Scientists use new programs to map connections of the human brain

We could use this to map good brains and map our brains as they neuroplastically and neurogenesis change as we recover. Talk to your neurologist to see that they are following this.
http://news.yahoo.com/scientists-programs-map-connections-human-brain-230940651.html

The structure of the human brain is perhaps, still, one of science’s greatest mysteries. As discovery paves the way through the human genome (our six billion basepairs of DNA) and human proteome (our vast array of proteins), one of the greatest remaining questions has been, “How do the neurons in our brain connect?” That mapping has been termed the connectome.

Scientists at the Max Planck Institute for Medical Research have utilized two newly developed computer programs to shed some light on the answer. Using both the KNOSSOS (aptly named for the legendary labyrinth) and RESCOP (no known Greek roots) the researchers were able to map roughly 100 neurons for over 70 students.

This is a massive step. Considering that there are over 70 billion neurons in our brain, all with variable connections to one another, even the fastest and powerful computers of today have been unable to generate models. And if there are 6.5 billion people on earth, each with slightly different connections, the calculations becomes endless.

RESCOP is designed to alleviate that second problem, by synthesizing the results from each of the subjects so that a general picture of the connections can be developed. KNOSSOS as its name implies, does the actual mapping of the neuronal connections. Subjects’ neurons are stained with a (safe) heavy metal which allows microscopes to see the connections between dendrites and axons. This three-dimensional picture is then recorded and analyzed, then repeated on a new section of neuron—a cumbersome process still. KNOSSOS is powerful enough that it can create and process the 3D pictures, and connect them to others roughly 50 times faster than previous programs.

There was also a time when mapping the human genome also seemed an endless task. And it has long past.

Patent - Pheromones and the Luteinizing Hormone for Inducing Proliferation of Neural Stem Cells and Neurogenesis

So I wonder where the research behind this patent is located and what it actually says.
http://www.freepatentsonline.com/y2011/0178009.html

United States Patent Application 20110178009

Kind Code:

A1

Abstract:

The present invention provides a method of increasing neural stem cell numbers or neurogenesis by using a pheromone, a luteinizing hormone (LH) and/or a human chorionic gonadotrophin (hCG). The method can be practiced in vivo to obtain more neural stem cells in situ, which can in turn produce more neurons or glial cells to compensate for lost or dysfunctional neural cells. The method can also be practiced in vitro to produce a large number of neural stem cells in culture. The cultured stem cells can be used, for example, for transplantation treatment of patients or animals suffering from or suspected of having neurodegenerative diseases or conditions.

Tobacco smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats

Someday a researcher will put together all this stuff on nicotine into a stroke protocol. I know this says smoke reduces neurogenesis but from 2005 is nicotine promotes recovery.
http://oc1dean.blogspot.com/2010/10/nicotine-and-stroke-rehab.html
and is it just the smoke that causes problems?
http://www.sciencedirect.com/science/article/pii/S0006899311013473

Abstract

Brain disorders and environmental factors can affect neurogenesis and gliogenesis in the hippocampus. These studies investigated the effects of chronic exposure to tobacco smoke on progenitor cell proliferation and the survival and phenotype of new cells in the dentate gyrus of adolescent rats. The rats were exposed to tobacco smoke for 4 hrs per day for 14 days. To investigate cell proliferation, the exogenous marker 5-bromo-2'-deoxyuridine (BrdU, 200 mg/kg, ip) was administered 2 hrs into the 4-hr smoke exposure session on day 14. The rats were sacrificed 2–4 hrs after the administration of BrdU. To investigate cell survival, the same dose of BrdU was administered 24 hrs before the start of the 14-day smoke exposure period. These rats were sacrificed 24 hrs after the last smoke exposure session. Tobacco smoke exposure decreased both the number of dividing progenitor cells (− 19%) and the number of surviving new cells (− 20%), labeled with BrdU in the dentate gyrus. The decrease in cell proliferation was not associated with an increase in apoptotic cell death, as shown by TUNEL analysis. Colocalization studies indicated that exposure to tobacco smoke decreased the number of new immature neurons (BrdU/DCX-positive) and transition neurons (BrdU/DCX/NeuN-positive) and increased the number of new glial cells (BrdU/GFAP-positive). These findings demonstrate that exposure to tobacco smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats. These effects may play a role in the increased risk for depression and cognitive impairment in adolescent smokers.

Highlights

► Tobacco smoke inhibits cell proliferation in the dentate gyrus of adolescent rats ► Tobacco smoke inhibits cell survival in the dentate gyrus of adolescent rats ► Tobacco smoke inhibits neurogenesis in the dentate gyrus of adolescent rats ► Tobacco smoke promotes gliogenesis in the dentate gyrus of adolescent rats

From 2005

Detecting a Possible Stroke Biomarker in Blood Serum

So I wonder if this is useful for ischemic strokes since the blood flow would be blocked, where would you get your blood sample?
http://www.nasw.org/users/mslong/2010/2010_04/Acrolein.htm
The adverse effects of many medical conditions are caused in part by oxidative stress, the damage caused by free radicals and peroxides in the body. Acrolein is one of the chemical products of these undesired reactions.

Consequently, the presence of acrolein in a blood sample is being investigated as a possible indicator of stroke (where rapid diagnosis and treatment is essential) and other medical conditions. Unfortunately, current methods of detecting acrolein involve a very dangerous (explosive) reaction, and/or slow quantification of the final chemical product of the assay.

