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 Autophagy Induction by Bexarotene Promotes Mitophagy in Presenilin 1 Familial Alzheimer's Disease iPSC-Derived Neural Stem Cells. Mol Neurobiol. 2019 Jun 16;: Authors: Martín-Maestro P, Sproul A, Martinez H, Paquet D, Gerges M, Noggle S, Starkov AA Abstract Adult neurogenesis defects have been demonstrated in the brains of Alzheimer's disease (AD) patients. The neurogenesis impairment is an early critical event in the course of familiar AD (FAD) associated with neuronal loss. It was suggested that neurologic dysfunction in AD may be caused by impaired functioning of hippocampal neural stem cells (NSCs). Multiple metabolic and structural abnormalities in neural mitochondria have long been suspected to play a critical role in AD pathophysiology. We hypothesize that the cause of such abnormalities could be defective elimination of damaged mitochondria. In the present study, we evaluated mitophagy efficacy in a cellular AD model, hiPSC-derived NSCs harboring the FAD-associated PS1 M146L mutation. We found several mitochondrial respiratory chain defects such as lower expression levels of cytochrome c oxidase (complex IV), cytochrome c reductase (complex III), succinate dehydrogenase (complex II), NADH:CoQ reductase (complex I), and also ATP synthase (complex V), most of which had been previously associated with AD. The mitochondrial network morphology and abundance in these cells was aberrant. This was associated with a marked mitophagy failure stemming from autophagy induction blockage, and deregulation of the expression of proteins involved in mitochondrial dynamics. We show that treating these cells with autophagy-stimulating drug bexarotene restored autophagy and compensated mitochondrial anomalies in PS1 M146L NSCs, by enhancing the clearance of mitochondria. Our data support the hypothesis that pharmacologically induced mitophagy enhancement is a relevant and novel therapeutic strategy for the treatment of AD. PMID: 31203573 [PubMed - as supplied by publisher]
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