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:

Saturday, February 11, 2017

Intranasal Administration of the Antisecretory Peptide AF-16 Reduces Edema and Improves Cognitive Function following Diffuse Traumatic Brain Injury in the Rat

Better to be rat than a human if having a brain injury.
Fredrik Clausen1*, Hans-Arne Hansson2, Johan Raud3 and Niklas Marklund1*
  • 1Dept. Neuroscience, Section of Neurosurgery, Uppsala University, Sweden
  • 2Institute of Biomedicine, University of Gothenburg, Sweden
  • 3Lantmännen AS Faktor AB, Sweden
A synthetic peptide with antisecretory activity, AF-16, improves injury-related deficits in water and ion transport and decreases intracranial pressure after experimental cold lesion injury and encephalitis although its role in traumatic brain injury (TBI) is unknown. AF-16 or an inactive reference peptide was administrated intranasally 30 min following midline fluid percussion injury (mFPI; n=52), a model of mild-moderate diffuse TBI in rats. Sham-injured (n=14) or naïve (n=24) animals were used as controls. The rats survived for either 48 h or 15 days. At 48 h, the animals were tested in Morris water maze (MWM) for memory function and brains analyzed for cerebral edema. Here, mFPI induced brain edema compared to sham or naïve controls that was significantly reduced by AF-16 treatment (p<0.05) although MWM performance was not altered. In the 15-day survival groups, the MWM learning and memory abilities as well as histological changes were analyzed. AF-16 treated brain-injured animals shortened both MWM latency and swim path in the learning trials and improved probe trial performance compared to brain-injured controls treated with the inactive reference peptide (p<0.05). A modest decrease by AF-16 on TBI-induced changes in hippocampal glial acidic fibrillary protein (GFAP) staining (p=0.11) was observed. AF-16 treatment did not alter any other immunohistochemical analyses (degenerating neurons, beta-amyloid precursor protein (β-APP) and Olig2). In conclusion, intranasal AF-16 attenuated brain edema and enhanced visuospatial learning and memory following diffuse TBI in the rat. Intranasal administration early post-injury of a promising neuroprotective substance offers a novel treatment approach for TBI.
Keywords: cerebral edema, Traumatic Brain Injury, intranasal, Neuroprotection, rat model
Citation: Clausen F, Hansson H, Raud J and Marklund N (2017). Intranasal Administration of the Antisecretory Peptide AF-16 Reduces Edema and Improves Cognitive Function following Diffuse Traumatic Brain Injury in the Rat. Front. Neurol. 8:39. doi: 10.3389/fneur.2017.00039

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