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1. Full Text Treatment of infantile-onset spinal muscular atrophy with nusinersen: a phase 2, open-label, dose-escalation study
by Finkel, Richard S, Dr and Chiriboga, Claudia A, MD and Vajsar, Jiri, MD and Day, John W, MD and Montes, Jacqueline, EdD and De Vivo, Darryl C, MD and Yamashita, Mason, MD and Rigo, Frank, PhD and Hung, Gene, MD and Schneider, Eugene, MD and Norris, Daniel A, PhD and Xia, Shuting, MS and Bennett, C Frank, PhD and Bishop, Kathie M, PhD
The Lancet (British edition), ISSN 0140-6736, 2016, Volume 388, Issue 10063, pp. 3017 - 3026
Internal Medicine | Medicine, General & Internal | Life Sciences & Biomedicine | General & Internal Medicine | Science & Technology | Injections, Spinal | Humans | RNA, Messenger - genetics | Patient Safety | Spinal Muscular Atrophies of Childhood - drug therapy | Female | Male | Oligonucleotides - adverse effects | Mutation | Oligonucleotides - administration & dosage | Oligonucleotides - pharmacokinetics | Care and treatment | RNA | Children's hospitals | Spinal muscular atrophy | Clinical trials | Analysis | Proteins | Spinal cord | Genetic disorders | Drug therapy | Drug dosages | Index Medicus | Abridged Index Medicus
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2. Full Text Peripheral SMN restoration is essential for long-term rescue of a severe spinal muscular atrophy mouse model
by Hua, Yimin and Sahashi, Kentaro and Rigo, Frank and Hung, Gene and Horev, Guy and Bennett, C. Frank and Krainer, Adrian R
Nature (London), ISSN 0028-0836, 10/2011, Volume 478, Issue 7367, pp. 123 - 126
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Neurology | Biological and medical sciences | Medical sciences | Diseases of striated muscles. Neuromuscular diseases | Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases | Spinal Cord - metabolism | Longevity - drug effects | Humans | Glycoproteins - metabolism | RNA, Messenger - analysis | Survival of Motor Neuron 2 Protein - metabolism | Motor Neurons - pathology | Muscular Atrophy, Spinal - genetics | Spinal Cord - pathology | Survival of Motor Neuron 2 Protein - genetics | Survival of Motor Neuron 1 Protein - genetics | RNA Isoforms - analysis | Glycoproteins - deficiency | Spinal Cord - cytology | Transgenes | Muscular Atrophy, Spinal - physiopathology | Motor Neurons - drug effects | Disease Models, Animal | Animals, Newborn | Muscular Atrophy, Spinal - metabolism | Oligonucleotides, Antisense - pharmacology | RNA Isoforms - genetics | Growth Hormone - metabolism | Alternative Splicing - genetics | Liver - metabolism | RNA, Messenger - genetics | Kaplan-Meier Estimate | Insulin-Like Growth Factor I - deficiency | Mice, Transgenic | Muscular Atrophy, Spinal - pathology | Motor Neurons - metabolism | Rotarod Performance Test | Alternative Splicing - drug effects | Animals | Carrier Proteins - metabolism | Oligonucleotides, Antisense - genetics | Oligonucleotides, Antisense - administration & dosage | Mice | Insulin-Like Growth Factor I - metabolism | Complications and side effects | Care and treatment | Gene mutations | Patient outcomes | Genetic aspects | Infants | Research | Diagnosis | Risk factors | Spinal muscular atrophy | Gene expression | Medical research | Rodents | Index Medicus
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3. Full Text Towards a therapy for Angelman syndrome by targeting a long non-coding RNA
by Meng, Linyan and Ward, Amanda J and Chun, Seung and Bennett, C. Frank and Beaudet, Arthur L and Rigo, Frank
Nature (London), ISSN 0028-0836, 02/2015, Volume 518, Issue 7539, pp. 409 - 412
