#WSF18: Harnessing the Power of Neuroplasticity

For all this firepower discussing neuroplasticity they never refer once to what research would look like to make it repeatable on demand.

World Science Festival - neuroplasticity

Can Hyperbaric Oxygen Repair the Damaged Brain?

I would trust this piece from Dana before the puff piece from HBOT pushers(Efrati). Your doctor can decipher the competing claims.
http://dana.org/news/features/detail.aspx?id=41174
While many agree that Efrati’s data are promising, a prior study run by the U.S. Air Force found no significant differences between hyperbaric oxygen treatment and a sham treatment on patients with mild traumatic brain injury (TBI). Both groups showed significant improvement over the course of the trial. Those results were published in the November 2012 issue of the Journal of Neurotrauma.

The HBOT pusher piece:

Hyperbaric Oxygen Induces Late Neuroplasticity in Post Stroke Patients - Randomized, Prospective Trial

Exercise Benefits the Healthy and Diseased Brain

Why the fuck doesn't your doctor have a specific exercise protocol for promoting neuroplasticity in your diseased brain? Incompetence? Stupidity? Doesn't care? Waiting for somebody else to address that issue?
http://www.dana.org/News/Exercise_Benefits_the_Healthy_and_Diseased_Brain/
Great stuff from the Dana Foundation.

“What’s good for the heart is good for the brain.”
That's the advice a physician might give to older patients who are concerned about staying mentally sharp as they get older. We know very well that physical activity keeps the heart healthy, and in recent years we have begun to understand how exercise affects the brain.
Exercise induces neuroplasticity, a collective term referring to various structural and functional brain changes that occur in response to experience. In a symposium at the 46^th annual meeting of the Society for Neuroscience in San Diego in November, researchers in the field discussed how exercise benefits the brains of healthy older adults and those of people with psychiatric and neurological diseases.
Psychologist Kirk Erickson of the University of Pittsburgh explained that most of us experience age-related decline in cognitive function, with abilities such as inductive reasoning, perceptual speed, and verbal memory declining sharply from about 60 years of age. Physical activity offers significant protection against age-related cognitive decline, however, and can improve mental function in older adults. [See A Purposeful Life is a Healthy Life]
He then described a number of longitudinal intervention studies performed in his lab investigating the underlying mechanisms by which exercise benefits brain structure and function in healthy older adults.
In 2009, Erickson and his colleagues reported that higher levels of aerobic exercise in elderly adults are associated with increased volume of the hippocampus, a brain structure known to be critical for memory formation, and that this in turn is related to enhanced spatial memory. [See One Man's Continuing Contribution to the Science of Memory] They went on to show that higher fitness levels are also associated with greater prefrontal cortex volume and better executive function, and that exercise enhances the integrity of white matter tracts throughout the brain.
Thus, exercise appears to have a protective effect on the brain's gray and white matter, making both more resilient to the effects of aging. Until recently, it was thought that the distribution of white matter in the brain was highly stable, but we now know that it can change rapidly in response to experience. And although studies consistently show that exercise increases expression of growth factor BDNF, it's still not clear exactly how the observed volume increases occur; they could be due to the production of new brain cells, the formation of new synaptic connections, or a combination of both.   
“I believe that exercise affects every organ of the body, and it's very likely that there are a multitude of pathways by which it affects the brain,” said Erickson, “but we can now begin to think about how changes at the molecular and cellular level influence behavioral outcomes.”
Erickson added that we still know very little about individual differences in how exercise affects the brain, and that people generally dislike the term “exercise,” which may discourage them from participating in research. He and his colleagues are now recruiting participants for the REACT! trial, a pilot study that will compare the effects of African dance and an educational discussion group on brain health, fitness levels, and quality of life in older African Americans, who are at higher risk of age-related cognitive decline than other populations.
Psychiatrist Sarah McEwan of the University of California, Los Angeles described her studies into how exercise benefits brain function in people diagnosed with schizophrenia. Schizophrenia is a severe, long-term mental health condition with symptoms that include delusions of persecution or grandeur, visual and auditory hallucinations, and disordered patterns of thought and behavior.
Previous studies have shown that people who have had schizophrenia for between 5 and 20 years have less grey matter volume in the dorosolateral prefrontal cortex. “This part of the brain is important for higher order processes such as top-down control, attention, and problem-solving,” McEwan said. “Although anti-psychotics are excellent for treating voices and delusions, there's nothing to treat the core cognitive dysfunctions, which are the most debilitating aspects of the disease.”
Last year, McEwan's lab published the first empirical study to examine the benefits of regular physical activity for patients in the early stages of the disease. They scanned the brains of 14 young adults who were experiencing their first schizophrenic episode, and found that those who reported having low levels of physical activity had reduced grey matter volume in the prefrontal cortex and hippocampus compared with the “high activity” group. Patients who reported greater levels of overall physical activity also performed slightly better on tests of verbal memory and social cognition.  
Together, these preliminary findings suggest that exercise-based interventions could improve brain health and cognitive function in patients experiencing their first schizophrenic episode. The findings need to be replicated in a larger study, however, and they do not address the effects of exercise in patients who have had the disease for longer periods of time.
“Patients deemed to be at high risk of developing schizophrenia tend to be more sedentary,” McEwan added, “and the first psychotic episode seems to be an excellent window during which we can try to intervene and improve patients' prognosis later on in life.”
Other recent research suggests that exercise can also be of benefit to people diagnosed with Parkinson's disease (PD), a progressive neurodegenerative disorder caused by the death of dopamine-producing neurons in the midbrain. PD leads to involuntary, shaky movements and other motor problems, as well as cognitive deficits. 
Neurologist Giselle Petzinger of the University of Southern California and her colleagues have been examining rodent models of Parkinson’s and translating their findings to studies in humans.
In the mouse models, neuronal death reduces dopamine levels in the striatum, a deep brain structure involved in reward, motivation, and movement, which normally receives inputs from the midbrain. This is accompanied by loss of dendritic spines, the tiny, finger-like protuberances at which neuronal signaling takes place.
Petzinger and her colleagues have shown that treadmill exercise reverses the loss of dendritic spines in the striatum in a mouse model of Parkinson’s by promoting the formation of new synaptic connections. And in a small pilot study of patients with early Parkinson’s published in 2013, they showed that intensive treadmill training elevates dopamine receptor levels in the striatum, and also improved patients’ postural control.
At the meeting, Petzinger presented preliminary evidence that exercise induces changes in neural circuits involved in attention. She noted, however, that some forms of exercise involve motor learning, and that this is likely to contribute to the protective effects.
Petzinger argues that exercise does not benefit overall brain health, but rather that different forms of exercise induce changes in specific neural circuits. She is now involved in a larger study comparing the effects of cardiovascular training and skill-based exercises in people with Parkinson’s.
“What we’re beginning to see is some evidence that both cardiovascular fitness and motor-related fitness seem to be associated with improved prefrontal cortex-related cognition,” she said. “We can now tease apart how exercise type may impact specific circuits and brain areas involved in cognition.”

