Neural Cell News Volume 4.37 | Sep 22 2010

TOP STORY

Scientists Identify a New Target for Alzheimer’s Disease 
Neurological researchers have found a new therapeutic target that can potentially lead to a new way to prevent the progression of Alzheimer’s disease. The target called neutral sphingomyelinase (N-SMase) is a protein that when activated, can cause a chain of reactions in the cell leading to neuronal death and memory loss. [Press release from Rush University Medical Center discussing online prepublication in the Journal of Neuroscience]

 

SCIENCE NEWS

Compound Boosts Marijuana-Like Chemical in the Body to Relieve Pain at Injury Site
The researchers discovered that the compound, URB937, did not enter the central nervous system but simply boosted the levels of anandamide in peripheral tissues. [Press release from University of California, Irvine discussing online prepublication in Nature Neuroscience]

For Neurons to Work as a Team, it Helps to Have a Beat
When it comes to conducting complex tasks, it turns out that the brain needs rhythm, according to researchers. [Press release from the University of California, Berkeley discussing online prepublication in the Proceedings of the National Academy of Sciences USA]

Alzheimer’s Drug Boosts Perceptual Learning in Healthy Adults
Research on a drug commonly prescribed to Alzheimer’s disease patients is helping neuroscientists better understand perceptual learning in healthy adults. [Press release from the University of California, Berkeley discussing online prepublication in Current Biology]

Increased Brain Protein Levels Linked to Alzheimer’s Disease
Elevated levels of a growth protein in the brains of Alzheimer’s disease patients is linked to impaired neurogenesis, say researchers. [Press release from the University of California, San Diego discussing online prepublication in The Journal of Neuroscience]

Nature Study: Discovery of Key Pathway Interaction may Lead to Therapies that Aid Brain Growth and Repair in Children and Adults
Researchers have discovered that the two major types of signaling pathways activated during brain cell development-the epidermal growth factor receptor pathway and the Notch pathway-operate together to determine how many and which types of brain cells are created during growth and repair in developing and adult brains. [Press release from the Children’s National Medical Center discussing online prepublication in Nature]

Preserving Nerve Cells in Motor Neuron Disease
A team of researchers has identified a way to prevent symptom onset, weight loss, and paralysis and extend survival in a mouse model of amyotrophic lateral sclerosis (ALS), providing a new avenue of research for the development of therapeutics for ALS and other motor neuron diseases. [Press release from ScienceDaily discussing online prepublication in the Journal of Clinical Investigation]

Study Links Normal Function of Protein, Not Its Build Up Inside Cells, to Death of Neurons
A study links muscle weakness and other symptoms of a rare neurodegenerative disease to a misstep in functioning of a normal protein, rather than its build-up inside cells. The finding offers insight into the mechanism driving common nervous system disorders like Parkinson’s and Alzheimer’s diseases. [Press release from PRNewswire discussing online prepublication in Neuron]

Acetylation May Contribute to Dementia and Alzheimer’s Disease
A new study uncovers a protein modification that may contribute to the formation of neuron-damaging neurofibrillary tangles in the human brain. The research may lead to new strategies for treatment of neurodegenerative diseases that result from pathological aggregation of tau protein. [Press release from EurekAlert! discussing online prepublication in Neuron]

Getting Off Tract: Polyglutamine Disease Involves Other Regions of Protein
Many genes code for proteins that have a “polyglutamine tract”. Nine inherited neurodegenerative diseases, including Huntington’s disease and spinocerebellar ataxia type 1 (SCA1), are associated with mutations that cause abnormally long polyglutamine tracts. One theory suggests that accumulation of proteins with extra glutamines damages and kills neurons. However, there is evidence that glutamine tract expansion alone is not sufficient to cause disease. [Press release from EurekAlert! discussing online prepublication in Neuron]

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Notch and EGFR Pathway Interaction Regulates Neural Stem Cell Number and Self-Renewal
Here researchers show that functional cell-cell interaction between neural progenitor cells and neural stem cells through EGFR and Notch signalling has a crucial role in maintaining the balance between these cell populations in the subventricular zone. [Nature]

Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels
Expression profiling and RNAi knockdown of candidate genes identified Piezo1 (Fam38A) to be required for mechanically activated currents in a mouse neuroblastoma cell line. [Science]

Blocking the Mitochondrial Apoptotic Pathway Preserves Motor Neuron Viability and Function in a Mouse Model of Amyotrophic Lateral Sclerosis (ALS)
Researchers found that neuronal deletion of Bax and Bak in a mouse model of familial ALS not only halted neuronal loss, but prevented axonal degeneration, symptom onset, weight loss, and paralysis and extended survival. [J Clin Invest]

Anandamide Suppresses Pain Initiation Through a Peripheral Endocannabinoid Mechanism
The results suggest that anandamide-mediated signaling at peripheral CB1 receptors controls the access of pain-related inputs to the CNS. Brain-impenetrant fatty acid amide hydrolase inhibitors, which strengthen this gating mechanism, might offer a new approach to pain therapy. [Nat Neurosci]

Native Functions of the Androgen Receptor Are Essential to Pathogenesis in a Drosophila Model of Spinobulbar Muscular Atrophy
The findings indicate that spinobulbar muscular atrophy pathogenesis is mediated by misappropriation of native protein function, a mechanism that may apply broadly to polyglutamine diseases. [Neuron]

Acetylation of Tau Inhibits Its Degradation and Contributes to Tauopathy
Neurodegenerative tauopathies characterized by hyperphosphorylated tau include frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer’s disease (AD). Reducing tau levels improves cognitive function in mouse models of AD and FTDP-17, but the mechanisms regulating the turnover of pathogenic tau are unknown. Researchers found that tau is acetylated and that tau acetylation prevents degradation of phosphorylated tau (p-tau). [Neuron]

SCA1-like Disease in Mice Expressing Wild-Type Ataxin-1 with a Serine to Aspartic Acid Replacement at Residue 776
Glutamine tract expansion triggers nine neurodegenerative diseases by conferring toxic properties to the mutant protein. In SCA1, phosphorylation of ATXN1 at Ser776 is thought to be key for pathogenesis. Here, researchers show that replacing Ser776 with a phosphomimicking Asp converted ATXN1 with a wild-type glutamine tract into a pathogenic protein. [Neuron]

Cholinergic Enhancement Augments Magnitude and Specificity of Visual Perceptual Learning in Healthy Humans
In this study, researchers increased synaptic levels of acetylcholine in the brains of healthy human subjects with the cholinesterase inhibitor donepezil (trade name: Aricept) and measured the effects of this cholinergic enhancement on visual perceptual learning. [Curr Biol]

Oscillatory Phase Coupling Coordinates Anatomically Dispersed Functional Cell Assemblies
The findings suggest that neuronal oscillations enable selective and dynamic control of distributed functional cell assemblies. [Proc Natl Acad Sci USA]

Increased BMP6 Levels in the Brains of Alzheimer’s Disease Patients and APP Transgenic Mice Are Accompanied by Impaired Neurogenesis
Researchers show here by qRT-PCR analysis that BMP6 mRNA levels were significantly increased in the hippocampus of human patients with Alzheimer’s disease and in APP transgenic mice compared to controls. [J Neurosci]

Fibrillar Amyloid-Beta-Activated Human Astroglia Kill Primary Human Neurons via Neutral Sphingomyelinase: Implications for Alzheimer’s Disease
The present study underlines the importance of neutral sphingomyelinase (N-SMase) in mediating the damaging effect of fibrillar amyloid-beta 1-42 (Abeta1-42) peptide-activated astroglia on neurons. [J Neurosci]

The Growth of Brain Tumors Can be Suppressed by Multiple Transplantation of Mesenchymal Stem Cells Expressing Cytosine Deaminase
Here, researchers showed a potential ex vivo therapy that used mesenchymal stem cells as cellular vehicles to deliver a bacterial suicide gene, cytosine deaminase to brain tumors. [Int J Cancer]
 