Tetsuo Nagano (University of Tokyo) and coworkers have reported an improved detection method for acrolein. Rapid concentration measurements, relevant for disease diagnostics, are detectable with their improved protocol.

Detecting acrolein.

A problem with current acrolein assays (wherein the chemical product of the assay emits light) is that fluorescence from blood serum interferes with light emitted from the assay. This means that the chemical product of the assay must be separated from the blood serum (a somewhat slow process).

The scientists' detection molecule, based in part on europium metal, gets around this limitation because it emits light for milliseconds after illumination. This might not seem like a long time, but carbon-based molecules in blood serum only emit fluorescence for nanoseconds after illumination.

By measuring the emitted light as a function of time, one can not only eliminate the interfering fluorescence from blood serum, but also determine the concentration of acrolein in the sample. The assay requires only 30 minutes and 100°C temperatures, a mild (and safe) protocol.

Furthermore, even acrolein concentrations of as little as 1 micromolar were detected via the assay, possibly a bit less sensitive when the procedure is performed in blood serum. The acrolein concentration relevant for disease states is around this value, implying convenient use in a medical diagnostics setting.

Implications.

Acrolein, a molecule that may serve as a useful indicator of stroke, heart disease, cancer, and many other medical conditions, can now be safely and rapidly detected in blood serum. This should accelerate studies aimed at utilizing acrolein in medical diagnostics.

Scientists discover potential stroke treatment that may extend time to prevent brain damage

So lets get phase II and III trials on this, Time is Brain, you know, ask your researcher/neurologist for what they are doing to advance this.
http://www.labspaces.net/112148/Scientists_discover_potential_stroke_treatment_that_may_extend_time_to_prevent_brain_damage
A naturally occurring substance shrank the size of stroke-induced lesions in the brains of experimental mice — even when administered as much as 12 hours after the event, Stanford University School of Medicine researchers have shown. The substance, alpha-B-crystallin, acts as a brake on the immune system, lowering levels of inflammatory molecules whose actions are responsible for substantial brain damage above and beyond that caused by the initial oxygen deprivation of a stroke.

The finding, which will be published online July 25 in Proceedings of the National Academy of Sciences, is of great potential significance. Every year brings nearly 800,000 new stroke patients in North America. "That's one every 40 seconds," said Gary Steinberg, MD, PhD, director of Stanford's Institute for Neuro-Innovation and Translational Neurosciences and one of the study's two senior authors. Steinberg is also the Bernard and Ronni Lacroute-William Randolph Hearst Professor of Neurosurgery and the Neurosciences, and chair of neurosurgery at the medical school.

The largest single cause of severe neurological disability and the third-leading cause of death in the United States, stroke accounts for an estimated $74 billion annually in related costs, including treatment and additional assistance for the three of every four stroke patients whose ability to perform the activities of daily life is impaired. Strokes are caused by a sudden drop in the flow of blood to the brain resulting from a clot or, less often, bleeding. One of every three stroke patients is under the age of 65. In all, there are 5.4 million stroke survivors in the United States and 15 million worldwide.

The only currently approved drug for stroke — tissue plasminogen activator, or tPA — dissolves clots that keep oxygenated blood from reaching brain tissue. To be effective, tPA must be administered within about 4.5 hours after the stroke. But patients' brains must first be scanned to rule out the possibility that the stroke was caused by bleeding, which tPA would exacerbate, rather than by blockage.

Moreover, tPA does nothing to counter the stroke's insidious inflammatory aftershock: a flood of noxious chemicals secreted by angry immune cells that rush in to the affected area, causing significant further damage.

Alpha-B-crystallin appears to act as a sponge, sopping up those bad actors and stopping inflammation from making a bad situation worse.

Alpha-B-crystallin is a major structural protein in the eye's lens. It is also constantly made in the heart. In other tissues, including the brain, its production can be triggered by stressful events, such as oxygen deprivation or excessive heat or cold. Growing evidence suggests that alpha-B-crystallin can help curb inflammatory activity in the brain.

"The brain doesn't roll over and play dead when it's under attack," said Lawrence Steinman, MD, the other senior author of the new study, who is the George A. Zimmermann Professor of Neurology and Neurological Sciences and Pediatrics as well as chair of Stanford's interdepartmental program in immunology.

In an earlier study, published in Nature in 2007, Steinman and his colleagues found that the presence of alpha-B-crystallin could help reduce the severity of brain damage caused by multiple sclerosis, a chronic, debilitating autoimmune disease of the brain. Other studies published this year by his group have shown that alpha-B-crystallin limits the damage caused by blood-supply cutoffs to heart tissue and the retina.

It seemed logical to see if this protein could mitigate the effects of a stroke. "We made a jump from its relevance in inflammatory diseases such as multiple sclerosis," Steinberg said. "To my knowledge, nobody had looked at concentrations of alpha-B-crystallin after a stroke, either in people or in an experimental animal model before."

So, along with first authors Ahmet Arac, MD, a postdoctoral scholar in Steinberg's lab, and Steinman's former graduate student Sarah Brownell, PhD, Steinberg and Steinman turned to a standard animal model: the laboratory mouse. They found that, in mice bioengineered to lack alpha-B-crystallin, experimentally induced stroke lesions were more massive than those induced in otherwise genetically similar mice whose cells were capable of making the protein. The alpha-B-crystallin-deficient mice had worse neurological function after the stroke than did the normal mice.

