Ask you competent? doctor if in the ensuing 8 years was ANYTHING DONE TO GET SURVIVORS CLOSER TO 100% RECOVERY! And keep asking until they acknowledge total failure on that front because 100% recovery isn't a goal in stroke research! All because we have fucking failures of stroke associations that don't listen to survivor needs!
Recent Progress in Therapeutic Strategies for Ischemic Stroke - 2016
Abstract
Possible
strategies for treating stroke include neuroprotection in the acute
phase of cerebral ischemia and stem cell therapy in the chronic phase of
cerebral ischemia. Previously, we have studied the temporal and spatial
expression patterns of c-fos, hypoxia inducible factor-1α (HIF-1α),
heat shock protein 70 (HSP70), and annexin V after 90 min of transient
middle cerebral occlusion in rats and concluded that there is a time
window for neuroprotection from 12 to 48 h after ischemia. In addition,
we have estimated the neuroprotective effect of glial cell line-derived
neurotrophic factor (GDNF) by injecting Sendai viral vector containing
the GDNF gene into the postischemic brain. This Sendai virus-mediated
gene transfer of GDNF showed a significant neuroprotective effect in the
ischemic brain. Additionally, we have administered GDNF and hepatocyte
growth factor (HGF) protein into the postischemic rat brain and
estimated the infarct size and antiapoptotic and antiautophagic effects.
GDNF and HGF significantly reduced infarct size, the number of
microtubule-associated protein 1 light chain 3 (LC3)-positive cells, and
the number of terminal deoxynucleotidyl transferase-mediated
dUTP-biotin in situ nick-end labeling (TUNEL)-positive cells, indicating
that GDNF and HGF were greatly associated with not only the
antiapoptotic effect but also the antiautophagic effects. Finally, we
have previously transplanted undifferentiated iPSCs into the ipsilateral
striatum and cortex at 24 h after cerebral ischemia. Histological
analysis was performed at 14 and 28 days after cell transplantation, and
we found that iPSCs could supply a great number of
doublecortin-positive neuroblasts but also formed tridermal teratoma in
the ischemic brain. Our results suggest that iPSCs have a potential to
provide neural cells after ischemic brain injury if tumorigenesis is
properly controlled. In the future, we will combine these strategies to
develop more effective therapies for the treatment of strokes.
Introduction
Stroke is the second leading cause of death in the world and results in a drastic reduction in the quality of life (30).
However, an effective therapy is not yet available. Both a better
understanding of the mechanisms of ischemic brain damage and a new
strategy for patients who have suffered a stroke are urgently required.
Multiple molecular penumbra has been proposed, and this attracts the
attention as the new concept for understanding the mechanisms of
ischemic brain. Possible strategies for treating ischemic strokes are
broadly categorized into two groups: (i) neuroprotection, which prevents
damaged neurons from death in the acute phase of cerebral ischemia, and
(ii) stem cell therapy, which can theoretically repair broken neuronal
networks with newly born neurons/glias in the chronic phase of cerebral
ischemia (Fig. 1).
In this review article, we focus on our findings with multiple
molecular penumbra, neurotrophic factors for neuroprotection, and the
transplantation of induced pluripotent stem cells (iPSCs) for stem cell
therapy.
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