Medicalnewstoday, Article Date: 04 Nov 2009 - 0:00 PST
Learning to talk also changes the way speech sounds are heard, according to a new study published in Proceedings of the National Academy of Sciences by scientists at Haskins Laboratories, a Yale-affiliated research laboratory. The findings could have a major impact on improving speech disorders. (read more)
Wednesday, November 4, 2009
Frataxin interacts with Isu1 through a conserved tryptophan in its beta-sheet.
Hum Mol Genet. 2009, Nov 2.
Leidgens S, De Smet S, Foury F.
Unité de Biochimie Physiologique, Institut des Sciences de la Vie, Université Catholique de Louvain, Croix du Sud 5-15, 1348 Louvain-la-Neuve, Belgium.
Keywords: Friedreich's ataxia, frataxin, iron-sulfur (Fe/S) clusters, Yfh1, Isu1, beta-sheet platform, Q129A, I130A, W131A(F), R141A, low aconitase activity, Gln-129, Trp-131, Arg-141, aromatic side chain.
Leidgens S, De Smet S, Foury F.
Unité de Biochimie Physiologique, Institut des Sciences de la Vie, Université Catholique de Louvain, Croix du Sud 5-15, 1348 Louvain-la-Neuve, Belgium.
Keywords: Friedreich's ataxia, frataxin, iron-sulfur (Fe/S) clusters, Yfh1, Isu1, beta-sheet platform, Q129A, I130A, W131A(F), R141A, low aconitase activity, Gln-129, Trp-131, Arg-141, aromatic side chain.
Monday, November 2, 2009
Iron Deficiency is the Most Common Deficiency Among People
November 02, 2009
http://www.associatedcontent.com/
Keyword: Dr. Timothy Stemmler, Wayne State University, University of Michigan-Dearborn, iron deficiency, Anemia, Parkinson's, Fredreich's Ataxia, frataxin.
http://www.associatedcontent.com/
Keyword: Dr. Timothy Stemmler, Wayne State University, University of Michigan-Dearborn, iron deficiency, Anemia, Parkinson's, Fredreich's Ataxia, frataxin.
Lundbeck starts clinical phase IIa with Lu AA24493 (cEPO) in Friedreich's ataxia in a study also assessing efficacy via biomarkers
PR-inside.com,
London, November , 02, 2009
Keywords: H. Lundbeck A/S, phase IIa clinical studies, project Lu AA24493, safety and
tolerability, Friedreich's ataxia, carbamoylated form of human erythropoietin (EPO), loss of haematopoietic effects, neuronal damage,
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Pharmacy Europe,
Latest News, Monday 2nd November 2009
Lundbeck starts clinical phase IIa with Lu AA24493 (cEPO)
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Reuters.com
Mon Nov 2, 2009 5:10am EST
Lundbeck says expands stroke drug candidate trials
London, November , 02, 2009
Keywords: H. Lundbeck A/S, phase IIa clinical studies, project Lu AA24493, safety and
tolerability, Friedreich's ataxia, carbamoylated form of human erythropoietin (EPO), loss of haematopoietic effects, neuronal damage,
----------------------------------------------------------
Pharmacy Europe,
Latest News, Monday 2nd November 2009
Lundbeck starts clinical phase IIa with Lu AA24493 (cEPO)
---------------------------------------------------------
Reuters.com
Mon Nov 2, 2009 5:10am EST
Lundbeck says expands stroke drug candidate trials
Saturday, October 31, 2009
Whole-body isometric force/torque measurements for functional assessment in neuro-rehabilitation: platform design, development and verification
OPEN ACCESS
Journal of NeuroEngineering and Rehabilitation 2009, 6:38doi:10.1186/1743-0003-6-38
Published: 30 October 2009
Abstract (provisional)
Background
One of the main scientific and technological challenges of rehabilitation bioengineering is the development of innovative methodologies, based on the use of appropriate technological devices, for an objective assessment of patients undergoing a rehabilitation treatment. Such tools should be as fast and cheap to use as clinical scales, which are currently the daily instruments most widely used in the routine clinical practice.
Methods
A human-centered approach was used in the design and development of a mechanical structure equipped with eight force/torque sensors that record quantitative data during the initiation of a predefined set of Activities of Daily Living (ADL) tasks, in isometric conditions.
Results
Preliminary results validated the appropriateness, acceptability and functionality of the proposed platform, that has become now a tool used for clinical research in three clinical centres.
Conclusions
This paper presented the design and development of an innovative platform for whole-body force and torque measurements on human subjects. The platform has been designed to perform accurate quantitative measurements in isometric conditions with the specific aim to address the needs for functional assessment tests of patients undergoing a rehabilitation treatment as a consequence of a stroke. The versatility of the system also enlightens several other interesting possible areas of application for therapy in neurorehabilitation, for research in basic neuroscience, and more.