The researchers also found that supplying synthetic alpha-B-crystallin to the deficient mice reduced brain-lesion sizes after a stroke, even when the substance was administered 12 hours after the stroke was induced. And they saw elevated alpha-B-crystallin levels in blood plasma from both human patients and mice after a stroke. (The human samples were obtained from study co-author Gregory Albers, MD, the Coy Foundation Professor of Neurology and Neurological Sciences and the director of the Stanford Stroke Center).

"In younger patients, the larger the stroke, the higher the concentration of alpha-B-crystallin," said Steinberg. Interestingly, increased alpha-B-crystallin levels were not detected in plasma from patients over the age of 80, whose strokes typically have worse consequences than those affecting younger patients.

Finally, the investigators demonstrated that alpha-B-crystallin-treated mice produce fewer inflammatory immune-signaling molecules and more anti-inflammatory ones than untreated mice.

At the doses given to the mice in this study, alpha-B-crystallin appeared to be nontoxic. "This is a naturally occurring molecule the body is already producing, although maybe just not enough of it," said Steinberg. "We're just supplementing it." If further studies by other labs and in other models confirm and extend the findings, alpha-B-crystallin may be an excellent candidate for clinical trials in stroke, Steinman and Steinberg both said.

"This is the first demonstration of an efficacious brain-protecting agent that targets the inflammatory aspect of stroke in a novel way, and it can be given at quite a delay," said Thomas Carmichael, MD, PhD, professor and vice chair of neurology at the David Geffen School of Medicine at UCLA. Carmichael, a stroke expert, did not participate in the study but is familiar with its methodology and results. "Tissue plasminogen activator has a fairly narrow risk-to-benefit ratio. The longer you wait, the more likely it is to stimulate a hemorrhage


So after your next stroke ask your ER doctor what treatments they are giving you to stop the cascade of cellular damage.

Inhibition of hippocampal neurogenesis by sleep deprivation is independent of circadian disruption and melatonin suppression

I know that for 4 years after my event I was not sleeping well, sleep apnea - still unresolved, no dreaming - resolved by moving my statin and anti-depressant pills to the morning from the evening. Of course I should not have done this without talking to my doctor but hell I know more that he does how various pills affect me.
http://www.sciencedirect.com/science/article/pii/S0306452211008426
I'm still sleep-deprived but it is better.

Abstract

Procedures that restrict or fragment sleep can inhibit neurogenesis in the hippocampus of adult rodents, although the underlying mechanism is unknown. We showed that rapid-eye-movement sleep deprivation (RSD) by the platform-over-water method inhibits hippocampal cell proliferation in adrenalectomized rats with low-dose corticosterone clamp. This procedure also greatly disrupts daily behavioral rhythms. Given recent evidence for circadian clock regulation of cell proliferation, we asked whether disruption of circadian rhythms might play a role in the anti-neurogenic effects of sleep loss. Male Sprague–Dawley rats were subjected to a 4-day RSD procedure or were exposed to constant bright light (LL) for 4 days or 10 weeks, a non-invasive procedure for eliminating circadian rhythms of behavior and physiology in this species. Proliferating cells in the granule cell layer of the dentate gyrus were identified by immunolabeling for the thymidine analogue 5-bromo-2-deoxyuridine. Consistent with our previous results, the RSD procedure suppressed cell proliferation by 50%. By contrast, although LL attenuated or eliminated daily rhythms of activity and sleep–wake without affecting daily amounts of REM sleep, cell proliferation was not affected. Melatonin, a nocturnally secreted neurohormone that is inhibited by light, has been shown to promote survival of new neurons. We found that 3-weeks of LL eliminated daily rhythms and decreased plasma melatonin by 88% but did not significantly affect either total cell survival or survival of new neurons (doublecortin+). Finally, we measured cell proliferation rates at the beginning and near the end of the daily light period in rats entrained to a 12:12 light/lark (LD) cycle, but did not detect a daily rhythm. These results indicate that the antineurogenic effect of RSD is not secondary to disruption of circadian rhythms, and provide no evidence that hippocampal cell proliferation and survival are regulated by the circadian system or by nocturnal secretion of pineal melatonin.

Highlights

Constant light suppresses daily sleep rhythms and plasma melatonin in rats. Four days of REM-sleep deprivation decreases hippocampal cell proliferation by 50%. Constant light for 4 days or 10 weeks does not affect hippocampal cell proliferation. Constant light for 3 weeks does not affect hippocampal cell survival. Proliferation does not vary between the beginning and end of the daily sleep phase.

Key words: neurogenesis; sleep deprivation; hippocampus; melatonin; circadian rhythms; constant light

Abbreviations: BrdU, 5-bromo-2′-deoxyuridine; CORT, corticosterone; CV, coefficients of variation; DAB, diaminobenzidine tetrahydrochloride; DCX, doublecortin; EEG, electroencephalogram; GCL, granule cell layer; LD, light/lark; LL, constant bright light; NREM, none-rapid-eye-movement; PB, phosphate buffer; PBS, phosphate buffered saline; RSD, rapid-eye-movement sleep deprivation; SD, sleep deprivation; SGZ, subgranular zone; TBS, Tris-buffered saline; ZT, zeitgeber time

Reduction in paracrine Wnt3 factors during aging causes impaired adult neurogenesis

I like the ability that they can reduce the decline in the ability to produce neural stem cells.
http://www.fasebj.org/content/early/2011/07/07/fj.11-184697.abstract

