Dr. Charles A Thornton MD
Neurologist | Vascular Neurology601 Elmwood Ave Box 278984 Rochester NY, 14642
Dr. Charles Thornton practices Neuropathology in Rochester, NY. Dr. Thornton studies, evaluates, diagnoses, and treats conditions that affect the nervous system. Neuropathologists are trained to fully understand and treat such conditions as Alzheimers disease and Parkinsons disease.
Education and Training
Univ Of Ia Coll Of Med- Iowa City Ia 1981
University of Ia Roy J & L Carver Com 1981
Baylor College of Medicine, Houston, Texas 1981
Psychiatry and NeurologyAmerican Board of Psychiatry and NeurologyABPN
- Expanded CUG repeats trigger aberrant splicing of ClC-1 chloride channel pre-mRNA and hyperexcitability of skeletal muscle in myotonic dystrophy.
- Computational method for reducing variance with Affymetrix microarrays.
- Myotonic syndromes.
- Molecular fingerprints of inflammatory myopathies.
- Reduced amount of mitochondrial DNA in aged human muscle.
- Gene expression profile of aging in human muscle.
- A muscleblind knockout model for myotonic dystrophy.
- Ribonuclear inclusions in skeletal muscle in myotonic dystrophy types 1 and 2.
- Skeletal muscle gene expression profiles in 20-29 year old and 65-71 year old women.
- Myotonic dystrophy type 1 is associated with nuclear foci of mutant RNA, sequestration of muscleblind proteins and deregulated alternative splicing in neurons.
- Truncated ClC-1 mRNA in myotonic dystrophy exerts a dominant-negative effect on the Cl current.
- Nuclear RNA foci in the heart in myotonic dystrophy.
- Failure of MBNL1-dependent post-natal splicing transitions in myotonic dystrophy.
- Reversal of RNA missplicing and myotonia after muscleblind overexpression in a mouse poly(CUG) model for myotonic dystrophy.
- RNA-dominant diseases.
- Chloride channelopathy in myotonic dystrophy resulting from loss of posttranscriptional regulation for CLCN1.
- Muscle growth after postdevelopmental myostatin gene knockout.
- Muscle chloride channel dysfunction in two mouse models of myotonic dystrophy.
- Severity, type, and distribution of myotonic discharges are different in type 1 and type 2 myotonic dystrophy.
- Huntington's disease--like 2 is associated with CUG repeat-containing RNA foci.
- Computerized hand grip myometry reliably measures myotonia and muscle strength in myotonic dystrophy (DM1).
- Muscleblind-like 1 interacts with RNA hairpins in splicing target and pathogenic RNAs.
- Myotonic dystrophy: RNA-mediated muscle disease.
- Correction of ClC-1 splicing eliminates chloride channelopathy and myotonia in mouse models of myotonic dystrophy.
- Sex-related differences in gene expression in human skeletal muscle.
- Cell-free cloning of highly expanded CTG repeats by amplification of dimerized expanded repeats.
- Dynamic combinatorial selection of molecules capable of inhibiting the (CUG) repeat RNA-MBNL1 interaction in vitro: discovery of lead compounds targeting myotonic dystrophy (DM1).
- Transcriptional and post-transcriptional impact of toxic RNA in myotonic dystrophy.
- Rational design of ligands targeting triplet repeating transcripts that cause RNA dominant disease: application to myotonic muscular dystrophy type 1 and spinocerebellar ataxia type 3.
- Reversal of RNA dominance by displacement of protein sequestered on triplet repeat RNA.
- Relation between extent of myostatin depletion and muscle growth in mature mice.
- Triplet-repeat oligonucleotide-mediated reversal of RNA toxicity in myotonic dystrophy.
- Scaled-down genetic analysis of myotonic dystrophy type 1 and type 2.
- Pentamidine reverses the splicing defects associated with myotonic dystrophy.
- Controlling the specificity of modularly assembled small molecules for RNA via ligand module spacing: targeting the RNAs that cause myotonic muscular dystrophy.
- Aberrant alternative splicing and extracellular matrix gene expression in mouse models of myotonic dystrophy.
- Expanded CTG repeat demarcates a boundary for abnormal CpG methylation in myotonic dystrophy patient tissues.
- Sarcolemmal-restricted localization of functional ClC-1 channels in mouse skeletal muscle.
- Bidirectional transcription stimulates expansion and contraction of expanded (CTG)*(CAG) repeats.
- Identification of restriction endonucleases sensitive to 5-cytosine methylation
- Replacement of the myotonic dystrophy type 1 CTG repeat with 'non-CTG repeat' insertions in specific tissues.
- Progressive myopathy in an inducible mouse model of oculopharyngeal muscular dystrophy.
- Stabilization of expanded (CTG)•(CAG) repeats by antisense oligonucleotides.
- Muscle weakness in myotonic dystrophy associated with misregulated splicing and
- Design of a bioactive small molecule that targets the myotonic dystrophy type 1 RNA via an RNA motif-ligand database and chemical similarity searching.
- Rationally designed small molecules targeting the RNA that causes myotonic dystrophy type 1 are potently bioactive.
- From dynamic combinatorial 'hit' to lead: in vitro and in vivo activity of compounds targeting the pathogenic RNAs that cause myotonic dystrophy.
- Targeting nuclear RNA for in vivo correction of myotonic dystrophy.
- Rational design of bioactive, modularly assembled aminoglycosides targeting the RNA that causes myotonic dystrophy type 1.
- RNA interference targeting CUG repeats in a mouse model of myotonic dystrophy.
- Induction and reversal of myotonic dystrophy type 1 pre-mRNA splicing defects by small molecules.
- Splicing biomarkers of disease severity in myotonic dystrophy.
- Reducing levels of toxic RNA with small molecules.
- Features of modularly assembled compounds that impart bioactivity against an RNA target.
- Detection of slipped-DNAs at the trinucleotide repeats of the myotonic dystrophy type I disease locus in patient tissues.
- Lomofungin and dilomofungin: inhibitors of MBNL1-CUG RNA binding with distinct cellular effects.
- Myotonic dystrophy.
- Loss of MBNL leads to disruption of developmentally regulated alternative polyadenylation in RNA-mediated disease.
- Short antisense-locked nucleic acids (all-LNAs) correct alternative splicing abnormalities in myotonic dystrophy.
- Identification and characterization of modified antisense oligonucleotides targeting DMPK in mice and nonhuman primates for the treatment of myotonic dystrophy type 1.
- Dmpk gene deletion or antisense knockdown does not compromise cardiac or skeletal muscle function in mice.
- Dose-Dependent Regulation of Alternative Splicing by MBNL Proteins Reveals Biomarkers for Myotonic Dystrophy.
- Myotonic dystrophy: approach to therapy.
- Targeting DMPK with Antisense Oligonucleotide Improves Muscle Strength in Myotonic Dystrophy Type 1 Mice.
- Detection of expanded RNA repeats using thermostable group II intron reverse transcriptase.
- Muscular Dystrophy
- Amyotrophic Lateral Sclerosis (als)
- Fellow 2005- American Academy of Neurology
- Member Scientific Advisory Board, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center 2006
- Member American Society of Gene Therapy 2008
- Strong Mem Hsp U Rochester, Neurology; Or Hlth Sci Univ Hosp, Neurology; Vet Affairs Med Ctr, Internal Medicine
- Oregon Health & Science University Affiliated Hospitals 1982
- U S DEPARTMENT OF VETERANS AFFAIRS
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Patient Experience with Dr. Thornton
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