Professor of Neurology, Professor of Neuroscience, Professor of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine; Director, Institute for Cell Engineering, Director, Morris K. Udall Parkinson's Disease Research Center,
Neurology
Dr. Ted M. Dawson, MD
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Dr. Ted M. Dawson works in the field of Neurology. He graduated from University of Utah School of Medicine. Doctor Ted M. Dawson, MD is a published doctor and has 100 publications published. The lastest was: 'TRPV1 on astrocytes rescues nigral dopamine neurons in Parkinson's disease via CNTF.'
Publications
- TRPV1 on astrocytes rescues nigral dopamine neurons in Parkinson's Disease via CNTF.
- Cognitive profile of LRRK2-related Parkinson's Disease.
- Parkin-independent mitophagy requires Drp1 and maintains the integrity of mammalian heart and Brain.
- LRRK2 Pathobiology in Parkinson's Disease.
- Early-onset Parkinson's Disease due to PINK1 p.Q456X mutation - Clinical and functional study.
- Conditional expression of Parkinson's Disease-related R1441C LRRK2 in midbrain dopaminergic neurons of mice causes nuclear abnormalities without neurodegeneration.
- Abberant protein synthesis in G2019S LRRK2 Drosophila Parkinson Disease-related phenotypes.
- Poly(ADP-ribose) polymerase-dependent energy depletion occurs through inhibition of glycolysis.
- Proneural Transcription Factor Atoh1 Drives Highly Efficient Differentiation of Human Pluripotent Stem Cells Into Dopaminergic Neurons.
- MiR-223 regulates the differentiation of immature neurons.
- Msp1/ATAD1 maintains mitochondrial function by facilitating the degradation of mislocalized tail-anchored proteins.
- Botch Is a γ-Glutamyl Cyclotransferase that Deglycinates and Antagonizes Notch.
- Parkin and PINK1: much more than mitophagy.
- Ribosomal Protein s15 Phosphorylation Mediates LRRK2 Neurodegeneration in Parkinson's Disease.
- A Randomized Clinical Trial of High-Dosage Coenzyme Q10 in Early Parkinson Disease: No Evidence of Benefit.
- Motor Neuron Death in ALS: Programmed by Astrocytes?
- MicroRNA-132 dysregulation in Toxoplasma gondii infection has implications for dopamine signaling pathway.
- Absence of C9ORF72 expanded or intermediate repeats in autopsy-confirmed Parkinson's Disease.
- Functional Interaction of Parkinson's Disease-Associated LRRK2 with Members of the Dynamin GTPase Superfamily.
- Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.
- Usp16: key controller of stem cells in Down Syndrome.
- Identification through high-throughput screening of 4'-methoxyflavone and 3',4'-dimethoxyflavone as novel neuroprotective inhibitors of parthanatos.
- Reprogramming cellular events by poly(ADP-ribose)-binding proteins.
- Neurodegenerative phenotypes in an A53T α-synuclein transgenic mouse model are independent of LRRK2.
- Botch promotes neurogenesis by antagonizing notch.
- Measuring the activity of leucine-rich repeat kinase 2: a kinase involved in Parkinson's Disease.
- Transcriptional responses to loss or gain of function of the leucine-rich repeat kinase 2 (LRRK2) gene uncover biological processes modulated by LRRK2 activity.
- Chemoproteomics-based design of potent LRRK2-selective lead compounds that attenuate Parkinson's Disease-related toxicity in human neurons.
- Iduna is a poly(ADP-ribose) (PAR)-dependent E3 ubiquitin ligase that regulates DNA damage.
- Inhibitors of LRRK2 kinase attenuate neurodegeneration and Parkinson-like phenotypes in Caenorhabditis elegans and Drosophila Parkinson's Disease models.
- Enhanced autophagy from chronic toxicity of iron and mutant A53T {alpha}-synuclein: Implications for neuronal cell death in Parkinson's Disease.
- A lysosomal lair for a pathogenic protein pair.
- Recent advances in the genetics of Parkinson's Disease.
- Iduna protects the Brain from glutamate excitotoxicity and stroke by interfering with poly(ADP-ribose) polymer-induced cell death.
- The AAA(+) ATPase Thorase Regulates AMPA Receptor-Dependent Synaptic Plasticity and Behavior.
- PARIS (ZNF746) repression of PGC-1α contributes to neurodegeneration in Parkinson's Disease.
- MicroRNAs in Parkinson's Disease.
- Poly(ADP-Ribose) (PAR) Binding to Apoptosis-Inducing Factor Is Critical for PAR Polymerase-1-Dependent Cell Death (Parthanatos).
- Resistance to MPTP-neuroToxicity in α-synuclein knockout mice is complemented by human α-synuclein and associated with increased Î&su...
- Dopaminergic Neuronal Loss, Reduced Neurite Complexity and Autophagic Abnormalities in Transgenic Mice Expressing G2019S Mutant LRRK2.
- Neuronal Activity Regulates Hippocampal miRNA Expression.
- Effect of Fenbendazole on Three Behavioral Tests in Male C57BL/6N Mice.
- Phosphorylation by the c-Abl protein tyrosine kinase inhibits parkin's ubiquitination and protective function.
- Reevaluation of phosphorylation sites in the Parkinson Disease-associated leucine-rich repeat kinase 2.
- Inhibitors of leucine-rich repeat kinase-2 protect against models of Parkinson's Disease.