Abstract

The mammalian brain contains neural stem cells (NSCs) that enable continued neurogenesis throughout adulthood. However, NSC function and/or numbers decline with increasing age. Adult hippocampal neurogenesis is unique in that astrocytes secreting Wnt3 promote NSC differentiation in a paracrine manner. Here, we show that both the levels of Wnt3 protein and the number of Wnt3-secreting astrocytes influence the impairment of adult neurogenesis during aging. The age-associated reduction in Wnt3 levels affects the regulation of target genes, such as NeuroD1 and retrotransposon L1, as well as the expression of Dcx, which is located adjacent to the L1 loci. Interestingly, the decline in the extrinsic Wnt3 levels and in the intracellular expression of the target genes with aging was reversible. Exercise was found to significantly increase de novo expression of Wnt3 and thereby rescue impaired neurogenesis in aged animals. Furthermore, the chromatin state of NeuroD1, L1, and the L1 loci near Dcx changed relative to Wnt3 levels in an age- or stimulus-associated manner. These results suggest that the regulation of paracrine factors plays a critical role in hippocampal aging and neurogenesis.—Okamoto, M., Inoue, K., Iwamura, H., Terashima, K., Soya, H., Asashima, M., Kuwabara, T. Reduction in paracrine Wnt3 factors during aging causes impaired adult neurogenesis.

Researchers at Brigham and Women's Hospital (BWH) have developed a platform technology for monitoring single-cell interactions in real-time

Tell your researchers that this functionality should be able to map neurons as they try to connect to each other. Watching it in real time would be useful in telling what some of the neuroplasticity and neurogenesis therapies are doing. And once we know that we should be able to come up with specific therapies that work. Heck, we should be able to do this in the next 30 years.
http://nextbigfuture.com/2011/07/researchers-at-brigham-and-womens.html
The ability to explore cell signalling and cell-to-cell communication is essential for understanding cell biology and developing effective therapeutics. However, it is not yet possible to monitor the interaction of cells with their environments in real time. Here, we show that a fluorescent sensor attached to a cell membrane can detect signalling molecules in the cellular environment. The sensor is an aptamer (a short length of single-stranded DNA) that binds to platelet-derived growth factor (PDGF) and contains a pair of fluorescent dyes. When bound to PDGF, the aptamer changes conformation and the dyes come closer to each other, producing a signal. The sensor, which is covalently attached to the membranes of mesenchymal stem cells, can quantitatively detect with high spatial and temporal resolution PDGF that is added in cell culture medium or secreted by neighbouring cells. The engineered stem cells retain their ability to find their way to the bone marrow and can be monitored in vivo at the single-cell level using intravital microscopy.

13 more pages of detail here:
http://www.nature.com/nnano/journal/vaop/ncurrent/extref/nnano.2011.101-s1.pdf
Someone has to push this kind of stuff so contact your researcher and your stroke association and ask them what they are going to do with this information.

testing bicycle riding as stroke rehabilitation

When I came back from Winnipeg I stopped at a friends cabin. There was a bicycle leaning against a car in the paved parking lot. I stared at it and decided it was time to see if I could still ride. I pried my left hand onto the handlebar. I tried about 6 times standing on my left leg to swing my right leg over the seat. Finally just put my right hand against the car. Luckily the left pedal was at the bottom of the arc., so I didn't have to counteract the spasticity to get it situated. I successfully did three loops around the parking lot. So now I have to get my bike out of the basement, pump up the two flat tires, lower the bike seat and add toe clips. Maybe I can finally have a sport that I can have the wind blowing through my sparse hairs again. Don't worry I'll be wearing a helmet.

Read my post on my epic failure before you even think about doing this.
http://oc1dean.blogspot.com/2011/08/epic-failure-at-bike-stroke-therapy.html

Billionaires and multi-millionaires wanted to sponsor stroke research prizes

Because of the pathetic slowness of stroke research findings I think we need a philanthropist to sponsor a prize for the next breakthrough in hyperacute, acute and chronic rehabilitation. The existing stroke associations have failed in helping survivors. A new foundation would need to be set up, run by driven survivors, it would only take 10-15 survivors. This could even help the philanthropist themselves when they have a stroke.

defeatist attitude about stroke from 2001

It seems that this article didn't reach any of the thousands of survivors via their doctors that populate the various stroke forums out there. This just proves how pathetically information is distributed to stroke medical staff and from there to survivors, and in 10 years it hasn't gotten any better.
http://long-term-care.advanceweb.com/Article/Breakthroughs-in-Stroke-Rehabilitation-2.aspx

Until now, "there's been a certain defeatist attitude about stroke," stated Joel Stein, PhD, director of the Stroke Rehabilitation Program at Spaulding Rehabilitation Hospital, in Boston, MA, and an assistant professor at Harvard Medical School. "It's been, I'm sorry. There's nothing we can do about it.' That's changing because people aren't accepting that as the end of the line."

Researchers connect neurons to computers to decipher the enigmatic code of neuronal circuits

Besides learning more about how the brain works they refer to a brain in a petri dish which I described here - http://oc1dean.blogspot.com/2011/05/stem-cell-technology-enables-new.html
I like the 40 neurons to create a network, I need small numbers to make up for the lost ones I have.
And the article link itself: http://medicalxpress.com/news/2011-07-neurons-decipher-enigmatic-code-neuronal.html
Doctoral student Shein and his supervisors, Prof. Yael Hanein of the School of Electrical Engineering and Prof. Eshel Ben-Jacob of the School of Physics and Astronomy, want to understand the brain's logic. They have developed a new kind of a lab-on-a-chip platform that may help neuroscientists understand one of the deepest mysteries of our brain –– how neuronal networks communicate and work together. The chip was recently described in an issue of the journal PLoS ONE.

