Stroke Stem Cell Treatment


Stem Cell Treatment for StrokeStem Cell Treatment for a Stroke is an option

What is a Stroke?

Stroke and Stem Cell Therapy

A stroke (Cerebrovascular Accident or CVA), is the rapid loss of brain function due to the blood supply to the brain being disturbed. This can be from ischemia from the lack of blood flow or from a blockage known as Thrombosis, an Arterial Embolism, or a Haemorrhage where blood is leaking out or inside the brain.

The affected area of the brain is unable to function correctly and may result in an inability to move especially in one or more limbs on one side of the body. Stroke can also cause an inability to understand speech or speak or see properly. 

A stroke is a medical emergency that needs immediate medical attention. Stroke can cause permanent neurological damage and ongoing complications, and death. It is the a leading cause of adult disability in the around the world.

Risk factors for stroke include ederly people,  high blood pressure (hypertension), a previous stroke or from a transient ischemic attack (TIA).

Other related risk conditions include diabetes, high cholesterol, cigarette smoking and atrial fibrillation. High blood pressure is the most important modifiable risk factor of stroke.

A silent stroke is a stroke that does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. A silent stroke still causes damage to the brain, and places the person at risk for both transient ischemic attack and a major stroke occuring in the future.

People who have suffered a major stroke are at risk of having silent strokes as well.Stem Cell Treatment for Stroke


Stroke rehabilitation.

Lancet. 2011 May 14;377(9778):1693-702

Authors: Langhorne P, Bernhardt J, Kwakkel G

Stroke is a common, serious, and disabling global health-care problem, and rehabilitation is a major part of patient care. There is evidence to support rehabilitation in well coordinated multidisciplinary stroke units or through provision of early supported provision of discharge teams. Potentially beneficial treatment options for motor recovery of the arm include constraint-induced movement therapy and robotics.

Promising interventions that could be beneficial to improve aspects of gait include fitness training, high-intensity therapy, and repetitive-task training. Repetitive-task training might also improve transfer functions. Occupational therapy can improve activities of daily living; however, information about the clinical effect of various strategies of cognitive rehabilitation and strategies for aphasia and dysarthria is scarce. Several large trials of rehabilitation practice and of novel therapies (eg, stem-cell therapy, repetitive transcranial magnetic stimulation, virtual reality, robotic therapies, and drug augmentation) are underway to inform future practice.

PMID: 21571152 [PubMed - in process]


Stem Cell Treatment for Stroke NIH Streaming Database:

Related Articles Therapeutic potential of AAV9-S15D-RLC gene delivery in humanized MYL2 mouse model of HCM. J Mol Med (Berl). 2019 May 17;: Authors: Yadav S, Yuan CC, Kazmierczak K, Liang J, Huang W, Takeuchi LM, Kanashiro-Takeuchi RM, Szczesna-Cordary D Abstract Familial hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder characterized by ventricular hypertrophy, myofibrillar disarray, and fibrosis, and is primarily caused by mutations in sarcomeric genes. With no definitive cure for HCM, there is an urgent need for the development of novel preventive and reparative therapies. This study is focused on aspartic acid-to-valine (D166V) mutation in the myosin regulatory light chain, RLC (MYL2 gene), associated with a malignant form of HCM. Since myosin RLC phosphorylation is critical for normal cardiac function, we aimed to exploit this post-translational modification via phosphomimetic-RLC gene therapy. We hypothesized that mimicking/modulating cardiac RLC phosphorylation in non-phosphorylatable D166V myocardium would improve heart function of HCM-D166V mice. Adeno-associated virus, serotype-9 (AAV9) was used to deliver phosphomimetic human RLC variant with serine-to-aspartic acid substitution at Ser15-RLC phosphorylation site (S15D-RLC) into the hearts of humanized HCM-D166V mice. Improvement of heart function was monitored by echocardiography, invasive hemodynamics (PV-loops) and muscle contractile mechanics. A significant increase in cardiac output and stroke work and a decrease in relaxation constant, Tau, shown to be prolonged in HCM mice, were observed in AAV- vs. PBS-injected HCM mice. Strain analysis showed enhanced myocardial longitudinal shortening in AAV-treated vs. control mice. In addition, increased maximal contractile force was observed in skinned papillary muscles from AAV-injected HCM hearts. Our data suggest that myosin RLC phosphorylation may have important translational implications for the treatment of RLC mutations-induced HCM and possibly play a role in other disease settings accompanied by depressed Ser15-RLC phosphorylation. KEY MESSAGES: HCM-D166V mice show decreased RLC phosphorylation and decompensated function. AAV9-S15D-RLC gene therapy in HCM-D166V mice, but not in WT-RLC, results in improved heart performance. Global longitudinal strain analysis shows enhanced contractility in AAV vs controls. Increased systolic and diastolic function is paralleled by higher contractile force. Phosphomimic S15D-RLC has a therapeutic potential for HCM. PMID: 31101927 [PubMed - as supplied by publisher]
Related Articles Fas ligand and nitric oxide combination to control smooth muscle growth while sparing endothelium. Biomaterials. 2019 May 07;212:28-38 Authors: Kural MH, Wang J, Gui L, Yuan Y, Li G, Leiby KL, Quijano E, Tellides G, Saltzman WM, Niklason LE Abstract Metallic stents cause vascular wall damage with subsequent smooth muscle cell (SMC) proliferation, neointimal hyperplasia, and treatment failure. To combat in-stent restenosis, drug-eluting stents (DES) delivering mTOR inhibitors such as sirolimus or everolimus have become standard for coronary stenting. However, the relatively non-specific action of mTOR inhibitors prevents efficient endothelium recovery and mandates dual antiplatelet therapy to prevent thrombosis. Unfortunately, long-term dual antiplatelet therapy leads to increased risk of bleeding/stroke and, paradoxically, myocardial infarction. Here, we took advantage of the fact that nitric oxide (NO) increases Fas receptors on the SMC surface. Fas forms a death-inducing complex upon binding to Fas ligand (FasL), while endothelial cells (ECs) are relatively resistant to this pathway. Selected doses of FasL and NO donor synergistically increased SMC apoptosis and inhibited SMC growth more potently than did everolimus or sirolimus, while having no significant effect on EC viability and proliferation. This differential effect was corroborated in ex vivo pig coronaries, where the neointimal formation was inhibited by the drug combination, but endothelial viability was retained. We also deployed FasL-NO donor-releasing ethylene-vinyl acetate copolymer (EVAc)-coated stents into pig coronary arteries, and cultured them in perfusion bioreactors for one week. FasL and NO donor, released from the stent coating, killed SMCs close to the stent struts, even in the presence of flow rates mimicking those of native arteries. Thus, the FasL-NO donor-combination has a potential to prevent intimal hyperplasia and in-stent restenosis, without harming endothelial restoration, and hence may be a superior drug delivery strategy for DES. PMID: 31102854 [PubMed - as supplied by publisher]

Quick Contact Form