free public luncheon briefing, “Moving Toward a Healthy Brain: Physical Activity and Brain Health,”

You do expect your stroke associations to go here to get the information and pass it on to all stroke doctors and stroke hospitals? But fuck, that won't occur, you will have to attend yourself because we have fucking failures of stroke associations doing nothing useful for survivors.
https://danablog.org/2016/09/02/free-public-briefing-on-physical-activity-and-brain-health/
It’s no secret that exercise and physical activity are central to public health. But does a healthy body equal a healthy brain?

Photo Credit: Shutterstock

Come to a free public luncheon briefing, “Moving Toward a Healthy Brain: Physical Activity and Brain Health,” hosted by the American Association for the Advancement of Science (AAAS), through the support of the Dana Foundation, and in conjunction with the Congressional Neuroscience Caucus.
Featuring:

• Sarah M. Ingersoll, MBA, Clinical Instructor of Neurology, Keck School of Medicine, University of Southern California
• Arthur Kramer, Ph.D., Senior Vice Provost for Research and Graduate Education, Professor of Psychology & Engineering, Northeastern University
• Moderator: Erin Heath, AAAS

Location:
B339 Rayburn House Office Building
Washington, DC
Time:
7 September 2016
12:00 PM – 1:00 PM
(Register by 10AM, September 7)
For questions, please contact Sean Gallagher at sgallagh@aaas.org
AAAS is a non-profit, non-partisan organization. Since it was founded in 1848, AAAS has been dedicated to the advancement of scientific knowledge for the good of society as a whole. http://www.aaas.org. The Dana Foundation is a private philanthropic organization that supports brain research through grants and educates the public about the successes and potential of brain research. http://www.dana.org

Joshua Gordon Named New Head of NIMH - National Institute of Mental Health

And if survivors had anything even remotely approaching a great stroke association we would be approaching him to see what science is needed to prevent the likely depression from stroke. But we don't and the opportunity will be fucking lost like everything to do with stroke research. And the boards of directors don't have enough sense to make this an objective of the president.
https://danablog.org/2016/08/01/joshua-gordon-named-new-head-of-nimh/
In late July, the National Institutes of Health (NIH) announced that it had finally completed its nearly year-long search for a new director of the National Institute of Mental Health (NIMH). Francis Collins, M.D., Ph.D., said that the agency had selected Joshua Gordon, M.D., Ph.D., currently an associate professor of psychiatry at Columbia University, to take the helm of the $1.5 billion federal agency governing mental health research, replacing former director Thomas Insel. He is expected to start in September.

In the press release announcing the selection, Collins said, “Josh is a visionary psychiatrist and neuroscientist with deep experience in mental health research and practice. He is exceptionally well qualified to lead the NIMH research agenda to improve mental health and treatments for mental illnesses. We’re thrilled to have him join the NIH leadership team.
Gordon, whose research program focused on integrative genetic models of psychiatric disease, spoke with the Dana Foundation about why he wanted to take on this new role in his career, the importance of collaboration and communication, and where he hopes to see the agency go under his leadership.

You’ve had quite a bit of success in academia. Why throw your hat in the ring to lead NIMH?
It’s a really exciting time in psychiatric neuroscience. And such an exciting time comes with a lot of possibilities—but also a lot of responsibilities for the field. In order to pursue those possibilities, with attention to tailoring neuroscience and basic research to really make a difference in people’s lives, requires a lot of thought and planning. So playing a role in how best to do that thought and planning moving forward is an exciting thing to take part in.

More at link.