Within it, Shein has applied advanced mathematical and engineering techniques to connect neurons with electronics and understand how neuronal networks communicate. Hoping to answer ultimate questions about how our neuronal circuits work, the researchers believe their tool can be also used to test new drugs. It might also advance artificial intelligence and aid scientists in rewiring artificial limbs to our brain.

Shedding light on a black box

There are relatively simple neural "firing" patterns that can be measured with sensory organs like the ears or eyes, but researchers know little about deep thought processes. Could the brain's electrical signals reveal the basis of thought itself?

"When we look at the neuronal networks operating in the ears or eyes, we have some idea about the coding schemes they utilize," explains Shein. A researcher can apply a stimulus such as a bright light, for example, and then monitor responses in the eye's neurons. But for more complex processes, like "thinking" or operating different sensory inputs and outputs together, "we are basically looking into a black box," he says.

The brain is composed of a daunting number of circuits interconnected with other countless circuits, so understanding of how they function has been close to impossible. But using engineered brain tissue in a Petri dish, Shein's device allows researchers to see what's happening to well-defined neural circuits under different conditions. The result is an active circuitry of neurons on a man-made chip. With it they can look for patterns in bigger networks of neurons, to see if there are any basic elements for information coding.

Investigating the activity of single neurons is not enough to understand how a network functions. With nanotechnological systems and tools, now researchers can explore activity patterns of many neurons simultaneously. In particular, they can investigate how several groups of neurons communicate with each other, says Shein.

The hierarchy of the brain

With these network engineering techniques, the scientists cultured different sized networks of neuronal clusters. Once they looked at these groups, they found rich and surprising behaviors which could not be predicted from what scientists know about single neurons.

The researchers were also able to measure patterns from nerve activity, at nodes where a number of nerves converged into networks. What they detected appears to show that neural networks have a hierarchical structure — large networks are composed of smaller sub-networks. This observation, and a unique setup using electrodes and living nerves, allowed them to create hierarchical networks in a dish.

The brain's circuits work like codes. They can see the patterns in the networks and simplify them, or control connectivity between cells to see how the neuronal network responds to various chemicals and conditions, the scientists report. One theory, proposed by Prof. Ben-Jacob, is that the human brain stores memories like a holograph of an image: small neural networks contain information about the whole brain, but only at a very low resolution.

So far the researchers are able to reveal that clusters of as few as 40 cells can serve as a minimal but sufficient functional network. This cluster is capable of sustaining neural network activity and communicating with other clusters. What this means exactly will be the next question.

Could adult hippocampal neurogenesis be relevant for human behavior?

One of your researchers should follow this up to see if this is generating enough new neurons to replace all the lost ones. I have 171 million to replace. I don't want to wait for 20 years before this is proven or not.

http://www.ncbi.nlm.nih.gov/pubmed/21736900
Abstract

Although the function of adult neurogenesis is still unclear, tools for directly studying the behavioral role of new hippocampal neurons now exist in rodents. Since similar studies are impossible to do in humans, it is important to assess whether the role of new neurons in rodents is likely to be similar to that in humans. One feature of adult neurogenesis that varies tremendously across species is the number of neurons that are generated, so a key question is whether there are enough neurons generated in humans to impact function. In this review we examine neuroanatomy and circuit function in the hippocampus to ask how many granule neurons are needed to impact hippocampal function and then discuss what is known about numbers of new neurons produced in adult rats and humans. We conclude that relatively small numbers of neurons could affect hippocampal circuits and that the magnitude of adult neurogenesis in adult rats and humans is probably larger than generally believed.

Exercise Supports Brain Repair For Stroke Victims

This sounds like they are just following the ideas in Spark by John Ratey about maximum exercise causing neurogenesis.
http://www.asianscientist.com/health-medicine/exercise-supports-brain-repair-stroke-victims/
Exercising as little as once a week might improve both memory and the ability to process information quickly in stroke victims, finds a study conducted at the University of South Australia.

The study investigating the effect of regular aerobic exercise on thinking and memory skills in people following a stroke, was recently completed by Dr. Michelle McDonnell, from the Sansom Institute for Health Research.

“We were testing the notion that exercise is not only good for the body but also the brain and the results have been very promising,” she says.

“We studied the ability to do things like remembering words or adding up numbers in people who had suffered a stroke and were taking part in regular exercise. Over the five month period of the study we have found solid evidence of improvements in memory and information processing for those participants engaged in regular exercise.”

Stroke is the leading cause of morbidity in Australia, with more than 300,000 Australians living with this devastating type of brain damage. On top of problems with walking and talking, more than two-thirds of stroke sufferers also experience problems with thinking and memory skills.

Dr. McDonnell says that exercise may increase blood circulation to the brain and alter connections between nerves that are interrupted by a stroke.

“We believe exercise might actually encourage re-wiring of the brain so we’re keen to continue our research with people who have suffered a stroke,” she says.

Dr. McDonnell is leading the study to investigate the effect of exercise on the brain and is looking for adults aged between forty-five and eighty who have suffered a stroke to take part in further research.

