Hope on the horizon for treating stroke

I hold no hope. It seems that 6+ years ago research suggested using neuregulin-1 as a hyperacute therapy, but I bet we never got human trials going. Failure once again. Why should this succeed since we have NO STROKE LEADERSHIP following up to make sure research is completed and protocols written? This is why stroke survivors need to be in charge, we know hold to handle difficult tasks, like trying to recover from stroke with NO useful help from your stroke hospital, doctors or therapists.

Extended therapeutic window and functional recovery after intraarterial administration of neuregulin-1 after focal ischemic stroke Nov. 2012

Hope on the horizon for treating stroke

A stroke treatment developed by researcher Byron Ford at the University of California, Riverside, has moved toward clinical trials.
The treatment focuses on neuregulins, a family of naturally occurring proteins that has shown promise for treating stroke, a leading cause of death in the United States and the major cause of long-term disability.
During stroke, blood supply to the brain is interrupted. Most often, an artery to the brain gets blocked by a clot or a blood vessel ruptures. With no blood — and therefore no oxygen or nutrients — reaching the brain, cells in the brain begin to die locally, at the “core,” within a couple of hours.  Subsequently, the core cells burst and release their components into the surrounding area, which then experiences a dramatic inflammatory response. This area, called the ischemic penumbra, dies over the course of several hours or days. Neuregulin-1, or NRG-1, one of four proteins in the neuregulin family, prevents this inflammation and cell death.

Byron Ford is a professor of biomedical sciences at UC Riverside. (UCR/Carrie Rosema)

“Cells in the core die by getting overexcited and exploding,” said Ford, a professor of biomedical sciences at the UCR School of Medicine, whose company, Brain-Gen, has patents for the use of NRG-1 to treat stroke. “Cells in the ischemic penumbra die by committing suicide. This happens, we believe, to prevent the whole brain from dying. An analogy: imagine a grenade is flung into a crowded theater, and a few people throw themselves on the grenade. They will die, but due to their sacrifice, others may very likely be spared.”
Brain-Gen is co-owned by his brother Gregory Ford, a neuroscientist and the dean of the College of Arts and Sciences at Fort Valley State University in Georgia. Byron Ford explained that Zensun Biotech, a Shanghai-based Chinese company with which Brain-Gen has recently partnered, has patents to use a particular form of neuregulin, called Neucardin, to treat heart failure. Zensun Biotech does not have patents, however, for Neucardin’s use in clinical trials for stroke. Brain-Gen tested Neucardin and found it works for stroke in animal models.
The two companies have signed an agreement to collaboratively move Neucardin toward clinical trials for stroke and to form a joint venture. The new company plans to approach the Food and Drug Administration, or FDA, to expand the use of Neucardin for stroke and to explore the possibility of securing funding from the National Institutes of Health, or NIH, with the aim of joining its StrokeNet clinical trials program.
Involving more than 200 hospitals in the country, StrokeNet conducts small and large clinical trials and research studies to advance acute stroke treatment, stroke prevention, and recovery and rehabilitation following a stroke.
“To our advantage, Zensun has already completed phase I and phase II clinical trials for heart failure and shown that Neucardin is safe and improves heart function in patients,” Ford said. “A stroke is like a heart attack in the brain. If the FDA says we can cross-reference Zensun’s data for approval to treat stroke, this would greatly expedite matters as we apply to become part of the NIH StrokeNet.”
Each year, nearly 800,000 Americans have a stroke, of which about 140,000 die. The “Stroke Belt,” an area in the southeastern United States and Mississippi Valley, has the highest rate of stroke mortality in the country.
Currently, the only FDA-approved drug to treat stroke is tissue plasminogen activator, or t-PA, which melts the clot. It has no effect on brain cells, however, and can be used only within a three-hour window from the witnessed time of stroke onset, beyond which t-PA damages blood vessels and causes bleeding. Further, only 3%-5% of stroke patients qualify for t-PA due to the limited time window and access to primary stroke centers. In contrast, Neucardin can be given to a patient more than 12 hours after a stroke and has been shown to be safe in patients.
Ford proposes that Neucardin be administered intravascularly to the patient along with t-PA to offer protection to the brain and potentially block t-PA’s negative effects that lead to bleeding in the brain.
“Neucardin can possibly be delivered in an ambulatory setting due to its relatively safe profile,” he said. “It can be given to the patient even before it has been determined if a stroke took place. It can also be delivered days following stroke to stimulate repair and regeneration in the brain. All this significantly boosts our hope for treating stroke.”

Elevating brain protein allays symptoms of Alzheimer's and improves memory

How closely is your doctor following this? You likely will need this whenever it becomes available.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013..
It seems that 4 years ago research suggested using neuregulin-1 as a hyperacute therapy, but I bet we never got human trials going. Failure once again.

