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.

Saturday, October 10, 2015

Ameliorative Effects of Antioxidants on the Hippocampal Accumulation of Pathologic Tau in a Rat Model of Blast-Induced Traumatic Brain Injury

I can't tell from this if this would be useful for stroke but hell that is what stroke associations are for. To answer fuckingly simple questions like these. Which they won't do. In my opinion they are totally worthlesss. They haven't proven me wrong yet. They won't even condescend to talk to me. Probably because I'm stupid from my stroke and have no medical training.
Is this better than fish oil?

Fish Oil Injection to Stroke Victims: Remedy for Brain Damage


Ameliorative Effects of Antioxidants on the Hippocampal Accumulation of Pathologic Tau in a Rat Model of Blast-Induced Traumatic Brain Injury

Xiaoping Du,1 Matthew B. West,1 Weihua Cheng,1 Donald L. Ewert,1 Wei Li,1 Debra Saunders,2 Rheal A. Towner,2 Robert A. Floyd,2 and Richard D. Kopke1,2,3

1Hough Ear Institute, Oklahoma City, OK 73112, USA
2Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
3Departments of Physiology and Otolaryngology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA

Received 22 July 2015; Accepted 15 September 2015

Academic Editor: Grégory Durand

Copyright © 2015 Xiaoping Du et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract

Traumatic brain injury (TBI) can lead to early onset dementia and other related neurodegenerative diseases. We previously demonstrated that damage to the central auditory pathway resulting from blast-induced TBI (bTBI) could be significantly attenuated by a combinatorial antioxidant treatment regimen. In the current study, we examined the localization patterns of normal Tau and the potential blast-induced accumulation of neurotoxic variants of this microtubule-associated protein that are believed to potentiate the neurodegenerative effects associated with synaptic dysfunction in the hippocampus following three successive blast overpressure exposures in nontransgenic rats. We observed a marked increase in the number of both hyperphosphorylated and oligomeric Tau-positive hilar mossy cells and somatic accumulation of endogenous Tau in oligodendrocytes in the hippocampus. Remarkably, a combinatorial regimen of 2,4-disulfonyl α-phenyl tertiary butyl nitrone (HPN-07) and N-acetylcysteine (NAC) resulted in striking reductions in the numbers of both mossy cells and oligodendrocytes positively labeled for these pathological Tau immunoreactivity patterns in response to bTBI. This treatment strategy represents a promising therapeutic approach for simultaneously reducing or eliminating both primary auditory injury and nonauditory changes associated with bTBI-induced hippocampal neurodegeneration.

3. Results
3.1. Effects of Blast Exposure and Antioxidant Treatment on Somatic Tau Staining in the Hippocampus

In uninjured brains, Tau localization is restricted to axons, resulting in a diffuse immunoreactivity pattern throughout the cortex and subcortical regions (Figures 1(a) and 1(d)) [27]. However, using an antibody against normal Tau protein (Tau-1), we observed a blast-induced accumulation of Tau-1-positive foci in the polymorphic layer of the dentate gyrus (PoDG) seven days after injury (Figures 1(b) and 1(e)). Upon closer examination, this atypical Tau immunostaining pattern was localized to the soma of small round cells, bearing large nuclei with limited axonal projections (arrows in Figures 1(d)–1(f)). These morphological features and distinct trauma-induced somatic Tau accumulation are consistent with characteristics associated with oligodendrocytes [28–33]. To confirm this characterization, relevant tissue sections were immunolabeled with oligodendrocyte specific protein antibody (OSPA) for colocalization evaluations with Tau-1. From this analysis, we determined that a large proportion of the Tau-1-positive cells were also OSPA-positive, confirming their characterization as oligodendrocytes, an example of which is shown in Figure 2. Formal quantification of these Tau-positive cell bodies in the PoDG revealed that bTBI induced a significant, yet delayed, increase in aberrant Tau-1 immunoreactivity in this region of the hippocampus, first evident at seven days after injury and persisting through the terminal sampling time point of 21 days after bTBI (, Figure 3).

Much more at link.

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