Role of mesenchymal stem cells in neurogenesis and nervous system repair

More stuff to research, hey they could be the start of magical stroke recovery.
http://www.sciencedirect.com/science/article/pii/S019701861100204X

Abstract

Bone marrow-derived mesenchymal stem cells (MSCs) are attractive candidates for use in regenerative medicine since they are easily accessible and can be readily expanded in vivo, and possess unique immunogenic properties. Moreover, these multipotent cells display intriguing environmental adaptability and secretory capacity. The ability of MSCs to migrate and engraft in a range of tissues has received significant attention. Evidence indicating that MSC transplantation results in functional improvement in animal models of neurological disorders has highlighted exciting potential for their use in neurological cell-based therapies. The manner in which MSCs elicit positive effects in the damaged nervous system remains unclear. Cell fusion and/or ‘transdifferentiation’ phenomena, by which MSCs have been proposed to adopt neural cell phenotypes, occur at very low frequency and are unlikely to fully account for observed neurological improvement. Alternatively, MSC-mediated neural recovery may result from the release of soluble molecules, with MSC-derived growth factors and extracellular matrix components influencing the activity of endogenous neural cells. This review discusses the potential of MSCs as candidates for use in therapies to treat neurological disorders and the molecular and cellular mechanisms by which they are understood to act.

Highlights

• MSCs are known to form mesenchymal derivatives but may also have a neurogenic function. • Evidence shows MSCs engrafted into the nervous system survive, migrate and positively effect recovery from neural deficits. • Three mechanisms by which MSCs may restore neural function have been proposed, with MSC-derived paracrine factors most likely to induce endogenous repair. • MSCs are potential candidates for use in therapies to treat neurological disorders.

Where do I go from here? Rehabilitation of a stroke survivor

From an India doctor, 292 pages that I haven't completely read. Rather distressing that it takes that many pages to tell us how little they really know about how to recover from a stroke.
http://www.nimhindia.org/neurorehabilitation.pdf#page=109

Perlecan domain V is neuroprotective and proangiogenic following ischemic stroke in rodents

Hey another hyperacute possibility, tell your researcher to start studying it.
http://www.jci.org/articles/view/46358?key=975ca4af1b533bd95895

Stroke is the leading cause of long-term disability and the third leading cause of death in the United States. While most research thus far has focused on acute stroke treatment and neuroprotection, the exploitation of endogenous brain self-repair mechanisms may also yield therapeutic strategies. Here, we describe a distinct type of stroke treatment, the naturally occurring extracellular matrix fragment of perlecan, domain V, which we found had neuroprotective properties and enhanced post-stroke angiogenesis, a key component of brain repair, in rodent models of stroke. In both rat and mouse models, Western blot analysis revealed elevated levels of perlecan domain V. When systemically administered 24 hours after stroke, domain V was well tolerated, reached infarct and peri-infarct brain vasculature, and restored stroke-affected motor function to baseline pre-stroke levels in these multiple stroke models in both mice and rats. Post-stroke domain V administration increased VEGF levels via a mechanism involving brain endothelial cell α5β1 integrin, and the subsequent neuroprotective and angiogenic actions of domain V were in turn mediated via VEGFR. These results suggest that perlecan domain V represents a promising approach for stroke treatment.

Scientists Discover How Best to Excite Brain Cells

If they could figure this out maybe they could figure out therapies that would help.
http://www.newswise.com/articles/scientists-discover-how-best-to-excite-brain-cells
ANN ARBOR, Mich.---Oh, the challenges of being a neuron, responsible for essential things like muscle contraction, gland secretion and sensitivity to touch, sound and light, yet constantly bombarded with signals from here, there and everywhere.
How on earth are busy nerve cells supposed to pick out and respond to relevant signals amidst all that information overload?
Somehow neurons do manage to accomplish the daunting task, and they do it with more finesse than anyone ever realized, new research by University of Michigan mathematician Daniel Forger and coauthors demonstrates. Their findings---which not only add to basic knowledge about how neurons work, but also suggest ways of better designing the brain implants used to treat diseases such as Parkinson's disease---were published July 7 in the online, open-access journal PLoS Computational Biology.
Forger and coauthors David Paydarfar at the University of Massachusetts Medical School and John Clay at the National Institute of Neurological Disorders and Stroke studied neuronal excitation using mathematical models and experiments with that most famous of neuroscience study subjects, the squid giant axon---a long arm of a nerve cell that controls part of the water jet propulsion system in squid.
Among the key findings: Neurons are quite adept at their job. "They can pick out a signal from hundreds of other, similar signals," said Forger, an associate professor of mathematics in the College of Literature, Science and the Arts and a research assistant professor of computational medicine and bioinformatics at the U-M Medical School.
Neurons discriminate among signals based on the signals' "shape," (how a signal changes over time), and Forger and coauthors found that, contrary to prior belief, a neuron's preference depends on context. Neurons are often compared to transistors on a computer, which search for and respond to one specific pattern, but it turns out that neurons are more complex than that. They can search for more than one signal at the same time, and their choice of signal depends on what else is competing for their attention.
"We found that a neuron can prefer one signal---call it signal A---when compared with a certain group of signals, and a different signal---call it signal B---when compared with another group of signals," Forger said. This is true even when signal A and signal B aren't at all alike.
The findings could contribute in two main ways to the design and use of brain implants in treating neurological disorders.
"First, our results determine the optimal signals to stimulate a neuron," Forger said. "These signals are much more effective and require less battery power than what is currently used." Such efficiency would translate into less frequent surgery to replace batteries in patients with brain implants.
"Second, we found that the optimal stimulus is context-dependent," he said, "so the best signal will differ, depending on the part of the brain where the implant is placed."
The research was funded by the Air Force Office of Scientific Research and the National Institutes of Health
More information:
Daniel Forger---http://www.math.lsa.umich.edu/people/facultyDetail.php?uniqname=forger

