza






Highlights

Sleep loss induces pericyte detachment from capillary walls.
Sleep loss reduces PDGFR-β and Connexin-43 expression in brain microvessels.
Pericyte detachment during sleep loss decreases claudin-5 and occludin expression.
Pericyte detachment during sleep loss increases blood-brain barrier permeability.
Sleep loss increases MMP-9, p-NFκB, A2A receptor expression in brain microvessels.

Abstract

Sleep loss in the rat increases blood-brain barrier permeability to circulating molecules by disrupting interendothelial tight junctions. Despite the description of the ultrastructure of cerebral microvessels and the evidence of an apparent pericyte detachment from capillary wall in sleep restricted rats the effect of sleep loss on pericytes is unknown. Here we characterized the interactions between pericytes and brain endothelial cells after sleep loss using male Wistar rats. Animals were sleep-restricted 20 h daily with 4 h sleep recovery for 10 days. At the end of the sleep restriction, brain microvessels (MVs) were isolated from cerebral cortex and hippocampus and processed for Western blot and immunocytochemistry to evaluate markers of pericyte-endothelial cell interaction (connexin 43, PDGFR-β), tight junction proteins, and proinflammatory mediator proteins (MMP9, A2A adenosine receptor, CD73, NFκB). Sleep restriction reduced PDGFR-β and connexin 43 expression in MVs; in addition, scanning electron microscopy micrographs showed that pericytes were detached from capillary walls, but did not undergo apoptosis (as depicted by a reduced active caspase-3 expression). Sleep restriction also decreased tight junction protein expression in MVs and increased BBB permeability to low- and high-molecular weight tracers in in vivo permeability assays. Those alterations seemed to depend on a low-grade inflammatory status as reflected by the increased expression of phosphorylated NFκB and A2A adenosine receptor in brain endothelial cells from the sleep-restricted rats. Our data show that pericyte-brain endothelial cell interaction is altered by sleep restriction; this evidence is essential to understand the role of sleep in regulating blood-brain barrier function.

No comments:

Post a Comment