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 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.
My back ground story is here:

Thursday, April 26, 2018

Old Drug May Get New Life in Parkinson's Prevention

With your chances of getting Parkinsons post stroke you'll want to ask your doctor what is being done to prevent that. S/he has had a year to come up with Parkinsons prevention and I bet nothing has been done on that.

Parkinson’s Disease May Have Link to Stroke March 2017


  And ask specifically what anti-TNF therapy is.

Old Drug May Get New Life in Parkinson's Prevention

Patients with inflammatory bowel disease (IBD) are at increased risk for Parkinson's disease (PD), but early treatment with anti–tumor necrosis factor (anti-TNF) therapy appears to offer protection, results of a large observational study suggest.
"We believe that our findings have potential clinical implications, including considering TNF-α inhibitors for Parkinson's disease prevention in high-risk individuals," Inga Peter, PhD, professor, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai in New York City, told Medscape Medical News.
The study was published online April 23 in JAMA Neurology.

Repurposing an Old Drug?

To compare the incidence of PD among adults with and without IBD and see whether the risk for PD among patients with IBD is altered by anti-TNF therapy, Peter and colleagues analyzed 16 years' worth of data on more than 170 million people in the Truven Health MarketScan claims database and the Medicare Supplemental Database. 
They identified 144,018 patients with IBD (mean age, 51 years; 44% men) and a matched cohort of 720,090 controls without IBD.
Overall, 1796 individuals had a diagnosis of PD. The incidence of PD was 28% higher in those with IBD (adjusted incidence rate ratio, 1.28; 95% confidence interval [CI], 1.14 - 1.44; P < .001). This association was seen in individuals with Crohn's disease and ulcerative colitis.
Of note, say the researchers, the incidence of PD was 78% lower in patients with IBD who received anti-TNF therapy compared with those who did not (adjusted incidence rate ratio, 0.22; 95% CI, 0.05 - 0.88; P = .03).
These findings support a role of systemic inflammation in the development of both PD and IBD, the researchers say. Further studies are needed to see whether anti-TNF therapy given to high-risk individuals may mitigate the risk for PD.
TNF inhibition has been considered as a therapeutic target for neurodegenerative diseases. Clinical trials have been conducted in Alzheimer's disease, amyotrophic lateral sclerosis, and multiple sclerosis  but not PD, "with some minor benefits observed in Alzheimer's patients only," said Peter. Several reasons could explain poor outcomes of these trials, she explained.
"One, TNF inhibition is ineffective once the disease is already established, and two, that TNF-α inhibitors do not cross blood-brain barrier. Our results indicate that reducing systemic inflammation earlier in life may help decrease the risk of Parkinson's disease. It can be testable in retrospective studies or in prospective clinical trials. However, the timing, dosage, and target population should be determined," said Peter.

Exciting Evidence

In a linked editorial,  Abby Olsen, MD, PhD, and colleagues from the Precision Neurology Program at Brigham and Women's Hospital in Boston, Massachusetts, note the study "builds on mounting genetic and molecular evidence supporting a causal association between the gut, systemic inflammation, and PD."

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