Social, emotional support more helpful to stroke patients than rehab

Which just means your insurance company will stop actual rehab because of the cost. You'll have to scream at your insurance carrier. This way they don't have to tell you the bad news that their rehab dept. is so bad that only 10% get to full recovery.
http://www.business-standard.com/article/news-ani/social-emotional-support-more-helpful-to-stroke-patients-than-rehab-118030500463_1.html

According to a recent study, providing stroke patients with social and emotional support is more helpful than sending them to a rehab.

The CMAJ-study suggested that when caring for stroke patients, health care providers should focus on the social and emotional issues facing patients, rather than only physical rehabilitation.

Harvard study shows the surprising impact of intermittent fasting on the aging process

And just when will this become a protocol at your hospital? Never? Because your hospital doesn't have anyone implementing research into stroke interventions?  How fucking incompetent is your hospital? You need to ask that question of your hospital board of directors.

https://ideapod.com/harvard-study-shows-impact-intermittent-fasting-aging-process/?

Countless research studies have shown the benefits of intermittent fasting, and now Harvard scientists have closely examined its impact on the aging process.

Intermittent fasting refers to an eating pattern that cycles between periods of fasting and eating. The most common intermittent fasting methods involve daily 16 hour fasts, or fasting for 24 hours, twice per week.

Advocates of intermittent fasting argue that humans have been fasting throughout our evolution. Sometimes it was because food wasn’t available, but it’s also been a core part of major religions including Islam, Christianity and Buddhism.

The Harvard study was published in the journal Cell Metabolism and reveals that intermittent fasting slows down the aging process.

That’s right. If you want to live longer, adapt your eating patterns to have periods of fasting and eating.

It’s all about your mitochondria

The research study examined the basic biology involved in our cells’ declining ability to process energy over time, which is what causes aging and age-related disease, and how embracing periods of fasting promotes healthy aging.

Mitochondria are organelles, or parts of a eukaryote cell. They make most of the cell’s supply of adenosine triphosphate, a molecule that provides cells with a source of energy. Their capacity to do so declines with age, but before this study the impact on metabolism and cellular function was previously unclear.

In the study, the researchers demonstrated a causal link between dynamic changes of mitochondrial networks and longevity. They did this by studying C. Elegans (nematode worms) which live just two weeks, enabling the studying of the aging process. They restricted the worms’ diets and found this restriction maintained the mitochondrial networks in a fused or “youthful” state.

“Low-energy conditions such as dietary restriction and intermittent fasting have previously been shown to promote healthy aging. Understanding why this is the case is a crucial step toward being able to harness the benefits therapeutically,” said Heather Weir, lead author of the study. “Our findings open up new avenues in the search for therapeutic strategies that will reduce our likelihood of developing age-related diseases as we get older.”

“Although previous work has shown how intermittent fasting can slow aging, we are only beginning to understand the underlying biology,” said William Mair, associate professor of genetics and complex diseases at Harvard Chan School and senior author of the study. “Our work shows how crucial the plasticity of mitochondria networks is for the benefits of fasting. If we lock mitochondria in one state, we completely block the effects of fasting or dietary restriction on longevity.”

Supporting a natural approach to health

Intermittent fasting has numerous benefits in addition to slowing down the aging process, including weight loss, lower blood pressure and reduced cholesterol.

It raises the question: why isn’t the food and pharmaceutical industries studying it?

Mark Mattson, the current Chief of the Laboratory of Neuroscience at the National Institute on Aging, asks just this question in the TED talk below.

In case you can’t watch the video right now, here’s an interesting section from the talk:

“Why is it that the normal diet is three meals a day plus snacks? It isn’t that it’s the healthiest eating pattern, now that’s my opinion but I think there is a lot of evidence to support that. There are a lot of pressures to have that eating pattern, there’s a lot of money involved. The food industry — are they going to make money from skipping breakfast like I did today? No, they’re going to lose money. If people fast, the food industry loses money. What about the pharmaceutical industries? What if people do some intermittent fasting, exercise periodically and are very healthy, is the pharmaceutical industry going to make any money on healthy people?”

If you’re hungry, don’t worry about it

We get used to having three meals a day, and always having snacks available when we feel hungry. But it turns out that hunger is your friend. Feeling full all the time only makes your body grow older, and being hungry is helping your body to maintain its youthful state.

