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Wednesday, October 16, 2013

Stem Cell Research : BrainStorm to Initiate Study for Multiple Sclerosis at Hadassah Medical Center

NEW YORK & PETACH TIKVAH, Israel--(BUSINESS WIRE)--October 15, 2013-- 
BrainStorm Cell Therapeutics (OTCQB: BCLI), a leading developer of adult stem cell technologies for neurodegenerative diseases, today announced that it will initiate a pre-clinical study for Multiple Sclerosis (MS) at the Hebrew University Hadassah Medical Center's SPF-grade animal laboratory in Jerusalem. The study was approved by the Institutional Animal Care and Use Committee (IACUC) of the Hebrew University.
Based on promising pre-clinical data published by the Company's Chief Scientist, Prof. Daniel Offen of Tel Aviv University, BrainStorm will conduct further studies using the Experimental Autoimmune Encephalomyelitis (EAE) animal model to evaluate MS as an additional indication for its NurOwn technology. Professor Dimitrios Karussis and Dr. Ibrahim Kassis, who have published extensively on pre-clinical research using the EAE model, will be the Principal Investigators of the study.
Prof. Karussis, a Key Opinion Leader in the field of MS, is Head of the multi-disciplinary MS Clinic and Center at Hadassah, member of the European Steering Committee for Bone Marrow Transplantation in MS, member of the Executive Board and Scientific Committee of the European School of Neuroimmunology (ESNI), and former board member of the European Council and Committee for Treatment and Research in MS. He has been the Principal Investigator of several multi-national clinical trials in MS conducted by global pharmaceutical companies.
About NurOwn(TM)
NurOwn is an autologous, adult stem cell therapy technology that induces bone marrow-derived mesenchymal stem cells (MSC) to secrete high levels of neurotrophic factors for protection of existing motor neurons, promotion of motor neuron growth, and re-establishment of nerve-muscle interaction. More information about NurOwn(TM) can be found at http://brainstorm-cell.com/index.php/science-a-technology/-nurown.
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Tuesday, October 15, 2013

Multiple Sclerosis: Functional change in brain as cause of cognitive disorders

Over the course of the disease, multiple sclerosis is very often combined with a deteriorating memory and attention deficits. Researchers at the University Department of Radiology and Nuclear Medicine at the MedUni Vienna have now demonstrated by means of a meta-analysis of functional image data that increased activations in the involuntary attention system in the brain are responsible for these disorders in MS patients.

MS patients generally often have problems with fading out what is unimportant. Says head of the study Veronika Schöpf: "They are practically in continuous alarm mode." The attention system is too highly activated and also notices – for example when watching the television or when talking to someone – completely unimportant extraneous noises. Because of this, concentrating on what is important is completely impossible or only possible to a limited extent. In addition, MS patients find it difficult to look for one specific thing and also find it. This high activation thus also leads to a poor memory and at the same time adversely affects the ability to take in new things.
In a meta-analysis in the top journal Neuroscience & Biobehavioral Reviews(Impact Factor 9.44) it has now been possible to prove that functional changes in the brain are responsible for these disorders and that these can also be depicted by means of functional imaging.
"In most people the centre for these activities lies in the right half of the brain, in many MS patients however it lies in the left side of the brain, as it does in many epilepsy patients," says the PhD student and primary author Kathrin Kollndorfer. This knowledge could now feed into the development of personalised treatments for people with  in order to counteract these cognitive disorders in good time.
With this, the working group at the MedUni Vienna has also achieved a better generalisability of the research results so far with regard to working memory and attention in patients with multiple sclerosis. "Most studies that have so far dealt with this question by means of functional imaging have mostly examined only very small and heterogeneous samples, which clearly differ with regard to age, gender or duration of illness. We have included in our evaluation everything in studies so far," explains Veronica Schöpf.
Multiple sclerosis is an incurable, chronic inflammatory disease of the central nervous system, which develops slowly at first and in later stages leads to greater and greater physical and mental handicaps. According to figures of the Austrian Multiple Sclerosis Society (ÖMSG) about 12,500 people suffer from this disease.
More information: Kollndorfer, K. et al. Altered likelihood of brain activation in attention and working memory networks in patients with multiple sclerosis: An ALE meta-analysis, Neuroscience & Biobehavioral Reviews.


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Sunday, October 13, 2013

Einstein's brain a wonder of connectedness

Information provided by Nina F., in Florida


Einstein brain connectivity
Theoretical physicist Albert Einstein had a brain that was not only bigger in many regions, but better connected than the brains of most people, a new study has found. (The Magnes Press)

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By Melissa Healy

Albert Einstein had a colossal corpus callosum. And when it comes to this particular piece of neural real estate, it's pretty clear that size matters.
Chances are, that brawny bundle of white matter cleaving the Swiss physicist's brain from front to back is part of what made his mind so phenomenally creative. The corpus callosum carries electrical signals between the brain's right hemisphere and its left. Stretching nearly the full length of the brain from behind the forehead to the nape of the neck, the corpus callosum is the dense network of neural fibers that make brain regions with very different functions work together.
When the corpus callosum works well, the human brain is a marvel of social, spatial and verbal reasoning. When it malfunctions, as it appears to do in autism, fetal alcohol syndrome and certain genetic disorders, as well as after traumatic brain injury, the effect on cognition can be disastrous.

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Oct 13, 2013 - New therapy gives hope to Multiple Sclerosis Patients

New strategy to treat multiple sclerosis shows promise in mice


New strategy to treat multiple sclerosis shows promise in mice
The new study showed the drug benztropine led to the repair of multiple sclerosis-damaged nerve fibers in animal models. Credit: Luke Lairson, The Scripps Research Institute.


Scientists at The Scripps Research Institute (TSRI) have identified a set of compounds that may be used to treat multiple sclerosis (MS) in a new way. 
Unlike existing MS therapies that suppress the immune system, the compounds boost a population of progenitor cells that can in turn repair MS-damaged nerve fibers.


One of the newly identified compounds, a Parkinson's disease drug called benztropine, was highly effective in treating a standard model of MS in mice, both alone and in combination with existing MS therapies.

"We're excited about these results, and are now considering how to design an initial clinical trial," said Luke L. Lairson, an assistant professor of Chemistry at TSRI and senior author of the study, which is reported online in Nature on October 9, 2013.

Lairson cautioned that benztropine is a drug with dose-related adverse side effects, and has yet to be proven effective at a safe dose in human MS patients. "People shouldn't start using it off-label for MS," he said.

A New Approach

An autoimmune disease of the brain and spinal cord, MS currently affects more than half a million people in North America and Europe, and more than two million worldwide. Its precise triggers are unknown, but certain infections and a lack of vitamin D are thought to be risk factors. The disease is much more common among those of Northern European heritage, and occurs about twice as often in women as in men.

In MS, immune cells known as T cells infiltrate the upper spinal cord and brain, causing inflammation and ultimately the loss of an insulating coating called myelin on some nerve fibers. As nerve fibers lose this myelin coating, they lose their ability to transmit signals efficiently, and in time may begin to degenerate. The resulting symptoms, which commonly occur in a stop-start, "relapsing-remitting" pattern, may include limb weakness, numbness and tingling, fatigue, vision problems, slurred speech, memory difficulties and depression, among other problems.

Current therapies, such as interferon beta, aim to suppress the immune attack that de-myelinates nerve fibers. But they are only partially effective and are apt to have significant adverse side effects.


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