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, October 30, 2024

Recent Progress in Therapeutic Strategies for Ischemic Stroke - 2016

 Ask your 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.
Figure 1. Therapeutic strategy for ischemic stroke. Possible therapeutic strategies for treating ischemic stroke include neuroprotection in the acute phase of cerebral ischemia, and stem cell therapy in the chronic phase of cerebral ischemia. CBF, cerebral blood flow; NTFs, neurotrophic factors; ad-GDNF, adenoviral vector containing glial cell line-derived neurotrophic factor; SeV-GDNF, Sendai virus vector containing glial cell line-derived neurotrophic factor.

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