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:

Sunday, February 26, 2017

Abstract WP118: Docosahexaenoic Acid Provides Neuroprotection by Increasing Neurogenesis After Experimental Stroke

These always seem to need more followup to be useful rather than doing it right in the first place and doing some real research. Regardless, I bet your doctor does nothing with this information.
A. Because s/he never read it.
B. Because s/he could not be bothered to understand how to implement it in a protocol.
C. It is not my job. I am waiting for SOMEONE ELSE TO SOLVE THE PROBLEM. Namely 100% recovery for all my stroke patients.

Abstract WP118: Docosahexaenoic Acid Provides Neuroprotection by Increasing Neurogenesis After Experimental Stroke

Nicolas G Bazan, Larissa Khoutorova, Sung-Ha Hong, Hemant Menghani, Ludmila Belayev


Introduction: Ischemic injury induces neurogenesis in the subventricular zone (SVZ) of the lateral ventricles and subgranular zone (SGZ) of dentate gyrus (DG), and it promotes the migration of neuroblasts, guided by blood vessels, into the ischemic damaged area. Recently, we have shown that docosahexaenoic acid (DHA; 22:6n-3) therapy improves functional and histological outcomes following experimental stroke. The objective, hence, is to determine whether DHA administration enhances endogenous neurogenesis after cerebral ischemia.
Methods: Twenty-one male SD rats were anesthetized with isoflurane and subjected to 2 h of middle cerebral artery occlusion (MCAo) by intraluminal filament. DHA (5 mg/kg, n=10) or saline (n=11) was administered intravenously at 3 h after onset of MCAo (n = 7-10 per group). BrdU was injected on days 4, 5 and 6. DCX (doublecortin), NeuN (a marker for mature neurons), ki-67 (marker for cell proliferation) have been used to test the proliferation, migration and differentiation of neural precursor cells. Behavioral tests were conducted on days 1, 2 and 3 and weeks 1 and 2. Immunohistochemistry with BrdU and ki-67, DCX or NeuN, and histopathology were performed on day 14.
Results: DHA-treated animals showed improved neurologic scores compared to the saline group during the two-week survival period. Total, cortical and subcortical infarct areas in the DHA-treated group were significantly attenuated at multiple bregma levels as well as total, cortical and subcortical infarct volumes by 42.4 %, by 47.5 %, and by 31.2 % compared to the vehicle-treated group. The number of BrdU+/ki-67+ cells in DHA-treated rats was increased in cortex by 88 %, SVZ by 40 % and DG by 270 % compared to saline-treated rats. DHA treatment increased the number of BrdU+/DCX+ cells in the cortex by 65 %, the SVZ by 29 % and the DG (by 58 %) compared to saline-treated group. In addition, the numbers of BrdU+/NeuN+ cells were increased in the cortex by 49 %, SVZ by 28 % and DG by 48% compared to vehicle treatment.
Conclusion: DHA increased neurogenesis by proliferation, differentiation and migration of neural stem cells in the DG, SVZ and peri-infarct area two weeks after ischemic stroke. In addition, DHA promoted neurobehavioral recovery and reduced infarct volume.

No comments:

Post a Comment