Extended therapeutic window and functional recovery after intraarterial administration of neuregulin-1 after focal ischemic stroke Nov. 2012

   

Elevating brain protein allays symptoms of Alzheimer's and improves memory

Boosting levels of a specific protein in the brain alleviates hallmark features of Alzheimer's disease in a mouse model of the disorder, according to new research published online August 25, 2016 in Scientific Reports.

The protein, called neuregulin-1, has many forms and functions across the brain and is already a potential target for brain disorders such as Parkinson's disease, amyotrophic lateral sclerosis and schizophrenia.
"Neuregulin-1 has broad therapeutic potential, but mechanistically, we are still learning about how it works," says the study's senior investigator Kuo-Fen Lee, a professor in the Salk Institute's Clayton Foundation Laboratories for Peptide Biology and holder of the Helen McLoraine Chair in Molecular Neurobiology. "We've shown that it promotes metabolism of the brain plaques that are characteristic of Alzheimer's disease."
Previously, researchers have shown that treating cells with neuregulin-1, for example, dampens levels of amyloid precursor protein, a molecule that generates amyloid beta, which aggregate and form plaques in the brains of Alzheimer's patients. Other studies suggest that neuregulin-1 could protect neurons from damage caused by blockage of blood flow.
In the new study, Lee's team tested this idea in a mouse model of Alzheimer's disease by raising the levels of one of two forms of neuregulin-1 in the hippocampus, an area of the brain responsible for learning and memory. Both forms of the protein seemed to improve performance on a test of spatial memory in the models.
What's more, the levels of cellular markers of disease—including the levels of amyloid beta and plaques—were noticeably lower in mice with more neuregulin-1 compared to controls.
The group's experiments suggest that neuregulin-1 breaks up plaques by raising levels of an enzyme called neprilysin, shown to degrade amyloid-beta. But that is probably not the only route through which neuregulin-1 confers its benefits, and the group is exploring other possible mechanisms—such as whether the protein improves signaling between neurons, which is impaired in Alzheimer's—says the study's first author Jiqing Xu, a research associate in Lee's group.
A neuregulin-1 treatment is not available on the market, though it is being explored in clinical trials as a potential treatment for chronic heart failure and Parkinson's disease. One advantage of neuregulin-1 as a potential drug is that it can cross the blood brain barrier, which means that it could be administered relatively noninvasively even though the efficiency is not clear. On the other hand, other research suggests too much of the protein impairs brain function. Working with chemists at Salk, Lee's team has come up with a small molecule that can raise levels of existing neuregulin-1 (rather than administering it directly) and are testing it in cells. This alternative therapy could be a better way to prevent plaques from forming because small molecules more readily cross the blood brain barrier.
The group is also interested in neuregulin-1 for its ties to schizophrenia. An alteration in the neuregulin-1 gene—a single change in one letter of the DNA code for the protein—has been found in families with schizophrenia and linked to late-onset Alzheimer's disease with psychosis. The protein may be a way to understand the overlap between Alzheimer's and other brain disorders, Lee says.
An important caveat is that the new research was conducted in a single type of mouse model of Alzheimer's. Lee's group is testing neuregulin-1's affects across other models. "There's much more work ahead before neuregulin-1 could become a treatment, but we are excited about its potential, possibly in combination with other therapeutics for Alzheimer's disease," Lee says.

Explore further: Immune cells may protect against Alzheimer's

Journal reference: Scientific Reports
Provided by: Salk Institute

Extended therapeutic window and functional recovery after intraarterial administration of neuregulin-1 after focal ischemic stroke

Only 7 years old so ask your doctor if human trials have occurred.
http://www.nature.com/jcbfm/journal/v26/n4/full/9600212a.html

Abstract

We have previously shown that neuregulin-1 (NRG-1) protects neurons from ischemic brain injury if administered before focal stroke. Here, we examined the therapeutic window and functional recovery after NRG-1 treatment in rats subjected to 90 mins of middle cerebral artery occlusion (MCAO) and 24 h of reperfusion. Neuregulin-1 (2.5 ng/kg bolus, 1.25 ng/kg/min infusion) reduced infarct volume by 89.2%41.9% (means.d.; n=8; P less than 0.01) if administered immediately after the onset of reperfusion.  Neuroprotection was also evident if NRG-1 was administered 4 h (66.4%52.6%; n=7; P less than 0.01) and 12 h (57.0%20.8%; n=8; Pless than 0.01) after reperfusion. Neuregulin-1 administration also resulted in a significant improvement of functional neurologic outcome compared with vehicle-treated animals (32.1%5.7%; n=9; Pless than 0.01). The neuroprotective effect of the single administration of NRG-1 was seen as long as 2 weeks after treatment. Neurons labeled with the neurodegeneration marker dye Fluoro-JadeB were observed after MCAO in the cortex, but the numbers were significantly reduced after NRG-1 treatment. These results indicate that NRG-1 is a potent neuroprotective compound with an extended therapeutic window that has practical therapeutic potential in treating individuals after ischemic brain injury.