Advances in Our Knowledge of Stroke Mechanisms and Therapy

I can't say that this has advanced my knowledge one bit.
http://www.dana.org/Publications/ReportOnProgress/Advances_in_Our_Knowledge_of_Stroke_Mechanisms_and_Therapy/

	Xuefang Ren, M.D. Department of Physiology and Pharmacology Experimental Stroke Core, Center for Basic and Translational Stroke Research West Virginia University
	James W. Simpkins, Ph.D. Department of Physiology and Pharmacology Experimental Stroke Core, Center for Basic and Translational Stroke Research West Virginia University

View Article as PDF
Stroke, the most common medical emergency, is a cerebrovascular accident that can cause death and long-term disability. Over 80 percent of all strokes are ischemic strokes, when a clot lodges in an artery supplying blood to the brain and the blood flow is reduced or blocked. A small percentage, caused by rupture of brain blood vessels, are called hemorrhagic strokes. Stroke risk factors are well known and include high blood pressure, elevated lipids, diabetes, smoking, heavy drinking, coronary artery disease, heart diseases, etc.
Both ischemic and hemorrhagic strokes may cause a variety of neurologic symptoms, including sudden death, loss of consciousness, one-sided numbness, weakness, paralysis, sudden deafness, visual impairment, or difficulty in speaking, thinking, or understanding speech. Specific symptoms correspond with the location of stroke injury. For example, stroke damage in the brain stem (a pivotal center in the regulation of cardiac and respiratory function) may cause sudden death; a clot or bleeding in middle cerebral artery (MCA) territory (including the motor cortex and the underlying caudate-putamen), may cause numbness, weakness or paralysis of the contralateral side of the body.

A computerized tomography (CT) scan or Magnetic Resonance Imaging (MRI) is required to distinguish ischemic and hemorrhagic strokes. One of these images is required for clinicians to decide on the therapeutic strategies for patients when a stroke occurs. There are different mechanisms and treatments for ischemic and hemorrhagic strokes. Here we focus on the description of our current knowledge of the mechanisms and current treatments for ischemic stroke.
Current Treatments
A stroke requires immediate medical attention and urgent care because stroke damage to the brain evolves every second. To date, intravenous thrombolytic agents (which pharmacologically dissolve clots) and surgical strategies (which retrieve clots by mechanical means) are used to treat acute ischemic stroke. Tissue plasma activator (tPA) is the only FDA approved medication for acute ischemic stroke and must be used within 4.5 hours from the time of the onset of symptoms of stroke. Other medical thrombolytic drugs such as streptokinase and aspirin, show higher mortality or disability, and a higher risk of brain hemorrhage. Surgical interventions should be performed within 6 hours of acute stroke symptoms, and only after a patient receives tPA. Considerable improvements in stroke outcome are seen with both tPA and surgical clot removal when used within their allowable time windows.

Mechanisms in Ischemic Stroke
Experimental animal stroke models and cell culture models were developed for stroke studies several decades ago and rigorous scientific investigations have been undertaken. Some models mimic pathophysiological changes in human stroke and address many puzzles in understanding stroke mechanisms, which are essential in developing effective therapeutic strategies for stroke patients.

Figure 1 describes our current understanding of stroke mechanism: during the first few hours, the primary ischemic stroke injury is due to the occlusion of the blood vessels. The occlusion leads to an insufficient energy supply to the brain tissue and causes neuronal death and neurological damage. Reduced oxygen supply compromises mitochondrial function and causes anaerobic glycolysis (transforms glucose to lactic acid when an insufficient amount of oxygen is available). Elevated levels of lactic acid make the brain tissue acid and results in decreased ATP production and reduced ion pumps activity on cell membrane. As a consequence, concentrations of protons, calcium, and sodium ions increase in the cells. This results in water influx into the cells, cell swelling, death, and formation of core infarction in primary stroke injury. This series of events evolve quickly in the primary stroke site, but might be salvageable by treatment within minutes to hours. Secondary stroke damage is initiated by post-stroke disruption of the blood-brain barrier (BBB), initiating a cascade damaging molecular processes. BBB is formed by endothelial cells surrounding the brain’s vasculature, which restrict access of molecules in the general circulation of the brain (See Figure 1 and following text).

(Click on image to view larger)

Figure 1. Mechanisms in Ischemic Stroke Damage.Ischemia causes immediate brain damage in primary stroke injury and delayed brain damage in secondary stroke injury. Mitochondrial failure plays a critical role in BBB opening that involves in vascular edema following stroke.