Link to full text: http://www.jneuroengrehab.com/content/pdf/1743-0003-6-38.pdf
Journal of NeuroEngineering and Rehabilitation 2009, 6:38doi:10.1186/1743-0003-6-38
Published: 30 October 2009
Abstract (provisional)
Background
One of the main scientific and technological challenges of rehabilitation bioengineering is the development of innovative methodologies, based on the use of appropriate technological devices, for an objective assessment of patients undergoing a rehabilitation treatment. Such tools should be as fast and cheap to use as clinical scales, which are currently the daily instruments most widely used in the routine clinical practice.
Methods
A human-centered approach was used in the design and development of a mechanical structure equipped with eight force/torque sensors that record quantitative data during the initiation of a predefined set of Activities of Daily Living (ADL) tasks, in isometric conditions.
Results
Preliminary results validated the appropriateness, acceptability and functionality of the proposed platform, that has become now a tool used for clinical research in three clinical centres.
Conclusions
This paper presented the design and development of an innovative platform for whole-body force and torque measurements on human subjects. The platform has been designed to perform accurate quantitative measurements in isometric conditions with the specific aim to address the needs for functional assessment tests of patients undergoing a rehabilitation treatment as a consequence of a stroke. The versatility of the system also enlightens several other interesting possible areas of application for therapy in neurorehabilitation, for research in basic neuroscience, and more.
Link to full text: http://www.jneuroengrehab.com/content/pdf/1743-0003-6-38.pdf
Friday, October 30, 2009
Progressive GAA·TTC Repeat Expansion in Human Cell Lines
OPEN ACCESS
Scott Ditch, Mimi C. Sammarco, Ayan Banerjee, Ed Grabczyk*
Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States of America
Abstract
Trinucleotide repeat expansion is the genetic basis for a sizeable group of inherited neurological and neuromuscular disorders. Friedreich ataxia (FRDA) is a relentlessly progressive neurodegenerative disorder caused by GAA·TTC repeat expansion in the first intron of the FXN gene. The expanded repeat reduces FXN mRNA expression and the length of the repeat tract is proportional to disease severity. Somatic expansion of the GAA·TTC repeat sequence in disease-relevant tissues is thought to contribute to the progression of disease severity during patient aging. Previous models of GAA·TTC instability have not been able to produce substantial levels of expansion within an experimentally useful time frame, which has limited our understanding of the molecular basis for this expansion. Here, we present a novel model for studying GAA·TTC expansion in human cells. In our model system, uninterrupted GAA·TTC repeat sequences display high levels of genomic instability, with an overall tendency towards progressive expansion. Using this model, we characterize the relationship between repeat length and expansion. We identify the interval between 88 and 176 repeats as being an important length threshold where expansion rates dramatically increase. We show that expansion levels are affected by both the purity and orientation of the repeat tract within the genomic context. We further demonstrate that GAA·TTC expansion in our model is independent of cell division. Using unique reporter constructs, we identify transcription through the repeat tract as a major contributor to GAA·TTC expansion. Our findings provide novel insight into the mechanisms responsible for GAA·TTC expansion in human cells.
Link to full text: http://www.plosgenetics.org/article/fetchObjectAttachment.action;jsessionid=1C3EDADDCEC7DDCE3438B379DC71EE00?uri=info%3Adoi%2F10.1371%2Fjournal.pgen.1000704&representation=PDF
Scott Ditch, Mimi C. Sammarco, Ayan Banerjee, Ed Grabczyk*
Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States of America
Abstract
Trinucleotide repeat expansion is the genetic basis for a sizeable group of inherited neurological and neuromuscular disorders. Friedreich ataxia (FRDA) is a relentlessly progressive neurodegenerative disorder caused by GAA·TTC repeat expansion in the first intron of the FXN gene. The expanded repeat reduces FXN mRNA expression and the length of the repeat tract is proportional to disease severity. Somatic expansion of the GAA·TTC repeat sequence in disease-relevant tissues is thought to contribute to the progression of disease severity during patient aging. Previous models of GAA·TTC instability have not been able to produce substantial levels of expansion within an experimentally useful time frame, which has limited our understanding of the molecular basis for this expansion. Here, we present a novel model for studying GAA·TTC expansion in human cells. In our model system, uninterrupted GAA·TTC repeat sequences display high levels of genomic instability, with an overall tendency towards progressive expansion. Using this model, we characterize the relationship between repeat length and expansion. We identify the interval between 88 and 176 repeats as being an important length threshold where expansion rates dramatically increase. We show that expansion levels are affected by both the purity and orientation of the repeat tract within the genomic context. We further demonstrate that GAA·TTC expansion in our model is independent of cell division. Using unique reporter constructs, we identify transcription through the repeat tract as a major contributor to GAA·TTC expansion. Our findings provide novel insight into the mechanisms responsible for GAA·TTC expansion in human cells.