If you haven’t already tried it, give intermittent fasting a shot. It’s a natural way to increase your lifespan.

PREGNANT women could hold the key to providing hope for stroke patients, following a breakthrough by Australian researchers.

Your doctor needs to followup this research and bring it into their hospital. Not following up is extreme incompetency. 
https://www.thesenior.com.au/health/new-hope-for-stroke-patients-2/

In a world first, scientists at Melbourne's La Trobe University have developed a groundbreaking treatment for stroke using discarded amniotic cells from pregnant women.

The teams found that injecting the stem cells - which line the amniotic sac during pregnancy and are discarded after birth - into stroke patients can significantly reduce brain injury and aid recovery.

Stroke is one of Australia's biggest killers and a leading cause of disability. Treatments for stroke are time critical and currently only a limited number of Australians have access to them.

The seven-year research project, led by La Trobe's Professor Chris Sobey and researchers from Monash University and Monash Health, found when human amnion epithelial cells were injected 90 minutes after stroke, the cells quickly homed in on the affected area of the brain, greatly reducing inflammation and nerve cell death.

"But what is particularly exciting about these new findings is that when the amniotic cells were administered as late as one or three days after stroke, there was accelerated healing and long term functional recovery was still greatly improved," Professor Sobey said.

Some of the most recent advancements in ischemic stroke treatment - strokes caused by a clot - can only be delivered within the first few hours of a stroke.

Professor Sobey said the reason this particular cell therapy was effective is because the cells are abundant, they are discarded after birth and don't require any treatment before being used.

"They already contain natural immune-suppressants, which means the patient's body won't reject them and they don't form tumours - both issues with other forms of cell therapy."

The first in-human trial in acute stroke patients will start soon, led by researchers at Monash Health and Monash University.

Recognise stroke: think FAST

F - Has their FACE drooped?

A - Can they lift both ARMS?

S - Is their SPEECH slurred and do they understand you?

T - Call 000, TIME is critical.

• More at strokefoundation.org.au

Compound repairs features of Alzheimer’s disease in mice

You'll want your doctor to follow this research because of your likely Alzheimer and Parkinsons risks.

Your chances of getting dementia.

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.

 

Your Parkinsons risk:

Parkinson’s Disease May Have Link to Stroke

Compound repairs features of Alzheimer’s disease in mice

At a Glance

• Researchers found that a compound called an NAD+ precursor helped mice with features of Alzheimer’s disease perform better on learning and memory tests.
• The findings pave the way for studies of the compound’s potential as an intervention for people with Alzheimer’s disease.

A mouse brain showing hallmarks of Alzheimer’s disease similar to that of the mice used in this study. Abnormal protein clumps are blue, blood vessels are red, and nerve cells are green.Alvin Gogineni, Genentech

Alzheimer’s disease is a brain disorder that slowly destroys thinking, memory, and language skills. It’s the most common cause of dementia among older people. Experts estimate that more than 5 million Americans are living with the disease. Symptoms usually begin after age 60. There is no cure.
The brain’s usual DNA repair activity is impaired in Alzheimer’s disease, leading to inflammation and dysfunction. A compound that the brain needs to regulate DNA repair and other key signaling pathways is known as nicotinamide adenine dinucleotide (NAD+). Because NAD+ declines with age, scientists have wondered whether boosting the level of NAD+ could help aging brain cells (neurons) to function better. One way to increase the cellular level is by giving an NAD+ precursor compound, such as nicotinamide riboside (NR). NR is a form of vitamin B3.
An international research team led by Dr. Vilhelm A. Bohr at NIH’s National Institute on Aging (NIA) set out to test whether NR supplements could normalize NAD+ levels in the brains of mice and counteract deficits in thinking and memory. The study was published online on February 5, 2018, in the Proceedings of the National Academy of Sciences.
The research team used findings from their previous studies with human cadaver brain tissue to develop a new strain of mice. These mice had the main features of human Alzheimer’s disease, such as the abnormal buildup of the proteins tau and amyloid-beta. The research team added the NR supplement to the mice’s drinking water for three months.
The team found that the NR-treated mice had less DNA damage, lower levels of neuron damage and death, increased production of new neurons, and lower brain inflammation than control mice. Mice who received NR had reduced tau in their brains, too, but amyloid-beta levels were unchanged. The NR-treated mice performed better than control mice on many learning and memory tests, such as a water maze. In addition, NR-treated mice had better muscle strength and endurance than controls.
The research team also tested human cells from people with and without Alzheimer’s disease. As in the mouse studies, NR decreased DNA damage in the cells from people with Alzheimer’s.
“The pursuit of interventions to prevent or delay Alzheimer’s and related dementias is an important national priority,” says NIA Director Dr. Richard J. Hodes. “We are encouraging the testing of a variety of new approaches, and this study’s positive results suggest one avenue to pursue further.”
“We are encouraged by these findings that see an effect in this Alzheimer’s disease model,” Bohr says. “We are looking forward to further testing of how NR or similar compounds might be pursued for their possible therapeutic benefit for people with dementia.”
The team is continuing to study the biological mechanisms of Alzheimer’s disease in preparation for possible studies of the approach in people.