Mitochondrial failure and BBB disruptionBBB opening is a key stage in secondary stroke injury and has been linked to increased stroke damage and vascular edema in animal models of stroke. Several groups have observed a biphasic BBB breakdown after transient stroke in animal models. The first BBB disruption occurs within several hours of the onset of ischemia and a second phase of BBB opening may happen after several days of ischemia. Recently, using an experimental model of stroke, our group has shown that mitochondria play a critical role in the first BBB opening¹. Due to lack of oxygen, mitochondrial failure decreases ATP production in the endothelial cells surrounding the blood vessels in the brain, causing a breakdown of the BBB and further exacerbating stroke damage².
We have also shown that lipopolysaccharide (LPS, an exotoxin extracted from bacteria and used to mimic bacterial infection) worsens stroke outcomes by the same mechanisms of compromised mitochondria in the endothelial cells^1-3. We have also found that a food preservative, tBHQ, interferes with mitochondrial function and worsens stroke outcome as well⁴. This evidence suggests that mitochondrial dysfunction plays a critical role in the first BBB disruption and acute stroke damage.
It is not known yet how the BBB is repaired after the initial first opening. There is a debate as to whether the second BBB opening contributes to brain damage or brain repair after stroke. More investigation is need to resolve this issue.
Reactive oxygen species (ROS) and stroke⁵About 95 percent of ROS, such as superoxide (O2•−) and hydrogen peroxide (H2O2) are derived from electron leakage during the activity of the mitochondrial respiratory chain, which generates ATP. These ROS are scavenged by manganese-superoxide dismutase (Mn-SOD or SOD2), catalase and glutathione peroxidase. Ischemic stress triggers a disturbance of the mitochondrial membrane potential and the normal proton gradient, which results in excessive ROS generation via electron transfer for the ATP synthesis.
The overproduction of ROS overwhelms oxidant scavenging capacity and establishes a vicious positive feedback loop in which increased ROS-induced ROS production. ROS also damage mitochondrial DNA, induce activation and secretion of matrix metalloproteinases (MMPs), activate inflammatory responses, and lead to cell swelling and death. This process causes BBB damage and secondary injury in acute stroke. However, ROS may also be involved in tissue remodeling and angiogenesis (new blood vessel formation) in the late phase of stroke.
Matrix metalloproteinases (MMPs) and stroke⁶MMPs, a large family of proteolytic enzymes, are present in various cells in latent forms and are capable of degrading all components of the extracellular matrix. ROS may induce activation and secretion of MMP-2 in astrocytes, MMP-3 and MMP-9 in endothelial cells and in neutrophils. The activated MMPs breakdown and degrade tight junctions, a critical component of the BBB, and contribute to BBB disruption and hemorrhagic transformation in acute stroke. Interestingly, evidence also suggest that MMPs participate in brain repair in the stroke late phase.

Inflammatory responses in the ischemic brain⁷
Our immune system protects the body from infections. We did not anticipate that the immune system would play a negative role in stroke by attacking brain tissue as it were “foreign”. However, this does happen in most of cases of acute strokes. Inflammatory responses are initiated in the clots causing the stroke. Platelets and white blood cells (WBCs) are trapped in the clot fibrin due to hypoxia and shear stress in small blood vessels. MMPs are released by leukocytes and facilitate the BBB opening. Following the BBB disruption, neutrophils, lymphocytes, and monocytes from peripheral blood infiltrate into the brain tissue. Pro-inflammatory cytokines⁸ and chemokine released by WBCs may destroy brain neurons directly or indirectly. The inflammatory cells currently being actively investigated include:
NeutrophilsNeutrophils, an essential part of the innate immune system, are one of the first peripheral responding WBCs to launch a defense against all classes of infections. Vesicles that contain various enzymes, including oxidase and MMPs are stored in neutrophils. Hypoxia induces the secretion of chemokines by neurons, which attract the migration of neutrophils; meanwhile hypoxia-induced ROS over-production activates the release of the MMPs from neutrophils that can attack BBB, permitting neutrophils to migrate into the ischemic brain tissue via the degraded BBB. From there, neutrophils phagocytose dying neurons and release a large amount of granules and ROS that may kill both dying and living neurons.

Antigen Presentation Cells (APCs)APCs are classified as professional APCs and non-professional APCs. The former includes macrophages, microglia, dendritic cells, B cells, and monocytes. From our basic immunology book, we know that professional APCs express major histocompatibility complex II (MHCII) on their surfaces and present antigens to T-cells. Non-professional APCs express MHC class 1 molecules on their surface. Following BBB disruption and the release of brain antigens into the periphery, these APCs present brain antigens to T-cells in the late stage of ischemic stroke, and they may be partially responsible for ischemia-induced dementia. However, in acute stroke, APCs may produce pro-inflammatory cytokines, such as TNF-α and IL-1β that contribute to post-stroke inflammation; they may also produce anti-inflammatory cytokines IL-10 and TGF-β, which promote healing and reduce inflammatory responses.
LymphocytesLymphocytes, including T-cells and B-cells belong to the adaptive immune system that involves both cellular and humoral immunity against antigens. Growing evidences indicate that T-cells and B-cells participate in the progression of ischemic stroke. Elevated antibodies (produced by B-cells) against brain antigens, and increased cytokines (secreted by T-cells and other WBCs) are detected in stroke, suggesting cellular and humoral responses to ischemic brain damage. Using the experimental stroke animal model, we have previously demonstrated that B-cells are protective in acute strokes .by secreting anti-inflammatory cytokine IL-10. Another group found that B-cells could impair cognitive behavioral outcomes and contribute to post-stroke dementia in the late phase.
Researchers are striving to identify the role of T cells in stroke. Tolerated T-cells that induce a TH2 cytokine response, including IL-4 and IL-10 secretion, reduce stroke infarction. TH1 cells, secreting pro-inflammatory cytokines (such as IL-1beta, TNF-alpha, and IFN-gamma,) exacerbate stroke. Mice, which have the recombination activation gene (RAG1) inactivated are deficient in T-cells and B-cells and are protected from ischemia. However, transfer of naive T-cells worsens stroke infarction following 24 hours reperfusion, suggesting that T-cells are detrimental early in stroke. It has been demonstrated that γδT cells (a unique T-cell subtype that links adaptive and innate immune system) contribute to brain damage by secreting a pro-inflammatory cytokine IL-17.
Other mechanismsScientists have also investigated other mechanisms in stroke, such as, glutamate and other excitatory neurotransmitters released by dying neurons which cause exotoxic damage to healthy neurons. MicroRNAs, a hot topic in life sciences, are changed in stroke animals and patients, and might be involved in brain damage and recovery as well. Other studies have also revealed that nitric oxide (NO) and peroxynitrite (ONOO−) produced simultaneously with superoxide in stroke, are detrimental to brain neurons.
Future perspectivesDespite the benefits afforded by tPA and surgical treatments, there is a desperate need to develop more effective therapies for stroke because very few stroke patients can meet the brief time window necessary for effective clot removal. While there are still debates as to whether we have successfully traveled from clot removal in early stroke to effective treatments in the second stroke injury, it is clear that we have gained more knowledge in the past two decades than any in our prior history. The failure of several clinical trials on some potential drugs raises questions about our complete understanding of the mechanisms in stroke. Given the complicated mechanisms revealed so far, drugs that target a single mechanism may not be able to stop the progression of post-stroke injury. However, if properly timed, we believe that preserving mitochondrial function in the BBB might be able to restrict the damage of stroke. We anticipate that a cocktail of compounds will be needed to preserve mitochondrial function representing a novel strategy for stroke treatments.
Further reading