Million-core ARM machine aims to simulate brain

Anything like this can only help stroke researchers understand what is going on in the brain, so when something goes wrong they can at least explain it.
http://www.zdnet.co.uk/news/emerging-tech/2011/07/08/million-core-arm-machine-aims-to-simulate-brain-40093356/
Manchester academics aim to use a million ARM processing cores to simulate the neuron network of the human brain and investigate new models of computing.

Manchester academics aim to use a million ARM processing cores to simulate the neuron network of the human brain. Photo credit: Manchester University

The bedrock of the SpiNNaker computing architecture is formed of 50,000 or so ARM 968-series multi-core, low-powered embedded processors, which passed their functionality tests "with flying colours", Manchester University said on Thursday.
"The most fundamental deliverable from this project is a generic computing platform that can be used to test hypotheses that are emerging from psychology and neuroscience about how information flows through the brain," Steve Furber, Manchester University's ICL processor of computer engineering and leader of the project, told ZDNet UK.

Read this

Scientists create brain-like computing component

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Furber also hopes that by closely approximating the structure of the brain, the researchers will investigate more distributed and resilient computer systems. "At the moment, the way we build computers is not able to cope with component failure, but the brain does. We don't know how to design things with that resilience," he said. Furber helped design the Advanced RISC Machine (ARM) 32-bit processor while at Acorn in the 1980s, before ARM was spun-off as a separate company.
Eventually, the chips will form a supercomputer built out of a SpiNNaker — spiking neural network — architecture, in which each chip sits within a two-dimensional mesh network connected to six or so others. Each processor has 18 cores and around 100 million transistors, and is attached to 128 megabytes of DRAM, which has a billion transistors. A single Intel Sandy Bridge-based Core i5-750 processor has 774 million transistors. Intel's server and supercomputing processor, the Xeon Nehalem-EX, has around 2.3 billion transistors.
Once built, the computer will be accessible to other academics and researchers via the internet, possibly through the UK's research network Janet, Furber said.

Testing the system

At the moment, the researchers are testing the system with a card containing four ARM processors, giving 72 cores in total; they then hope to expand this and build a card-based system of 1,000 cores. By the end of the year the researchers hope to assemble a SpiNNaker architecture with 10,000 cores and anticipate achieving a million cores by the end of 2012, Furber said.

The way we build computers is not able to cope with component failure, but the brain does. We don't know how to design things with that resilience.

– Steve Furber

Each chip will mimic the spikes that neurons produce when they pass information between one another. "A spike is basically a fixed-energy impulse, so what you need to communicate is which neuron spiked and when it spiked," Furber said. "When a processor that's modelling a neuron computes that that neuron should spike it drops a 32-bit identifier into a 40-bit packet that goes into the local fabric", at which point an on-chip router steers the packet to where it must go, Furber explained.
Because any processor can be turned into any particular neuron, the entire supercomputer can be modified, so while it can only simulate around one percent of the human brain, it can be modified to simulate different parts for other experiments.
"Imagine our machine as a giant FPGA [field-programmable gate array] where the individual components are not logic gates, but are neurons," Furber explained. "Configuring a big machine is a significant software challenge, which we are working our way up towards."
To that end, the researchers have ported a variant of high-level programming language Python to work on the SpiNNaker architecture.

Toward a wholly digital brain?

A complete simulation of the entire brain is still far off. In June, a French academic predicted that a digital brain would be possible by around 2023.

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Furber estimates the SpiNNaker architecture has a rough scale limit of around four billion neurons, compared to the 100 billion in the human brain, but with research this barrier could be broken.
"The real limit from our point of view is the kind of research budget that we can expect to get as a university research group," Furber said. Additionally, he feels that the community SpiNNaker is targeted at, such as neuroscientists and psychologists, would not "sensibly be able to exploit" a whole brain model because understanding of this part of the brain is patchy.
"In the cortex there are tens of different types of neurons and they interconnect with each other in specific ways and information about the ways they connect and the strength is almost nonexistent," he said.
The project has been funded by a £5m grant from the EPSRC, of which Manchester received £2.5m, with the rest going to the universities of Southampton, Cambridge and Sheffield. Additionally, Manchester has received some further small grants for the project, and an earlier grant of £750,000.
The researchers chose to use ARM because of Furber's familiarity with the architecture and the relatively low power consumption — one watt per processor — of the ARM 968 chips.

