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, April 14, 2019

Therapeutic Potential of FAK Inhibitor After Stroke in Neuroprotection and Neurogenesis

Is this enough for your stroke hospital to contact researchers and get human clinical trials done? OR WILL THEY DO NOTHING LIKE THEIR USUAL INCOMPETENCE?

Therapeutic Potential of FAK Inhibitor After Stroke in Neuroprotection and Neurogenesis



Authors' Affiliations

Hannah M. Malone, Department of Biomedical Sciences, College of Medicine, East Tennessee State University, Johnson City, TN. Dr. Cuihong Jia, Department of Biomedical Sciences, College of Medicine, East Tennessee State University, Johnson City, TN. Dr. Theo Hagg, Department of Biomedical Sciences, College of Medicine, East Tennessee State University, Johnson City, TN.

Location

BEECH MTN. ROOM 120

Start Date

4-12-2019 10:20 AM

End Date

4-12-2019 10:35 AM

Faculty Sponsor’s Department

Biomedical Sciences

Name of Project's Faculty Sponsor

Dr. Theo Hagg

Type

Oral Presentation

Classification of First Author

Graduate Student-Doctoral

Project's Category

Healthcare and Medicine, Traumatic Brain Injury, Stroke

Abstract

Stroke increases neurogenesis (birth of new neurons) through upregulation of ciliary neurotrophic factor (CNTF), a potent neurogenic cytokine made almost exclusively in the central nervous system. Previous study found that CNTF is induced and needed to stimulate neurogenesis in the subventricular zone (SVZ) of mouse brain in a stroke model. CNTF also has a neuroprotective function. Focal adhesion kinase (FAK), protein tyrosine kinase 2, is ubiquitously expressed in various cell types and mediates cell adhesion and migration. We previously discovered that systemic inhibition of FAK upregulates CNTF expression in the SVZ, making FAK a pharmacological target to increase CNTF to promote neurogenesis and neuroprotection after stroke. This study examined whether systemic FAK inhibitor treatment after stroke regulates SVZ neurogenesis and neuroprotection using a middle cerebral artery occlusion (MCAO) to induce a stroke in adult male C57BL/6 mice. A filament was inserted in the external carotid artery and then fed through the carotid bifurcation into the internal carotid artery to the base of the middle cerebral artery. After 30 minutes of occlusion, the filament was removed to restore blood flow. Mice were randomly assigned to receive 3 daily doses of saline or FAK inhibitor (FAK14, i.p., 3 mg/kg) and treatment started at 6 hours, 12 days, or 58 days after MCAO. Because CNTF has a neuroprotective function, the amount of tissue damage was analyzed to compare treatment groups. The neuroprotective role of FAK14 was examined by measuring MCAO-induced infarction. The infarct size was measured using the absence of NeuN (neuronal cell marker) and GFAP (activated astrocytes) and presence of CD68 (activated microglia). FAK14 given at 6 hours post-stroke reduced the infarct size to 38% of the uninjured side of the brain compared to 46% with saline. Proliferating cells were labeled by injecting bromodeoxyuridine (BrdU, 50 mg/kg), the mice were processed 2 h after the last BrdU injection, and proliferated cells in the SVZ were counted with unbiased stereology. There were no significant differences in the total numbers of BrdU+ cells between saline and FAK14 at 3, 14 and 60 days. Future studies are needed to confirm the levels of CNTF at the various times of treatment. If there is no difference in CNTF expression or increased expression of counteracting cytokines, no difference in neurogenesis between groups would be expected. The neuroprotective effect of FAK14 during the acute phase following injury could provide novel pharmacological options to stroke patients extending the current therapeutic treatment window.

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