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.

Friday, January 22, 2016

D-4F Decreases White Matter Damage After Stroke in Mice

WHO THE FUCK IS GOING TO RUN WITH THIS AND CREATE A HUMAN CLINICAL TRIAL?
I bet nothing will occur because we have NO stroke leadership or stroke strategy. We are completely fucked because we have fucking failures for stroke associations. I weep for your children and grandchildren. Will no one think of the children?
http://stroke.ahajournals.org/content/47/1/214.abstract?sid=8b5c9623-0660-4b66-9300-3785a8d2c58e 
  1. Jieli Chen, MD
+ Author Affiliations
  1. From the Department of Neurology, Henry Ford Hospital, Detroit, MI (X.C., M.C., A.Z., C.C., T.Y., R.N., J.C.); and Department of Physics, Oakland University, Rochester, MI (M.C.).
  1. Correspondence to Jieli Chen, MD, Neurology Research, E&R Bldg, Room No 3091, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202. E-mail jieli@neuro.hfh.edu

Abstract

Background and Purpose—Stroke-induced neuroinflammation and white matter damage are associated with neurological deficits. Whether D-4F, an apolipoprotein A-I mimetic peptide, treatment of stroke decreases neuroinflammation and white matter damage and improves functional outcome has not been investigated.
Methods—Adult male C57BL/6 mice were subjected to permanent middle cerebral artery occlusion (MCAo) and were orally administered saline as a vehicle control and different doses of D-4F (2, 4, 8, 16, or 32 mg/kg) starting at 2 h after MCAo and daily until euthanized at 7 days after MCAo. D-4F treatment did not alter the blood levels of high-density lipoprotein, total cholesterol, triglyceride, blood–brain barrier leakage, and infarction volume compared with control group.
Results—D-4F (16 mg/kg) treatment of stroke significantly improved functional outcome, increased the white matter density and the number of oligodendrocyte progenitor cells in the ischemic boundary zone of the ipsilateral striatum, and increased myelin basic protein, insulin-like growth factor-1 (IGF1), but decreased inflammatory factor Toll-like receptor-4 and tumor necrosis factor-α expression in the ischemic brain 7 days after MCAo (P<0.05, n=11/group). The neurite/axonal outgrowth in primary cultured neurons was significantly increased when treated with D-4F (100 ng/mL) and IGF1 (100 ng/mL) compared with the nontreatment control. Inhibition of IGF1 significantly attenuated D-4F or IGF1 treatment–induced axonal outgrowth. D-4F-treatment did not increase oligodendrocyte–progenitor cell proliferation but decreased oligodendrocyte–progenitor cell death.
Conclusions—D-4F treatment initiated 2 h after MCAo decreases neuroinflammation and white matter damage and improves functional outcome after stroke. D-4F-induced increase in IGF1 may contribute to D-4F–induced neurite/axonal outgrowth after stroke.
 

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