Link to full text: http://www.plosgenetics.org/article/fetchObjectAttachment.action;jsessionid=1C3EDADDCEC7DDCE3438B379DC71EE00?uri=info%3Adoi%2F10.1371%2Fjournal.pgen.1000704&representation=PDF
Thursday, October 29, 2009
Researchers Find Brain Cell Transplants Help Repair Neural Damage
ScienceDaily (Oct. 29, 2009) — A Swiss research team has found that using an animal's own brain cells (autologous transplant) to replace degenerated neurons in select brain areas of donor primates with simulated but asymptomatic Parkinson's disease and previously in a motor cortex lesion model, provides a degree of brain protection and may be useful in repairing brain lesions and restoring function. (read more)
Neuroprotective effects of blockers for T-type calcium channels
Molecular Neurodegeneration 2009, 4:44doi:10.1186/1750-1326-4-44
Published: 28 October 2009
OPEN ACCESS
Norelle C Wildburger , Avary Lin-Ye , Michelle A Baird , Debin Lei and Jianxin Bao
Abstract
Cognitive and functional decline with age is correlated with deregulation of intracellular calcium, which can lead to neuronal death in the brain. Previous studies have found protective effects of various calcium channel blockers in pathological conditions. However, little has been done to explore possible protective effects of blockers for T-type calcium channels, which forms a family of FDA approved anti-epileptic drugs. In this study, we found that neurons showed an increase in viability after treatment with either L-type or T-type calcium channel antagonists. The family of low-voltage activated, or T-type calcium channels, comprise of three members (Cav3.1, Cav3.2, and Cav3.3) based on their respective main pore-forming alpha subunits: alpha 1G, alpha 1H, and alpha 1I. Among these three subunits, alpha 1H is highly expressed in hippocampus and certain cortical regions. However, T-type calcium channel blockers can protect neurons derived from alpha 1H-/- mice, suggesting that neuroprotection demonstrated by these drugs is not through the alpha 1H subunit. In addition, blockers for T-type calcium channels were not able to confer any protection to neurons in long-term cultures, while blockers of L-type calcium channels could protect neurons. These data indicate a new function of blockers for T-type calcium channels, and also suggest different mechanisms to regulate neuronal survival by calcium signaling pathways. Thus, our findings have important implications in the development of new treatment for age-related neurodegenerative disorders.
Link to full text: http://www.molecularneurodegeneration.com/content/pdf/1750-1326-4-44.pdf
Published: 28 October 2009
OPEN ACCESS
Norelle C Wildburger , Avary Lin-Ye , Michelle A Baird , Debin Lei and Jianxin Bao
Abstract
Cognitive and functional decline with age is correlated with deregulation of intracellular calcium, which can lead to neuronal death in the brain. Previous studies have found protective effects of various calcium channel blockers in pathological conditions. However, little has been done to explore possible protective effects of blockers for T-type calcium channels, which forms a family of FDA approved anti-epileptic drugs. In this study, we found that neurons showed an increase in viability after treatment with either L-type or T-type calcium channel antagonists. The family of low-voltage activated, or T-type calcium channels, comprise of three members (Cav3.1, Cav3.2, and Cav3.3) based on their respective main pore-forming alpha subunits: alpha 1G, alpha 1H, and alpha 1I. Among these three subunits, alpha 1H is highly expressed in hippocampus and certain cortical regions. However, T-type calcium channel blockers can protect neurons derived from alpha 1H-/- mice, suggesting that neuroprotection demonstrated by these drugs is not through the alpha 1H subunit. In addition, blockers for T-type calcium channels were not able to confer any protection to neurons in long-term cultures, while blockers of L-type calcium channels could protect neurons. These data indicate a new function of blockers for T-type calcium channels, and also suggest different mechanisms to regulate neuronal survival by calcium signaling pathways. Thus, our findings have important implications in the development of new treatment for age-related neurodegenerative disorders.
Link to full text: http://www.molecularneurodegeneration.com/content/pdf/1750-1326-4-44.pdf
Epilepsy Drugs Could Treat Alzheimer's And Parkinson's
ScienceDaily (Oct. 29, 2009) — Researchers in the USA have discovered a potential new function for anti-epileptic drugs in treating neurodegenerative disorders such as Alzheimer's and Parkinson's disease. The study, published in BioMed Central's open access journal Molecular Neurodegeneration, found that neurons in the brain were protected after treatment with T-type calcium-channel blockers, which are commonly used to treat epilepsy. (read more)
Saturday, October 24, 2009
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