The American Heart Association Stroke Outcome Classification: Executive Summary

What took them so long to figure out that the stroke world needs a standardized, comprehensive classification system to document the resultant impairment, They still do not understand that the first part needed is a damage diagnosis, doing it the impairment way is using secondary impacts rather than primary impacts. A start, but survivors would give them an earful on where to get something useful.
http://circ.ahajournals.org/content/97/24/2474.full
Stroke remains one of the major public health problems in the United States today, with approximately 500 000 new or recurrent cases occurring each year.¹ About 4 000 000 persons alive today have survived a stroke and have some neurological deficits. Although the magnitude of healthcare resources used to treat and rehabilitate stroke survivors is considerable, to date a standardized, comprehensive classification system to document the resultant impairments and disability has not been developed.
Successful management of any disabling disease, including stroke, should benefit from the use of a classification system to judge the impact of treatment, particularly emerging therapies. Participants in the Methodologic Issues in Stroke Outcome Symposium² determined that the complex nature of stroke recovery demands clarification of its natural history and classification of the variable patterns of functional recovery. For stroke survivors to receive the best care, a comprehensive stroke outcome classification system is needed to direct appropriate therapeutic interventions.³ Building on the work and recommendations of the Stroke Outcome Symposium, the American Heart Association Classification of Stroke Outcome Task Force has worked to develop a valid and reliable global classification system that accurately summarizes the neurological impairments, disabilities, and handicaps that occur after stroke.
The development of a stroke outcome classification system is predicated on the belief that neurological deficits often lead to permanent impairments, disabilities, and compromised quality of life.^{4 5 6} Although a person's ability to complete daily functional tasks is thought to be largely dependent on and often limited by the type and degree of impairment, additional factors are often relevant in the ultimate determination of functional outcome.^{7 8 9} Thus, a classification of stroke outcome should include the broad range of disabilities and impairments as well as the relationship of disability and impairment to independent function.
It is important to underscore that impairment alone does not define level of disability. In a study of stroke survivors¹⁰ it was determined that although a disability is most directly influenced by impairments, current stroke scales that measure impairments only partially explained the level of disability, handicap, or quality of life for those surviving at least 6 months. Some persons adapt well to many and/or severe impairments caused by stroke. Others with only minimal neurological impairments can be severely disabled. Many factors determine function, including the influence of poststroke rehabilitation training and the physical and social environments.
Approach to Stroke Assessment
The schema for the stroke outcome classification score presented here is conceptually similar to the New York Heart Association functional and therapeutic classification of patients with diseases of the heart framework.¹¹ However, unlike heart disease, in which the primary limitation is impairment of physical activity due to chest pain, shortness of breath, and fatigue, stroke impairs many critical neurological functions, resulting in a greater number and broader range of physical and social disabilities. The AHA Stroke Outcome Classification (AHA.SOC) score (Figure) classifies the severity and extent of neurological impairments that are the basis for disability. The classification also identifies the level of independence of stroke patients according to basic and more complex activities of daily living both at home and in the community. The classification score is meant to describe the limitations resulting from the current stroke. It is not an evaluation of disabilities caused by other neurological events. Furthermore, it is a summary score. The task force recommends that clinicians support their rating decisions with standardized assessment instruments whenever possible.
Stroke remains one of the major public health problems in the United States today, with approximately 500 000 new or recurrent cases occurring each year.¹ About 4 000 000 persons alive today have survived a stroke and have some neurological deficits. Although the magnitude of healthcare resources used to treat and rehabilitate stroke survivors is considerable, to date a standardized, comprehensive classification system to document the resultant impairments and disability has not been developed.
Successful management of any disabling disease, including stroke, should benefit from the use of a classification system to judge the impact of treatment, particularly emerging therapies. Participants in the Methodologic Issues in Stroke Outcome Symposium² determined that the complex nature of stroke recovery demands clarification of its natural history and classification of the variable patterns of functional recovery. For stroke survivors to receive the best care, a comprehensive stroke outcome classification system is needed to direct appropriate therapeutic interventions.³ Building on the work and recommendations of the Stroke Outcome Symposium, the American Heart Association Classification of Stroke Outcome Task Force has worked to develop a valid and reliable global classification system that accurately summarizes the neurological impairments, disabilities, and handicaps that occur after stroke.
The development of a stroke outcome classification system is predicated on the belief that neurological deficits often lead to permanent impairments, disabilities, and compromised quality of life.^{4 5 6} Although a person's ability to complete daily functional tasks is thought to be largely dependent on and often limited by the type and degree of impairment, additional factors are often relevant in the ultimate determination of functional outcome.^{7 8 9} Thus, a classification of stroke outcome should include the broad range of disabilities and impairments as well as the relationship of disability and impairment to independent function.
It is important to underscore that impairment alone does not define level of disability. In a study of stroke survivors¹⁰ it was determined that although a disability is most directly influenced by impairments, current stroke scales that measure impairments only partially explained the level of disability, handicap, or quality of life for those surviving at least 6 months. Some persons adapt well to many and/or severe impairments caused by stroke. Others with only minimal neurological impairments can be severely disabled. Many factors determine function, including the influence of poststroke rehabilitation training and the physical and social environments.
Approach to Stroke Assessment
The schema for the stroke outcome classification score presented here is conceptually similar to the New York Heart Association functional and therapeutic classification of patients with diseases of the heart framework.¹¹ However, unlike heart disease, in which the primary limitation is impairment of physical activity due to chest pain, shortness of breath, and fatigue, stroke impairs many critical neurological functions, resulting in a greater number and broader range of physical and social disabilities. The AHA Stroke Outcome Classification (AHA.SOC) score (Figure) classifies the severity and extent of neurological impairments that are the basis for disability. The classification also identifies the level of independence of stroke patients according to basic and more complex activities of daily living both at home and in the community. The classification score is meant to describe the limitations resulting from the current stroke. It is not an evaluation of disabilities caused by other neurological events. Furthermore, it is a summary score. The task force recommends that clinicians support their rating decisions with standardized assessment instruments whenever possible.