Athersys Announces Groundbreaking Data Showing Neuroprotective Effects of MultiStem Therapy for Traumatic Brain Injury
The study demonstrates that intravenous injection of MultiStem(R), Athersys’ multipotent adult progenitor stem cell therapy product, provides neurovascular protection after traumatic brain injury in an established preclinical model of brain injury. [Athersys, Inc. Press Release]

ImmunoCellular Therapeutics Announces Long-Term Disease-Free Survival Data from Phase I Study in Glioblastoma
ImmunoCellular Therapeutics, Ltd., a biotechnology company focused on the development of novel immune-based cancer therapies, announced long-term data from a Phase I clinical trial of ICT-107, the Company’s lead cancer vaccine candidate for the treatment of glioblastoma multiforme (GBM), the most common and aggressive form of brain cancer. [Immunocellular Therapeutics, Ltd. Press Release]

Data Published in Journal of Neuroimmunology Suggest Anti-Inflammatory Role for Lead VBL Therapeutics Compound in CNS Inflammatory Diseases
VBL Therapeutics, a clinical-stage biotechnology company committed to the development of novel treatments for immune-inflammatory diseases and cancer, announced the publication of preclinical data in the Journal of Neuroimmunology finding that its lead development candidate VB-201 significantly delayed the onset and severity of experimental autoimmune encephalomyelitis (EAE) in mice. [VBL Therapeutics, Inc. Press Release]

$40 Million Awarded to Trace Human Brain’s Connections
The National Institutes of Health awarded grants totaling $40 million to map the human brain’s connections in high resolution. Better understanding of such connectivity promises improved diagnosis and treatment of brain disorders. [National Institutes of Health Press Release]

Rexahn Pharmaceuticals Announces Publication of Study on Neuroprotective Effects of Clavulanic Acid
Rexahn Pharmaceuticals, Inc., a clinical stage pharmaceutical company developing and commercializing potential best in class oncology and CNS therapeutics, announced the publication of a research article in Drug Development Research (71:351-357, 2010) on the neuroprotective effects of clavulanic acid, the active pharmaceutical ingredient of Serdaxin®, Rexahn’s lead CNS therapeutic currently in Phase II clinical trials. [Rexahn Pharmaceuticals, Inc. Press Release]

European Medicines Agency and U.S. Food and Drug Administration Extend Confidentiality Arrangements Indefinitely
The European Medicines Agency and the U.S. Food and Drug Administration have extended their confidentiality arrangements related to medicinal products for human and veterinary use, following the positive experience gained since the initial arrangements were signed in September 2003. [Food and Drug Administration, United States]

FDA to Review Medical Products Alongside Medicare
A new process to review medical products at the U.S. Food and Drug Administration in tandem with the nation’s Medicare insurance program could help speed up coverage decisions. [Food and Drug Administration, United States]

NHGRI Funds Development of Third Generation DNA Sequencing Technologies
More than $18 million in grants to spur the development of a third generation of DNA sequencing technologies was announced by the National Human Genome Research Institute (NHGRI). [National Institutes of Health, United States]

Innovative Emerging Molecular Analysis Technologies (SBIR R43/R44) (RFA-CA-10-013) [National Institutes of Health, United States]

National Human Genome Research Institute; Notice of Closed Meeting (FR Doc. 2010-23027) [National Institutes of Health, United States]

National Cancer Institute; Notice of Closed Meeting (FR Doc. 2010-23144) [National Institutes of Health, United States]

Center for Scientific Review; Notice of Closed Meetings (FR Doc. 2010-23143) [National Institutes of Health, United States]
 
Center for Scientific Review; Notice of Closed Meetings (FR Doc. 2010-23275) [National Institutes of Health, United States]

National Institute of Neurological Disorders and Stroke; Notice of Closed Meeting (FR Doc. 2010-23156) [National Institutes of Health, United States]