References: NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency. Yujun Hou, Sofie Lautrup, Stephanie Cordonnier, Yue Wang, Deborah L. Croteau, Eduardo Zavala, Yongqing Zhang, Kanako Moritoh, Jennifer F. O’Connell, Beverly A. Baptiste, Tinna V. Stevnsner, Mark P. Mattson and Vilhelm A. Bohr. PNAS 2018; published ahead of print February 5, 2018, https://doi.org/10.1073/pnas.1718819115 (link is external).

Funding: NIH’s National Institute on Aging (NIA) and ChromaDex.

New stem-cell based stroke treatment repairs damaged brain tissue

In case you are wondering what else AB126 is used for, here it is:

AB126. Enzyme replacement therapy in patient with mucopolysaccharidosis type I: a case report

The stem cell treatment here, which of course no one in  stroke will followup with human testing. I have 10 posts on exosomes back to March, 2011. Your doctors can explain their incompetency in not getting researchers to followup and create translation interventions from them.

New stem-cell based stroke treatment repairs damaged brain tissue

Human clinical trials could begin as early as next year, Really? Ask your doctor for followup reports.

Date:

February 15, 2018

Source:

University of Georgia

Summary:

Researchers have developed a new treatment for stroke that reduces brain damage and accelerates the brain's natural healing tendencies in animal models.

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FULL STORY

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Exosomes, shown as small red punctate clusters, are taken up by neurons, shown as green cell extensions surrounding a blue nucleus.

Credit: UGA

A team of researchers at the University of Georgia's Regenerative Bioscience Center and ArunA Biomedical, a UGA startup company, have developed a new treatment for stroke that reduces brain damage and accelerates the brain's natural healing tendencies in animal models. They published their findings in the journal Translational Stroke Research.

The research team led by UGA professor Steven Stice and Nasrul Hoda of Augusta University created a treatment called AB126 using extracellular vesicles (EV), fluid-filled structures known as exosomes, which are generated from human neural stem cells.
Fully able to cloak itself within the bloodstream, this type of regenerative EV therapy appears to be the most promising in overcoming the limitations of many cell therapies-with the ability for exosomes to carry and deliver multiple doses-as well as the ability to store and administer treatment. Small in size, the tiny tubular shape of an exosome allows EV therapy to cross barriers that cells cannot.
"This is truly exciting evidence, because exosomes provide a stealth-like characteristic, invisible even to the body's own defenses," said Stice, Georgia Research Alliance Eminent Scholar and D.W. Brooks Distinguished Professor in the College of Agricultural and Environmental Sciences. "When packaged with therapeutics, these treatments can actually change cell progression and improve functional recovery."
Following the administration of AB126, the researchers used MRI scans to measure brain atrophy rates in preclinical, age-matched stroke models, which showed an approximately 35 percent decrease in the size of injury and 50 percent reduction in brain tissue loss -- something not observed acutely in previous studies of exosome treatment for stroke.
Outside of rodents, the results were replicated by Franklin West, associate professor of animal and dairy science, and fellow RBC members using a porcine model of stroke-the only one of its kind in the U.S.
Based on these pre-clinical results, ArunA Biomedical plans to begin human studies in 2019, said Stice, who is also chief scientific officer of ArunA Biomedical.
"Until now, we had very little evidence specific to neural exosome treatment and the ability to improve motor function," said Stice. "Just days after stroke, we saw better mobility, improved balance and measurable behavioral benefits in treated animal models."
Named as part of the 'stroke belt' region, Georgia continues to exceed the national average in stroke deaths, which is the third leading cause of death in the U.S., with more than 140,000 Americans dying each year, according to the Centers for Disease Control and Prevention.
ArunA recently unveiled advances to the company's proprietary neural cell platform for the production of exosome manufacturing. Today, ArunA's manufacturing process positions the company to produce AB126 exosomes at a scale to meet early clinical demand. The company has plans to expand this initiative beyond stroke for preclinical studies in epilepsy, traumatic brain and spinal cord injuries later this year.
Researchers also plan to leverage collaborations with other institutions through the National Science Foundation Engineering Research Center for Cell Manufacturing Technologies, based at the Georgia Institute of Technology and supported by $20 million in NSF funding.
Stice, the UGA lead for CMaT, and industry partners like ArunA Biomedical, will develop tools and technologies for the consistent and low-cost production of high-quality living therapeutic cells that could revolutionize treatment for stroke, cancer, heart disease and other disorders.