1. Doll, D. N. et al. Mitochondrial crisis in cerebrovascular endothelial cells opens the blood-brain barrier. Stroke; a journal of cerebral circulation46, 1681-1689, doi:10.1161/STROKEAHA.115.009099 (2015).

2. Hu, H. et al. Mitochondrial Impairment in Cerebrovascular Endothelial Cells is Involved in the Correlation between Body Temperature and Stroke Severity. Aging and disease7, 14-27, doi:10.14336/AD.2015.0906 (2016).

3. Doll, D. N. et al. Lipopolysaccharide exacerbates infarct size and results in worsened post-stroke behavioral outcomes. Behavioral and brain functions : BBF11, 32, doi:10.1186/s12993-015-0077-5 (2015).

4. Sun, J., Hu, H., Ren, X. & Simpkins, J. W. Tert-butylhydroquinone compromises survival in murine experimental stroke. Neurotoxicology and teratology54, 15-21, doi:10.1016/j.ntt.2016.01.004 (2016).

5. Kalogeris, T., Bao, Y. & Korthuis, R. J. Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning. Redox biology2, 702-714, doi:10.1016/j.redox.2014.05.006 (2014).

6. Turner, R. J. & Sharp, F. R. Implications of MMP9 for Blood Brain Barrier Disruption and Hemorrhagic Transformation Following Ischemic Stroke. Frontiers in cellular neuroscience10, 56, doi:10.3389/fncel.2016.00056 (2016).

7. Iadecola, C. & Anrather, J. The immunology of stroke: from mechanisms to translation. Nature medicine17, 796-808, doi:10.1038/nm.2399 (2011).

8. Doll, D. N., Rellick, S. L., Barr, T. L., Ren, X. & Simpkins, J. W. Rapid mitochondrial dysfunction mediates TNF-alpha-induced neurotoxicity. Journal of neurochemistry132, 443-451, doi:10.1111/jnc.13008 (2015).

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The Neuro Funding Rollercoaster

This is where a great stroke leader would shine, first by creating a stroke strategy and tying research proposals to that strategy which should be able to shake money out of foundations wanting to solve all the problems in stroke. That does mean getting away from this fucking 'happy talk' that everything in stroke is hunky-dory. But we have jackshit for stroke leaders and have for decades.

From the Dana Foundation;

The Neuro Funding Rollercoaster

Editor’s Note: Compared to the money dedicated to cancer and cardiology, funding for neuroscience research has lagged behind for decades. But things are starting to change. From the White House’s Brain Initiative to the Ice Water Challenge for ALS to some recent sizeable gifts to universities, money for brain research appears to be on the rise. But, as our author explains, research and development funding from private and corporate lenders for cognitive neuroscience—an area that he has spent years tracking—is also vital to the quality of life for millions of people. 

More at link.

Editor’s Note: Compared to the money dedicated to cancer and cardiology, funding for neuroscience research has lagged behind for decades. But things are starting to change. From the White House’s Brain Initiative to the Ice Water Challenge for ALS to some recent sizeable gifts to universities, money for brain research appears to be on the rise. But, as our author explains, research and development funding from private and corporate lenders for cognitive neuroscience—an area that he has spent years tracking—is also vital to the quality of life for millions of people. - See more at: http://www.dana.org/Cerebrum/2016/The_Neuro_Funding_Rollercoaster/#sthash.2qs92aPN.dpuf

Submit Nominations for European Brain Awareness Week Award

I wish they would change this to Brain results award. 

Submit Nominations for European Brain Awareness Week Award

Every 67 Seconds: Genetics in Alzheimer’s Disease

Every 40 seconds someone has a stroke and yet our fucking failures of stroke associations can't get stroke front and center in the publics' consciousness and get research dollars allocated to solve all the problems in stroke. And the reason for that is because they refuse to publicly state that everything in stroke is a failure. All you get from them is 'Happy talk'.  Fucking worthless pieces of shit. 

Every 67 Seconds: Genetics in Alzheimer’s Disease

Genes passed down from generation to generation within families are the main culprit in contracting Alzheimer’s disease. Recent research for the disease is focusing on individual variations of these genes, instead of trying to find a “one size fits all” treatment.
That was part of the message delivered by Richard Mayeux, the Gertrude H. Sergieysky co-director of the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center. Mayeux’s talk on the role that genetics plays in Alzheimer’s disease last Thursday evening at the 92nd Street Y in Manhattan came at an opportune time. November is both National Alzheimer’s Disease Awareness month and National Epilepsy Awareness Month.
Mayeux, M.D., MS.c., who is also Professor of Neurology, Psychiatry, and Epidemiology and a member of the Dana Alliance for Brain Initiatives, has been featured in the New York Academy of Sciences podcast series, Dementia Decoded. His research on genomes aims to understand the differences in gene structure and what it could mean for future treatment.

