Deans' stroke musings: Can angiogenesis be exploited to improve stroke outcome? Mechanisms and therapeutic potential.

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.

Sunday, June 9, 2013

Can angiogenesis be exploited to improve stroke outcome? Mechanisms and therapeutic potential.

Hell yes. I'm sure your doctor will not be able to have a protocol for your use to help your recovery about this.
http://212.250.180.69/cs/111/0171/1110171.pdf
A B S T R A C T
Recent developments in our understanding of the pathophysiological events that follow acute
ischaemic stroke suggest an important role for angiogenesis which, through new blood vessel
formation, results in improved collateral circulation and may impact on the medium-to-long term
recovery of patients. Future treatment regimens may focus on optimization of this process in the
ischaemic boundary zones or ‘penumbra’ region adjacent to the infarct, where partially affected
neurons exposed to intermediate perfusion levels have the capability of survival if perfusion is
maintained or normalized. In this review, we present evidence that angiogenesis is a key feature
of ischaemic stroke recovery and neuronal post-stroke re-organization, examine the signalling
mechanisms through which it occurs, and describe the therapeutic potential of treatments aimed
at stimulating revascularization and neuroprotection after stroke.
ANGIOGENESIS AFTER STROKE: EVIDENCE
FOR ITS OCCURRENCE AND IMPORTANCE
Folkman introduced the concept of angiogenesis as a
necessity for tumour growth in 1971 [1]. Its importance
in other pathological conditions, including rheumatoid
arthritis, diabetes, myocardial infarction and stroke,
was soon realized. Krupinski et al. [2,3] demonstrated
for the first time that capillary density was increased
around infarcts in post-mortem brains of patients who
had survived acute ischaemic stroke for up to several
weeks (Figure 1). Significantly, capillary density could
be correlated with time of survival after stroke. The same
group has described the revascularization process after
MCAO[MCA(middle cerebral artery) occlusion] in a rat
model using brain vascular casts [4]. The data suggested
that new blood vessels, initiated through vascular buds,
formed regular connections with intact microvessels
within 1 week of ischaemia, the patterns being similar
to those seen in the normal brain (Figure 2).