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Story Source:
Materials provided by University of Georgia. Note: Content may be edited for style and length.

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Journal Reference:

1. Robin L. Webb, Erin E. Kaiser, Shelley L. Scoville, Tyler A. Thompson, Sumbul Fatima, Chirayukumar Pandya, Karishma Sriram, Raymond L. Swetenburg, Kumar Vaibhav, Ali S. Arbab, Babak Baban, Krishnan M. Dhandapani, David C. Hess, M. N. Hoda, Steven L. Stice. Human Neural Stem Cell Extracellular Vesicles Improve Tissue and Functional Recovery in the Murine Thromboembolic Stroke Model. Translational Stroke Research, 2017; DOI: 10.1007/s12975-017-0599-2

Stroke survivors walk again after Stanford injects stem cells into brain

I'd need to see videos of before and after before I believe this. Not sure why it showed up in my news feeds 2 years later.
https://www.telegraph.co.uk/science/2016/06/03/stroke-survivors-walk-again-after-stanford-injects-stem-cells-in/?WT.mc_id=tmg_share_em

• Sarah Knapton, Science Editor

3 June 2016 • 6:00am

Stroke survivors who believed they would be paralysed or need a wheelchair for the rest of their lives are walking and moving again following a ground-breaking stem cell treatment.

18 patients who agreed to allow doctors to drill a hole in their skull and inject stem cells into the damaged part of their brain have made a ‘remarkable’ recovery.

Incredibly, it worked for patients whose strokes had occurred between six months and three years previously. Historically doctors have believed that the brain will no longer regenerate after six months.

 

Patients who were in wheelchairs are walking now. Their ability to move around has recovered visibly. That’s unprecedented.Prof Gary Steinberg

But the new therapy essentially turns the adult brain back to an infant brain so that it can rebuild itself.

Scientists at Stanford University School of Medicine believe the therapy could also work for other neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s and Lou Gehrig’s Disease.

“The remarkable recovery we saw in many of these chronic stroke patients was quite surprising,” said Prof Gary Steinberg, Chair of Neurosurgery at Stanford, who has spent 15 years researching stem cells.

“This wasn’t just ‘they couldn’t move their thumb and now they can’. Patients who were in wheelchairs are walking now. Their ability to move around has recovered visibly. That’s unprecedented.

“The study changes our prior notion that patients can’t recover much more after the first six months following a stroke because the circuits are dead, or irreversibly damaged.

“Clearly the circuits can be resurrected by this treatment and we are still investigating how they are being jump-started.”

The stem cells in question were taken from the bone marrow of two donors. Scientists had previously believed that stem cells could not integrate into the brain to become neurons. But it now appears they secrete powerful chemicals for growth and regeneration which the brain can use to restore function.

“In a simple sense, the stem cell transplant turns the adult brain in a neonatal of infant brain which recovers well after a stroke or other injury,” added Prof Steinberg.

Prof Gary Steinberg  Credit: Stanford University 

“This could revolutionise our concept of what happens after no only stroke but traumatic brain injury and ever neurodegenerative disorders. We thought these brain circuits were dead and we’ve learned that they’re not.”