Through the use of genome-wide association studies, Mayeux and his colleagues are examining common genetic variants to see if any variant is associated with the traits common to the disease. (See more about the gene involvement in the brain in our Brain in the News article, Genetics and the Brain.) Mayeux believes that developing successful treatments will depend on better understanding genetic and environmental influences. His research team has learned that treatment will be tied to each patient’s individual genetic profile and specific gene structure. Mayeux outlined examples of individuals with varying levels of APOe, a protein that is heavily involved in Alzheimer’s, and the different ways that it influences how each individual processes amyloid. Factors such as these, as well as many others, make each patient unique. He described future treatment for the disease as “precision medicine,” such as the way cancers, brain tumors, etc., are cared for.
Mayeux said that he and other specialists submit their research findings and family studies to a large database open to all qualified scientists. With the Obama Administration’s $50 million reallocation towards Alzheimer’s research, funds have been committed to study the genome in more detail, and the use of Mayeux’s and other scientists’ datasets will help in conducting more accurate analyses. In the Q&A, Mayeux expressed his enthusiasm for a breakthrough and the renewed pharmaceutical interest –
“I’m more than halfway through my career – and I’ve never been more excited.”
With life spans expanding due to advances in almost every other area of medicine, Mayeux’s research is vital to the future of the nation’s healthcare system. According to the Alzheimer’s Association, about 5.3 million people (7 million in the US have survived a stroke) in the United States suffer from Alzheimer’s disease, and a new person is diagnosed every 67 seconds. Heathcare costs to treat the disease in 2015 are estimated at more than $200 billion. (Without Action, Financial Cost of Strokes to Reach $2.2 Trillion by 2050)
To see Richard Mayeux and other specialists speak more about Alzheimer’s disease, check out the Dana Foundation’s YouTube playlist, Dana Alliance Experts on Dementia/Alzheimer’s Disease.

Disorders of Consciousness: Brain Death, Coma, and the Vegetative and Minimally Conscious States -

You need to be extremely concerned about this. There was not enough discussion of locked-in syndrome so it is unlikely your doctor will know what to do in that case. Or the common misdiagnosis of stroke as drunkeness or balance issues.
http://www.dana.org/Publications/ReportOnProgress/Disorders_of_Consciousness__Brain_Death,_Coma,_and_the_Vegetative_and_Minimally_Conscious_States/

How to Reduce Your Risk of Alzheimer’s Without Taking Drugs

This article from Dana Foundation summarizes a lot of the information I have scattered about my blog. Compare this to what your doctor is giving you.
http://www.dana.org/alzrisk/

Can Hearing Loss Predict—or Lead to—Cognitive Decline?

Is your doctor assigning your cognitive decline post-stroke to the stroke because of  Occams' Razor  rather than really finding out the cause?
http://www.dana.org/News/Can_Hearing_Loss_Predict%E2%80%94or_Lead_to%E2%80%94Cognitive_Decline_/

The Neurobiology of Resilience

I should be studied, having a stroke, losing my job, getting divorced. Any one of those three should have slammed me to the ground and left me there.
What is your doctor doing to enhance your resilience?
http://dana.org/Briefing_Papers/The_Neurobiology_of_Resilience/

Students: Design a Brain Experiment

Students: Design a Brain Experiment

The Dana Foundation is asking U.S. high school students to submit their most creative brain experiment ideas to the fourth annual Design a Brain Experiment Competition. Submissions must test an idea about the brain, anything from examining the effects of art on the adolescent brain to exploring alternative treatments for Alzheimer's disease. Students should not complete their experiments, so be creative!

 

I'm sure you can promote some ideas to your grandchildren.

PTSD Awareness Day: The Future of Treatment

Is your doctor even aware of PTSD from stroke or any of these solutions?
http://danablog.org/2014/06/27/ptsd-awareness-future-of-treatment/
Although they do only focus on war survivors and make no mention of  marijuana for PTSD.

‘Smart’ Drugs Alter Developing Brain

Whom is going to research if these cognitive enhancing drugs help a survivors recovery?  This is from the Dana Foundation so I expected a much more complete story.  After my next stroke I will find some way to get them because this:
Maybe Ritalin from this research in 1998.
The article here:
‘Smart’ Drugs Alter Developing Brain 

At Neuroscience 2012, Barbara Sahakian, a psychiatrist at the University of Cambridge, led a rousing discussion regarding the ethics surround the use of so-called "smart" drugs, or drugs that improve attention, memory, wakefulness and cognitive capabilities. In her talk, Sahakian highlighted that the number of young students and professionals using such drugs is only growing-and stressed the pros and cons of such use must be discussed in the context of both the individual and society at large. It was one of the most talked about speeches at the conference that year.
Certainly, cognitive enhancement, by any means, remains a controversial issue. But Julian Savulescu, the Uehiro Chair in Practical Ethics at the University of Oxford, says, on the whole, there is a lot of benefit to cognitive enhancement. He says that the ability to enhance memory and learning, even through the use of drugs, offers healthy people not only the ability to improve their academic performance but also their overall well-being and life success. And that, he argues, provides an economic benefit to society at large.
"I think there are a lot of good reasons to take 'smart' drugs. Overwhelmingly, there are a weight of reasons in favor of taking them," he says. "There are only two good objections to it that I see. One is that their use may be potentially exacerbating social injustice. But I think that's easily addressed by making sure people have basic access to them in the same way they have access to basic education. The second objection is one of safety. That they might be risky and we just don't know the long-term effects of their use. And that's a scientific question that needs to be answered."
To date, there has been a serious lack of research concerning the effects of these drugs, many of which are available without a prescription over the Internet, in healthy individuals. A recent review from researchers at the Drexel University College of Medicine suggests the use of cognitive enhancing drugs may have unintended and quite negative consequences, particularly in young brains.
- See more at: http://www.dana.org/News/Details.aspx?id=115099#sthash.7ShljdNO.dpuf