- NMDA-induced neuronal survival is mediated through nuclear factor I-A in mice.
- Endonuclease G does not play an obligatory role in poly(ADP-ribose) polymerase-dependent cell death after transient focal Cerebral ischemia.
- Genetic animal models of Parkinson's Disease.
- GTPase activity plays a key role in the pathobiology of LRRK2.
- PINK1-dependent recruitment of Parkin to mitochondria in mitophagy.
- Functional identification of neuroprotective molecules.
- The role of parkin in familial and sporadic Parkinson's Disease.
- Unexpected lack of hypersensitivity in LRRK2 knock-out mice to MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine).
- SnapShot: pathogenesis of Parkinson's Disease.
- Neuronal NOS and cyclooxygenase-2 contribute to DNA damage in a mouse model of Parkinson Disease.
- Parkin protects against LRRK2 G2019S mutant-induced dopaminergic neurodegeneration in Drosophila.
- Abnormal localization of leucine-rich repeat kinase 2 to the endosomal-lysosomal compartment in lewy body Disease.
- Poly(ADP-ribose) signals to mitochondrial AIF: a key event in parthanatos.
- Leucine-rich repeat kinase 2 expression leads to aggresome formation that is not associated with alpha-synuclein inclusions.
- S-nitrosylation of XIAP compromises neuronal survival in Parkinson's Disease.
- CHIP regulates leucine-rich repeat kinase-2 ubiquitination, degradation, and Toxicity.
- Parthanatos, a messenger of death.
- What causes cell death in Parkinson's Disease?
- Mitochondrial and nuclear cross talk in cell death: parthanatos.
- Value of genetic models in understanding the cause and mechanisms of Parkinson's Disease.
- Role of tuberin in neuronal degeneration.
- The chaperone activity of heat shock protein 90 is critical for maintaining the stability of leucine-rich repeat kinase 2.
- Advances in neuronal cell death 2007.
- Lysine 63-linked polyubiquitin potentially partners with p62 to promote the clearance of protein inclusions by autophagy.
- Parkinson's Disease genetic mutations increase cell susceptibility to stress: mutant alpha-synuclein enhances H2O2- and Sin-1-induced cell death.
- DJ-1 gene deletion reveals that DJ-1 is an atypical peroxiredoxin-like peroxidase.
- A hierarchical NGF signaling cascade controls Ret-dependent and Ret-independent events during development of nonpeptidergic DRG neurons.
- Ataxia telangiectasia mutated (ATM) signaling network is modulated by a novel poly(ADP-ribose)-dependent pathway in the early response to DNA-damaging agents.
- MPTP and DSP-4 susceptibility of substantia nigra and locus coeruleus catecholaminergic neurons in mice is independent of parkin activity.
- Relative sensitivity of parkin and other cysteine-containing enzymes to stress-induced solubility alterations.
- The role of stem cells in Parkinson's Disease.
- Poly(ADP-ribose) (PAR) polymer is a death signal.
- Apoptosis-inducing factor mediates poly(ADP-ribose) (PAR) polymer-induced cell death.
- Localization of LRRK2 to membranous and vesicular structures in mammalian Brain.
- Kinase activity of mutant LRRK2 mediates neuronal Toxicity.
- Taming the clot-buster tPA.
- Diagnosis and treatment of Parkinson Disease: molecules to medicine.
- Identification of far upstream element-binding protein-1 as an authentic Parkin substrate.
- Parkin blushed by PINK1.
- Inclusion body formation and neurodegeneration are parkin independent in a mouse model of alpha-synucleinopathy.
- Parkin-mediated lysine 63-linked polyubiquitination: a link to protein inclusions formation in Parkinson's and other conformational Diseases?
- Neuroprotection by pharmacologic blockade of the GAPDH death cascade.
- A nitric oxide signaling pathway controls CREB-mediated gene expression in neurons.
- Lessons from Drosophila models of DJ-1 deficiency.
- Leucine-rich repeat kinase 2 (LRRK2) interacts with parkin, and mutant LRRK2 induces neuronal degeneration.
- Failures and successes of clinical trials for Parkinson Disease treatments.
- Parkinson's Disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity.
- Alpha-synuclein and Parkinson's Disease: implications from the screening of more than 1,900 patients.
- Accumulation of the authentic parkin substrate aminoacyl-tRNA synthetase cofactor, p38/JTV-1, leads to catecholaminergic cell death.
- Abeta deposition is associated with enhanced cortical alpha-synuclein lesions in Lewy body Diseases.
- Bcl-x is required for proper development of the mouse substantia nigra.
- Alpha-synuclein phosphorylation enhances eosinophilic cytoplasmic inclusion formation in SH-SY5Y cells.
- The road to survival goes through PARG.
- Parkin mediates nonclassical, proteasomal-independent ubiquitination of synphilin-1: implications for Lewy body formation.
Schools
University of Utah
University Ut
Hospital University Pa
Johns Hopkins University
Procedures Preformed
- EEG (Electroencephalogram)
- EMG (Electromyography)
Conditions Treated
- Alzheimer's Disease
- Brain Aneurysm
- Carpal Tunnel Syndrome
- Cerebral Artery Thrombosis
- View All
Doctors Specialties
- Neurology
Accepted Insurances
Education
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University of Pennsylvania Health System -
University of Utah -
University of Utah School of Medicine
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