All the patients involved in the trial had suffered ischemic strokes where a clot prevents blood getting to the brain, which leads to brain cell death. The procedure involved drilling a small hole in the skull above the damaged area so that SB623 stem cells could be injected at several spots around the edge of the injury.

The patients, who had an average age of 61,  only needed a local anaesthetic and were sent home the following day. Although many complained of initial headaches, because of the surgical procedure, there were no long-term side-effects.

Afterwards they were monitored with blood tests, clinical evaluations and brain imaging. Intriguingly the implanted stem cells do not survive very long in the brain, but recovery continued even after they had vanished.

There was an overall 11.4 point improvement on the Fugl-Meyer test, which gauges how well stoke pateints can move and there has been no relapse since the injection,n which was carried out up to two years ago.

Repression of adenosine triphosphate binding cassette transporter ABCG2 by estrogen increases intracellular glutathione in brain endothelial cells following ischemic reperfusion injury

Over my head but it talks about neuroprotection against ischemic injury, so go ask your doctor whom she is following up with to get this tested in humans.
https://www.sciencedirect.com/science/article/pii/S0197458018300642

• Jin A. Shin^{a, 1},
• Sae Im Jeong^{b, 1},
• Hye Won Kim^a,
• Gyeonghui Jang^a,
• Dong-Ryeol Ryu^c,
• Young-Ho Ahn^d,
• Ji Ha Choi^a,
• Youn-Hee Choi^e,
• Eun-Mi Park^{a, ,}

 Show more

https://doi.org/10.1016/j.neurobiolaging.2018.02.020

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Highlights

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Estrogen decreased basal protein level of ABCG2 in the brain of OVX mice.

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Estrogen prevented ischemia-induced brain ABCG2 level in OVX mice.

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ABCG2 siRNA transfection reduced OGD-induced injury in bEnd.3 cells.

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Estrogen enhanced survival in bEnd.3 cells transfected with ABCG2 siRNA against OGD.

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ABCG2 inhibition increased intracellular glutathione in bEnd.3 cells exposed to OGD.

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Abstract

The adenosine triphosphate-binding cassette efflux transporter ABCG2 which is located in the blood-brain barrier limits the entry of endogenous compounds and xenobiotics into the brain, and its expression and activity are regulated by estrogen. This study was aimed to define the role of ABCG2 in estrogen-mediated neuroprotection against ischemic injury. ABCG2 protein levels before and after ischemic stroke were increased in the brain of female mice by ovariectomy, which were reversed by estrogen replacement. In brain endothelial cell line bEnd.3, estrogen reduced the basal ABCG2 protein level and efflux activity, and protected cells from ischemic injury without inducing ABCG2 expression. When bEnd.3 cells were transfected with ABCG2 small interfering RNA (siRNA), ischemia-induced cell death was reduced, and the intracellular concentration of glutathione, an antioxidant that is transported by ABCG2, was increased. In addition, after ischemic stroke in ovariectomized mice, estrogen prevented the reduction of intracellular glutathione level in brain microvessels. These data suggested that the suppression of ABCG2 by estrogen is involved in neuroprotection against ischemic injury by increasing intracellular glutathione, and that the modulation of ABCG2 activity offers a therapeutic target for brain diseases in estrogen-deficient aged women.

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Graphical abstract

Keywords

• ABCG2;
• brain endothelial cell;
• estrogen;
• glutathione;
• ischemic stroke;
• neuroprotection

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1. All authors disclose that there are no actual or potential conflicts of interest.

2. This study was supported by the National Research Foundation of Korea (NRF) grants funded by the Korea government (MSIP) (2010-0011353 and 2014R1A2A1A11051461).

3. The data contained in the manuscript being submitted have not been previously published, have not been submitted elsewhere and will not be submitted elsewhere while under consideration at Neurobiology of Aging.

4. Animal experiments in the present paper comply with the NIH and Ewha Womans University guidelines for Laboratory Animals Care and Use, and the study was approved by the Institutional Animal Care and Use Committee of the Medical School of Ewha Womans University.

5. All authors have reviewed the contents of the manuscript being submitted, approve of its contents and validate the accuracy of the data.

Corresponding author: Eun-Mi Park, Department of Pharmacology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, 1071 Anyangcheon-ro, Yangcheon-gu, Seoul, 07985, Republic of Korea, Tel.: 82-2-2650-5743, Fax: 82-2-2653-8891.