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | RNA, Antisense - deficiency | Gene Silencing - drug effects | Memory Disorders - genetics | Male | Memory Disorders - complications | Obesity - genetics | Angelman Syndrome - therapy | Brain - metabolism | Time Factors | Oligonucleotides, Antisense - therapeutic use | Angelman Syndrome - genetics | Female | Neurons - metabolism | Neurons - drug effects | Disease Models, Animal | Oligonucleotides, Antisense - pharmacology | Obesity - complications | Mice, Inbred C57BL | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | RNA, Long Noncoding - genetics | Angelman Syndrome - complications | Brain - drug effects | Genomic Imprinting - genetics | Phenotype | Animals | Oligonucleotides, Antisense - genetics | RNA, Antisense - antagonists & inhibitors | Alleles | Memory Disorders - therapy | Obesity - therapy | Fathers | Mice | RNA, Long Noncoding - antagonists & inhibitors | Ubiquitin-Protein Ligases - genetics | RNA, Antisense - genetics | RNA | Gene therapy | Health aspects | Methods | Proteins | Genetic disorders | Rodents | DNA methylation | Protein expression | Ribonucleic acid--RNA | Binding sites | Index Medicus
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4. Full Text Premature polyadenylation-mediated loss of stathmin-2 is a hallmark of TDP-43-dependent neurodegeneration
by Melamed, Ze’ev and López-Erauskin, Jone and Baughn, Michael W and Zhang, Ouyang and Drenner, Kevin and Sun, Ying and Freyermuth, Fernande and McMahon, Moira A and Beccari, Melinda S and Artates, Jon W and Ohkubo, Takuya and Rodriguez, Maria and Lin, Nianwei and Wu, Dongmei and Bennett, C. Frank and Rigo, Frank and Da Cruz, Sandrine and Ravits, John and Lagier-Tourenne, Clotilde and Cleveland, Don W
Nature neuroscience, ISSN 1097-6256, 02/2019, Volume 22, Issue 2, pp. 180 - 190
Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Spinal Cord - metabolism | Humans | Motor Cortex - pathology | Motor Neurons - pathology | Nerve Degeneration - metabolism | Nerve Degeneration - pathology | DNA-Binding Proteins - metabolism | Motor Neurons - metabolism | Amyotrophic Lateral Sclerosis - pathology | Motor Cortex - metabolism | Spinal Cord - pathology | Amyotrophic Lateral Sclerosis - metabolism | Polyadenylation | Female | Membrane Proteins - metabolism | Complications and side effects | Amyotrophic lateral sclerosis | Research | Gene mutations | Neurons | Motor neurons | Motors | mRNA | Cortex (motor) | Ribonucleic acid--RNA | Gene expression | Stathmin | Proteins | Regeneration | Reduction | DNA-binding protein | Neurodegeneration | Stem cells | Fibroblasts | Dementia disorders | Mutation | Frontotemporal dementia | Pluripotency | Deoxyribonucleic acid--DNA | Index Medicus
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5. Full Text The Power of Human Protective Modifiers: PLS3 and CORO1C Unravel Impaired Endocytosis in Spinal Muscular Atrophy and Rescue SMA Phenotype
by Hosseinibarkooie, Seyyedmohsen and Peters, Miriam and Torres-Benito, Laura and Rastetter, Raphael H and Hupperich, Kristina and Hoffmann, Andrea and Mendoza-Ferreira, Natalia and Kaczmarek, Anna and Janzen, Eva and Milbradt, Janine and Lamkemeyer, Tobias and Rigo, Frank and Bennett, C. Frank and Guschlbauer, Christoph and Büschges, Ansgar and Hammerschmidt, Matthias and Riessland, Markus and Kye, Min Jeong and Clemen, Christoph S and Wirth, Brunhilde
American journal of human genetics, ISSN 0002-9297, 09/2016, Volume 99, Issue 3, pp. 647 - 665
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Membrane Glycoproteins - metabolism | Synaptic Transmission - genetics | Calcium - metabolism | Neuromuscular Junction - metabolism | Humans | Actins - metabolism | Male | Muscular Atrophy, Spinal - genetics | Survival of Motor Neuron 2 Protein - genetics | Survival of Motor Neuron 1 Protein - genetics | Endocytosis - genetics | Microfilament Proteins - metabolism | Microfilament Proteins - genetics | Neuromuscular Junction - pathology | Carrier Proteins | Disease Models, Animal | Oligonucleotides, Antisense | Muscular Atrophy, Spinal - pathology | Zebrafish - genetics | Membrane Glycoproteins - genetics | Phenotype | Animals | Axons - pathology | Zebrafish - metabolism | Quaternary Ammonium Compounds - metabolism | Presynaptic Terminals - metabolism | Mice | Pyridinium Compounds - metabolism | Proteins | Genotype & phenotype | Neuromuscular diseases | Gene expression | Rodents | Index Medicus
