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.

Wednesday, November 16, 2016

Antibiotic restores cell communication in brain areas damaged by Alzheimer's disease

Ask your doctor and hospital what they are doing to followup on this research. Would it be useful after stroke? Glutamate poisoning is one of the 5 causes of neuronal death in the first week.  Does your doctor know that? I don't care that this was just in mice, research followup is needed and our fucking failures of stroke associations will do nothing.
http://medicalxpress.com/news/2016-11-antibiotic-cell-brain-areas-alzheimer.html
New research from the Djavad Mowafaghian Centre for Brain Health at UBC has found a way to partially restore brain cell communication around areas damaged by plaques associated with Alzheimer's disease.
The findings, published this week in Nature Communications, demonstrate a possible target and a potential drug treatment to reduce damage to the brain that occurs in the early stages of Alzheimer's disease. Using Ceftriaxone, an FDA-approved antibiotic used to treat bacterial infections, researchers were able to reduce synaptic disruption and clear the lines of neuronal communication in mice.
Amyloid plaques of -amyloid deposits develop in brain regions of patients with Alzheimer's disease, These plaques are linked to the damage found in Alzheimer's disease because they prevent and are toxic to nerve cells. The researchers found that the around these plaques show high levels of glutamate, a signaling molecule essential to communication between brain cells, accompanying high levels of hyperactivity in glia, the brain's support cells. It's in this glutamate-rich environment that communication between neurons is changed or disrupted, causing neurons to die in the later stages of the disease.
"By imaging the glial cells and glutamate itself around the plaques, we were able to see that the cells were not able to 'remove' the glutamate accumulating in these areas. By using Ceftriaxone, we were able to up-regulate glutamate transport," explains Dr. MacVicar, principal investigator and professor of psychiatry. "By restoring , we were able to mostly restore neuronal activity."
The team's findings have implications for treatment of early symptoms of Alzheimer's disease.
"This dysfunction in cell communication occurs at a very early stage in the disease, before memory impairment is detectable," says Dr. Jasmin Hefendehl, a former Postdoctoral Fellow in Dr. MacVicar's lab and the lead author on the paper. "This makes our discovery particularly interesting, as it opens a window for an early intervention strategy to possibly prevent or delay neuron and memory loss."
Ceftriaxone is an antibiotic that is commonly administered before some types of surgery to prevent infections. Although a recent clinical trial failed to see improvements for treating (ALS), the researchers are hopeful about its potential for early intervention in treating Alzheimer's disease.
More information: J. K. Hefendehl et al, Mapping synaptic glutamate transporter dysfunction in vivo to regions surrounding Aβ plaques by iGluSnFR two-photon imaging, Nature Communications (2016). DOI: 10.1038/ncomms13441

Journal reference: Nature Communications search and more info website
Provided by: University of British Columbia

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