Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, February 22, 2018

Central Infusion of IGF-1 Increases Hippocampal Neurogenesis and Improves Neurobehavioral Function following Traumatic Brain Injury

Would this help post stroke?  What leader in stroke will make sure followup occurs? 

Central Infusion of IGF-1 Increases Hippocampal Neurogenesis and Improves Neurobehavioral Function following Traumatic Brain Injury

To cite this article:
Dr. Shaun W. Carlson and Dr. Kathryn E Saatman. Journal of Neurotrauma. February 2018, ahead of print. https://doi.org/10.1089/neu.2017.5374
Online Ahead of Editing: February 17, 2018

ABSTRACT

Traumatic brain injury (TBI) produces neuronal dysfunction and cellular loss that can culminate in lasting impairments in cognitive and motor abilities. Therapeutic agents that promote repair and replenish neurons after TBI hold promise in improving recovery of function. Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor capable of mediating neuroprotective and neuroplasticity mechanisms. Targeted overexpression of IGF-1 enhances the generation of hippocampal newborn neurons in brain-injured mice; however, the translational neurogenic potential of exogenously administered IGF-1 after TBI remains unknown. In a mouse model of controlled cortical impact (CCI), continuous intracerebroventricular infusion of recombinant human IGF-1 (hIGF) for 7 days, beginning 15min post-injury, resulted in a dose-dependent increase in the number of immature neurons in the hippocampus. Infusion of 10μg/d IGF-1 produced detectable levels of hIGF-1 in the cortex and hippocampus and a concomitant increase in Akt activation in the hippocampus. Both motor function and cognition were improved over 7 days following injury in IGF-1 treated cohorts. Vehicle treated brain-injured mice showed reduced hippocampal immature neuron density relative to sham controls at 7 days post-injury. In contrast, the density of hippocampal immature neurons in brain-injured mice receiving acute onset IGF-1 infusion was significantly higher than in injured mice receiving vehicle and equivalent to that in sham-injured control mice. Importantly, the neurogenic effect of IGF-1 was maintained with as much as a 6 hr delay in the initiation of infusion. These data suggest that central infusion of IGF-1 enhances the generation of immature neurons in the hippocampus, with a therapeutic window of at least 6 hrs post-injury, and promotes neurobehavioral recovery after TBI.

 

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