Deans' stroke musings: Examining the proliferation and fate of new cells in the brain following chronic cerebral hypoperfusion

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, January 25, 2012

Examining the proliferation and fate of new cells in the brain following chronic cerebral hypoperfusion

About time someone looked at new neurons after stroke. From the 2011 Canadian Stroke Congress.
page 119 here:
http://www.strokecongress.org/2011/wp-content/uploads/2011/12/CSC_Abstracts.pdf
Human and animal studies demonstrate that during stroke recovery the brain has a remarkable ability for innate repair. This is hypothesized to be partly due to newly dividing cells localized in the known neurogenic regions of the subgranular zone (SGZ) and subventricular zone (SVZ), as well as the infarct area. In rodents, this has primarily been shown following middle cerebral artery occlusion. Little is known whether a similar response occurs following cerebral hypoperfusion. To determine the proliferative response following cerebral hypoperfusion, we quantified proliferation one week following bilateral common carotid artery occlusion (2VO). Male Long Evans rats were randomly assigned to 2VO or sham surgery and compared to home cage controls. Proliferating cells were labeled with bromodeoxyuridine (BrdU, 2h) and brains were processed by immunohistochemistry for BrdU, doublecortin (DCX, immature neurons) and glial fibrillary acidic protein (GFAP, astrocytes). As expected BrdU+ cells were present in the SVZ and SGZ of all rats. However, qualitatively more BrdU+ cells were found in 2VO rats as compared to controls. In the SGZ, there was a 1.5 and 2.5 fold increase in BrdU+ cells in the 2VO animals compared to sham and home cage controls, respectively. BrdU+ cells were also observed in hypoperfused rats in the prefrontal cortex (bregma +2.96) and the striatum (bregma +1.18). The cells in these two regions were not positive for DCX or GFAP, suggesting that they are neither immature neurons nor astrocytes. Following 2VO there is an increase in proliferation in the known adult neurogenic regions and striatum, which is commonly observed
in other stroke models. To our knowledge, this is the first identification of cell division in the cortex following chronic hypoperfusion. This is exciting as these newly dividing cells may be able to be harnessed in order to enhance functional recovery.