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6. Full Text Antisense oligonucleotide therapy for spinocerebellar ataxia type 2
by Scoles, Daniel R and Meera, Pratap and Schneider, Matthew D and Paul, Sharan and Dansithong, Warunee and Figueroa, Karla P and Hung, Gene and Rigo, Frank and Bennett, C. Frank and Otis, Thomas S and Pulst, Stefan M
Nature (London), ISSN 0028-0836, 04/2017, Volume 544, Issue 7650, pp. 362 - 366
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Humans | Male | Spinocerebellar Ataxias - therapy | RNA, Messenger - metabolism | Ataxin-2 - genetics | Action Potentials | RNA, Messenger - biosynthesis | Ataxin-2 - metabolism | Oligonucleotides, Antisense - therapeutic use | Female | Disease Models, Animal | Spinocerebellar Ataxias - genetics | Movement | Purkinje Cells - metabolism | RNA, Messenger - genetics | Gene Expression Regulation | Mice, Transgenic | Spinocerebellar Ataxias - physiopathology | Spinocerebellar Ataxias - pathology | Ataxin-2 - deficiency | Phenotype | Rotarod Performance Test | Animals | Mice | Purkinje Cells - pathology | Antisense nucleic acids | Care and treatment | Genetic aspects | Purkinje cells | Health aspects | Spinocerebellar ataxia | Proteins | Studies | Disease | Neurodegeneration | Rodents | Amyotrophic lateral sclerosis | Nervous system | Mutation | FDA approval | Drug dosages | Deoxyribonucleic acid--DNA | Index Medicus
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7. Full Text Increased 4R-Tau Induces Pathological Changes in a Human-Tau Mouse Model
by Schoch, Kathleen M and DeVos, Sarah L and Miller, Rebecca L and Chun, Seung J and Norrbom, Michaela and Wozniak, David F and Dawson, Hana N and Bennett, C. Frank and Rigo, Frank and Miller, Timothy M
Neuron (Cambridge, Mass.), ISSN 0896-6273, 06/2016, Volume 90, Issue 5, pp. 941 - 947
Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | RNA Splicing - drug effects | Oligonucleotides, Antisense - pharmacology | Seizures - genetics | Humans | tau Proteins - toxicity | Solubility | tau Proteins - metabolism | Exons - genetics | Seizures - metabolism | tau Proteins - chemistry | Seizures - chemically induced | Brain - metabolism | Nesting Behavior - drug effects | Animals | Mutation - drug effects | Protein Isoforms - metabolism | tau Proteins - genetics | Models, Biological | RNA Splicing - genetics | Oligonucleotides, Antisense - administration & dosage | Mice | Phosphorylation - drug effects | Trinucleotide Repeat Expansion - drug effects | Infusions, Intraventricular | Physiological aspects | Nervous system diseases | Seizures (Medicine) | Dementia | Pathology | Phosphorylation | Rodents | Software | Behavior | Alzheimers disease | Pharmaceuticals | Index Medicus
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8. Full Text Antisense-based therapy for the treatment of spinal muscular atrophy
by Rigo, Frank and Hua, Yimin and Krainer, Adrian R and Frank Bennett, C
The Journal of cell biology, ISSN 0021-9525, 10/2012, Volume 199, Issue 1, pp. 21 - 25
Life Sciences & Biomedicine | Science & Technology | Cell Biology | Oligonucleotides, Antisense - pharmacology | Humans | RNA, Messenger - genetics | Mice, Transgenic | Muscular Atrophy, Spinal - genetics | Animals | Survival of Motor Neuron 1 Protein - antagonists & inhibitors | Survival of Motor Neuron 2 Protein - genetics | Survival of Motor Neuron 1 Protein - genetics | Muscular Atrophy, Spinal - drug therapy | Mice | Survival of Motor Neuron 2 Protein - antagonists & inhibitors | RNA, Messenger - drug effects | Care and treatment | Children | Spinal muscular atrophy | Diseases | Index Medicus
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