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.

Thursday, February 4, 2016

Improving Brain’s Garbage Disposal May Slow Alzheimer’s Disease

We need this and soon. But because we have NO stroke leadership or strategy nothing will get done on this.
Your 33% dementia chance post-stroke from an Australian study?  May 2012.
Then this study came out and seems to have a range from 17-66%. December 2013.
A 20% chance in this research.   July 2013.

http://medicalxpress.com/news/2015-01-scientists-heart-disease-clues-alzheimer.html

 Improving Brain’s Garbage Disposal May Slow Alzheimer’s Disease

A drug that boosts activity in the brain’s “garbage disposal” system can decrease levels of toxic proteins associated with Alzheimer’s disease and other neurodegenerative disorders and improve cognition in mice, a new study by neuroscientists at Columbia University Medical Center (CUMC) and New York State Psychiatric Institute (NYSPI) has found. The study was published today in the online edition of Nature Medicine.

“We have identified a new way to activate the brain’s garbage disposal system, and have shown that we can effectively use a drug to activate this system and slow down disease in a mouse model,” said study leader Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at CUMC and NYSPI. “This has the potential to open up new avenues of treatment for Alzheimer’s and many other neurodegenerative diseases.”
The drug used was rolipram, which causes nausea and thus is not a good drug for use in humans. However, similar drugs do not incur nausea as a side effect and can be potentially tested in clinical trials quickly.
To remain healthy, brain cells must continually clear out old, worn, or damaged proteins, a task performed by a small molecular cylinder called the proteasome. The proteasome acts as a kind of garbage disposal, grinding up the old proteins so they can be recycled into new ones. In neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s, proteins tagged for destruction accumulate in the brain’s neurons, suggesting that the cell’s proteasomes are impaired.
Using a genetically engineered mouse, the researchers first discovered that tau—a protein that accumulates in Alzheimer’s, frontotemporal degeneration, and other brain diseases—sticks to the proteasome and slows down the protein disposal process.
“Something profoundly bad happens to proteasomes in diseases where abnormal proteins accumulate,” said the study’s first author, Natura Myeku, PhD, an associate research scientist in the pathology and cell biology department at CUMC. “Our work on tau showed that even when proteasomes are removed from the diseased brains they remain defective and can’t chew up proteins compared with proteasome from normal brains.”
Administering rolipram activated the proteasome and restored protein disposal. The drug also improved memory in diseased mice to levels seen in healthy mice.
Rolipram has been tested before in mice, and was shown to improve memory. But the new research shows a previously unknown function of the drug that produces a physical change in the proteasome and increases its activity.
“We have uncovered a mechanism by which we can activate proteasomes,” said Dr. Myeku. “However, we still don’t have a full picture how those changes cause proteasomes to become super proteasomes that are able to remove toxic proteins from the brain. For now, it’s exciting to know that brain proteasomes can be repaired, which will allow us to develop better drugs.”
Drugs that target proteasomes in this way should work for any neurodegenerative disease caused by the accumulation of abnormal proteins, including Alzheimer’s, frontotemporal degeneration, Huntington’s, and Parkinson’s.
Dr. Duff noted, “Even though much work has been done, we still don’t know exactly which form of a particular protein is toxic to the brain. This has made it difficult to develop drugs to treat neurodegenerative diseases. In Alzheimer’s disease, the problem is compounded because several types of abnormal protein can accumulate in a person’s brain, including amyloid, tau, alpha-synuclein, and TDP43. We think that a well-functioning proteasome will be able to clear out everything at once.”
“This exciting research from Dr. Duff’s team advances our basic understanding of the proteasome system, provides a way to repair the system when it breaks, and holds the potential to alleviate symptoms of neurodegenerative disorders,” said Rod Corriveau, PhD, program director at the National Institute of Health’s National Institute of Neurological Disorders and Stroke, which provided funding for the study.
About the paper:
The study is titled, “Tau-driven 26S proteasome impairment and cognitive dysfunction can be prevented early in disease by activating cAMP-PKA signaling.” The other contributors are: Catherine L. Clelland (CUMC), Sheina Emrani (CUMC), Nikolay V. Kukushkin (Harvard Medical School), Wai Haung Yu (CUMC) and Alfred L. Goldberg (Harvard Medical School).
The study was supported by grants from the National Institute of Neurological Disorders and Stroke (NS074593), the CurePSP Foundation, the National Institute of General Medical Sciences (GM051923), the Fidelity Biosciences Research Initiative, and the Multiple Myeloma Research Foundation.

The researchers declare no financial or other conflicts of interest.

Columbia University Medical Center provides international leadership in basic, preclinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest faculty medical practices in the Northeast. For more information, visit cumc.columbia.edu or columbiadoctors.org.

 

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