 At Neuroscience 2012, Barbara Sahakian, a psychiatrist at the University of Cambridge, led a rousing discussion regarding the ethics surround the use of so-called "smart" drugs, or drugs that improve attention, memory, wakefulness and cognitive capabilities. In her talk, Sahakian highlighted that the number of young students and professionals using such drugs is only growing-and stressed the pros and cons of such use must be discussed in the context of both the individual and society at large. It was one of the most talked about speeches at the conference that year.

Certainly, cognitive enhancement, by any means, remains a controversial issue. But Julian Savulescu, the Uehiro Chair in Practical Ethics at the University of Oxford, says, on the whole, there is a lot of benefit to cognitive enhancement. He says that the ability to enhance memory and learning, even through the use of drugs, offers healthy people not only the ability to improve their academic performance but also their overall well-being and life success. And that, he argues, provides an economic benefit to society at large.

"I think there are a lot of good reasons to take 'smart' drugs. Overwhelmingly, there are a weight of reasons in favor of taking them," he says. "There are only two good objections to it that I see. One is that their use may be potentially exacerbating social injustice. But I think that's easily addressed by making sure people have basic access to them in the same way they have access to basic education. The second objection is one of safety. That they might be risky and we just don't know the long-term effects of their use. And that's a scientific question that needs to be answered."

To date, there has been a serious lack of research concerning the effects of these drugs, many of which are available without a prescription over the Internet, in healthy individuals. A recent review from researchers at the Drexel University College of Medicine suggests the use of cognitive enhancing drugs may have unintended and quite negative consequences, particularly in young brains.

PTSD Awareness Day: The Future of Treatment

Come on Dana Foundation I expected more of you. No mention of marijuana as a treatment for PTSD.  I'm sure they have hundreds of employees and they can't keep up-to-date on research involving PTSD or at least know how to use Google Scholar.  GAH!!!!!
http://danablog.org/2014/06/27/ptsd-awareness-future-of-treatment/

Uncovering the Mysteries of Myelin

From the Dana Foundation. I still don't know whether we lose myelin as part of our stroke damage or not.  Ask your doctors if myelin repair is needed in our white matter after a stroke. A neurologist  told me that after 2 years you wouldn't get any recovery because the myelin sheath of the connector neurons would have demyelinated by now. He was blowing smoke out his ass because he was trying to use big words to deflect the question I had asked him about, ' How many stroke survivors go insane because their motor control functions have taken over their executive controls?'  It was a damned simple question and yet he had no clue to the answer. After that debacle I pretty much knew there was no point in asking him any further questions, or seeing any stroke doctor ever again.
http://www.dana.org/News/Uncovering_the_Mysteries_of_Myelin/

Treating Post-Traumatic Stress: Public Briefing

Since PTSD can be an aftereffect of stroke I would fully expect every stroke hospital to be sending a person to this, along with the ASA and NSA. You don't really believe that will occur, Do you?

Prevalence of PTSD in Survivors of Stroke and Transient Ischemic Attack: A Meta-Analytic Review 

And look at this, an actual treatment:

Medical Marijuana – A Magic Bullet for Treating PTSD?

 Send those emails to your hospital, Only you can change how stroke is treated. I bet your hospital will prove their failures once again.

The briefing:
http://danablog.org/2014/04/30/treating-post-traumatic-stress-public-briefing/
Through the support of the Dana Foundation, the American Association for the Advancement of Science (AAAS) is hosting a public luncheon briefing on treating post-traumatic stress.
Post-traumatic stress (PTS) or post-traumatic stress disorder can afflict individuals after a trauma or life-threatening event. It affects more than five million adults per year and is a particular concern for the military. Come hear about how PTS affects service members and veterans and how researchers are treating PTS through different styles of therapy:
Friday, May 9, 2014
12:00-1:30 p.m.
2168 Rayburn House Office Building
RSVP: http://events.signup4.com/posttraumaticstress
Featuring:
The Honorable Chaka Fattah, D-PA
General Peter Chiarelli, U.S. Army (Retired), CEO, One Mind
Kathleen Chard, PhD, Professor of Psychiatry and Behavioral Neuroscience, University of Cincinnati
JoAnn Difede, PhD, Professor of Psychology in Psychiatry, Weill Cornell Medical College
Moderator Alan Leshner, PhD, CEO of AAAS
For questions, please contact Sara Spizzirri at 202-326-6789 or by email at sspizzir@aaas.org

Stroke’s Global Burden of Death and Disability Highlights Need for Awareness, Prevention, and Rehabilitative Strategies

A great paper from the Dana Foundation. I'll comment on several sections. Full paper available at link.
http://www.dana.org/media/detail.aspx?id=44906

Few medical conditions, neurological or otherwise, exact a greater public-health toll than stroke, a fact underscored by a new published report on the global burden of stroke. An acute brain injury that may begin insidiously years prior, stroke is now the second leading cause of death and the third most common cause of disability worldwide. Nearly 17 million people in the world will have a first stroke in the next year, and 33 million people are stroke survivors.
In the U.S., stroke is the No. 1 cause of serious long-term disability. Approximately 800,000 strokes occur annually in this country, and about 130,000 people die annually from stroke. The risk of stroke has decreased by roughly 70 percent in the U.S. since incidence was first tracked in the mid-1900’s, a downward trend that has not plateaued, suggesting there is still room for improvement. Stroke risk factors are well known, and experts estimate that 80 percent of strokes could be prevented with better management of hypertension, blood lipids, and glucose.
Getting Aggressive About Prevention
“Most people believe there could be substantial, dramatic stroke reduction if we just really aggressively managed the risk factors we currently know about,” says Walter Koroshetz, M.D., deputy director of the National Institute for Neurological Disorders and Stroke and a member of the Dana Alliance for Brain Initiatives. “In many diseases, you need a major scientific breakthrough to make a difference. That’s not true with stroke.”
Except you could reduce stroke risk by hundreds of percents following these;
Green tea and coffee 20%  - Green tea, coffee may reduce stroke risk by 20 percent

Potassium 21%   Why eat three bananas a day?
 Marijuana buds 50%  A Marijuana Bud A Day Keeps The Stroke Away

 Dietary magnesium 8% Higher magnesium intake associated with reduced ischemic stroke risk

Mediterranean diet 30% - Mediterranean Diet Proven Key In Avoiding Heart Disease And Stroke

lycopene - tomatoes 55%  -Tomatoes Linked to Lower Stroke Risk


Fish 6% - Does Eating Two Fish a Day REALLY Keep the Chance of Stroke Away?

 Chocolate eating 17%Eating small bar of chocolate cuts risks of stroke in men

Walking 43% - Walking wards off stroke for women

Speed walking 50% - Speed Walking Halves Stroke Risk
Dietary fiber 7% -    More Dietary Fiber Might Help Thwart Stroke

Total 307%

Opening the Window for Acute Treatment
Public-health advocates have tried for years to drive home the message that strokes require immediate medical attention, ever since a treatment became available that could help some people with ischemic stroke, which occurs when blood flow to part of the brain is restricted by a clot or narrowed blood vessel. Tissue plasminogen activator, or tPA, is still the only drug approved for treating acute stroke, but its use is severely limited, largely because published guidelines call for it to be administered within three hours of stroke onset for most patients. Some experts have criticized these guidelines and are calling for them to be revised.
With a pathetic 12% efficacy that means that they are lying about 88% of the results 

Public Awareness Still Lacking
The advent of tPA has triggered a system-wide reorganization of stroke urgent care that is still evolving nearly 17 years later. For example, specialized stroke centers have been established where expert care, along with the tools and technologies for swift, accurate diagnosis, is readily available. A tiered system based on minimum requirements, much like the system that designates hospitals as Level 1-4 trauma centers depending on their capabilities, is being put in place for stroke care as well, so that patients can be transported to the most advanced center in their area. While there have been vast improvements, a number of obstacles remain. Primary among them is public awareness, experts say.
“Public knowledge about stroke is still very low,” says Caplan. “This is the more difficult problem, because a lot of people don’t know they’ve had a stroke.”
The real problem here is that there is no easy objective way to diagnose a stroke. Friends have been in ERs for hours because the stroke hadn't established severe enough effects to be obvious. That should be accomplished with the tricorder possibly thru one of these 17 ways. 
Better Rehab Through Brain Science
The Global Burden of Disease report underscores the dichotomy between richer, developed countries like the U.S., where the majority of people who suffer a stroke survive, and poorer, developing countries where people are more likely to die from a stroke. While cutting stroke deaths is a major global-health goal, better recovery and rehabilitation strategies are desperately needed to address the ever-growing population of stroke survivors who struggle to function with varying degrees of disability.
“We have in the U.S. alone 800,000 people who have a stroke each year. So the question becomes, what can be done to return functional recovery to those patients?” says Koroshetz. “That’s where the really interesting science is, because it intersects with the area of neuroplasticity–how the brain learns to function for a particular purpose and how it rewires itself to get lost function back.”
You have this all wrong, you need to stop the neuronal cascade of death resulting in much less death and disability. The silo of rehabilitation is not where the breakthroughs are going to occur because no one knows exactly how to make neuroplasticity repeatable.
Brain Recovery Not Passive
Armed with such investigational tools, neuroscience has already revealed some fundamental principles of recovery in the brain. “The general rule, at least in the cortex, is that somehow the brain recovers function after an initial injury, whether it’s a stroke or some other lesion,” says Koroshetz. “Now people are studying how that happens, and the hope is that we can translate that to therapeutic strategies.”
One key finding already, Koroshetz says, is that recovery from injury is not “passive.” Rather, it requires enhancement by active exposure to sensory stimuli or motor practice. He points to the LEAPS study, which was the first large randomized, controlled clinical trial that investigated recovery of locomotor function in people who had had a stroke. The NIH-funded study compared two fairly intensive therapies: treadmill walking vs. strength and balance training performed at home with a physical therapist. A third group, serving as controls, received “standard of care”–whatever physical therapy or rehab they were getting as part of their regular medical care.
‘Standard of Care’ Substandard?
What the hell is the standard of care for stroke? Does anyone know?