Professor, Neurology, Yale University School of Medicine
Neurology
Dr. Stephen M. Strittmatter, MD
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Stephen M. Strittmatter is an expert in the field of Neurology. He went to Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is one of the top medical schools in the US. Johns Hopkins University School of Medicine is ranked 3/29 in Research/PrimaryCare. Stephen Strittmatter has written publications. He has 101 publications published with PubMed. The lastest publication is: 'Parkinson's disease: nigral receptor changes support peptidergic role in nigrostriatal modulation.'
Publications
- Metabotropic glutamate receptor 5 couples cellular prion protein to intracellular signalling in Alzheimer's Disease.
- Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1-/- Mice.
- Gene-Silencing Screen for Mammalian Axon Regeneration Identifies Inpp5f (Sac2) as an Endogenous Suppressor of Repair after Spinal Cord Injury.
- Intravitreal Delivery of Human NgR-Fc Decoy Protein Regenerates Axons After Optic Nerve Crush and Protects Ganglion Cells in Glaucoma Models.
- Therapeutic Molecules and Endogenous Ligands Regulate the Interaction between Brain Cellular Prion Protein (PrPC) and Metabotropic Glutamate Receptor 5 (mGluR5).
- Progressive retinal degeneration and accumulation of autofluorescent lipopigments in Progranulin deficient mice.
- Human NgR-Fc Decoy Protein via Lumbar Intrathecal Bolus Administration Enhances Recovery from Rat Spinal Cord Contusion.
- Overcoming Drug Development Bottlenecks With Repurposing: Old drugs learn new tricks.
- Minimum Information About a Spinal Cord Injury Experiment (MIASCI) - a proposed reporting standard for spinal cord injury experiments.
- Diffusion Tensor Imaging as a Predictor of Locomotor Function Following Experimental Spinal Cord Injury and Recovery.
- Nogo limits neural plasticity and recovery from injury.
- Fyn kinase inhibition as a novel therapy for Alzheimer's Disease.
- Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein.
- Multimodal exercises simultaneously stimulating cortical and brainstem pathways after unilateral corticospinal lesion.
- Delayed amyloid plaque deposition and behavioral deficits in outcrossed A?PP/PS1 mice.
- Anatomical plasticity of adult brain is titrated by nogo receptor 1.
- Amyloid-? induced signaling by cellular prion protein and Fyn kinase in Alzheimer Disease.
- Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons.
- Recovery from chronic spinal cord contusion after nogo receptor intervention.
- Cartilage acidic protein-1B (LOTUS), an endogenous Nogo receptor antagonist for axon tract formation.
- Membrane type matrix metalloproteinase-3 regulates neuronal responsiveness to myelin through Nogo Receptor 1 cleavage.
- Myelin associated inhibitors: A link between injury-induced and experience-dependent plasticity.
- Differential but competitive binding of Nogo and MHCI to PIR-B provides an inhibition of cells.
- A Multi-domain Fragment of Nogo-A Protein Is a Potent Inhibitor of Cortical Axon Regeneration via Nogo Receptor 1.
- Inosine augments the effects of a nogo receptor blocker and of environmental enrichment to restore skilled forelimb use after stroke.
- Neuroscience. Lynx for braking plasticity.
- Sortilin-mediated endocytosis determines levels of the frontotemporal Dementia protein, progranulin.
- Genetic reduction of striatal-enriched tyrosine phosphatase (STEP) reverses cognitive and cellular deficits in an Alzheimer's Disease mouse model.
- Nogo receptor deletion and multimodal exercise improve distinct aspects of recovery in cervical spinal cord injury.
- Genetic deletion and pharmacological inhibition of Nogo-66 receptor impairs cognitive outcome after traumatic brain injury in mice.
- MAG and OMgp synergize with Nogo-A to restrict axonal growth and neurological recovery after spinal cord trauma.
- Memory impairment in transgenic Alzheimer mice requires cellular prion protein.
- Combination of NEP 1-40 treatment and motor training enhances behavioral recovery after a focal cortical infarct in rats.
- Rho-associated kinase II (ROCKII) limits axonal growth after trauma within the adult mouse spinal cord.
- LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology.
- Reticulon-4A (Nogo-A) redistributes protein disulfide isomerase to protect mice from SOD1-dependent amyotrophic lateral sclerosis.
- Cellular prion protein mediates the toxicity of beta-amyloid oligomers: implications for Alzheimer Disease.
- An unbiased expression screen for synaptogenic proteins identifies the LRRTM protein family as synaptic organizers.
- Ibuprofen enhances recovery from spinal cord injury by limiting tissue loss and stimulating axonal growth.
- Genetic variants of Nogo-66 receptor with possible association to schizophrenia block myelin inhibition of axon growth.
- Functional MRI and other non-invasive imaging technologies: providing visual biomarkers for spinal cord structure and function after injury.
- Release of MICAL autoinhibition by semaphorin-plexin signaling promotes interaction with collapsin response mediator protein.
- The N-terminal domain of Nogo-A inhibits cell adhesion and axonal outgrowth by an integrin-specific mechanism.
- Toll-like receptor 3 is a potent negative regulator of axonal growth in mammals.
- ROCK and Rho: biochemistry and neuronal functions of Rho-associated protein kinases.
- Nogo-A marks motor neuron Disease.
- Response to correspondence: Kim et al., "axon regeneration in young adult mice lacking Nogo-A/B." Neuron 38, 187-199.
- Functional axonal regeneration through astrocytic scar genetically modified to digest chondroitin sulfate proteoglycans.
- Characterization of myelin ligand complexes with neuronal Nogo-66 receptor family members.
- The CRMP family of proteins and their role in Sema3A signaling.
- Subcutaneous Nogo receptor removes brain amyloid-beta and improves spatial memory in Alzheimer's transgenic mice.
- The Nogo-Nogo receptor pathway limits a spectrum of adult CNS axonal growth.
- Delayed Nogo receptor therapy improves recovery from spinal cord contusion.
- Identification of a receptor necessary for Nogo-B stimulated chemotaxis and morphogenesis of endothelial cells.
- RanBPM contributes to Semaphorin3A signaling through plexin-A receptors.
- Alzheimer precursor protein interaction with the Nogo-66 receptor reduces amyloid-beta plaque deposition.
- Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain ...
- Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.
- Nogo-A interacts with the Nogo-66 receptor through multiple sites to create an isoform-selective subnanomolar agonist.
- Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury.
- Regulating axon growth within the postnatal central nervous system.
- Blockade of Nogo-66, myelin-associated glycoprotein, and oligodendrocyte myelin glycoprotein by soluble Nogo-66 receptor promotes axonal sprouting and recovery after s...
- Nogo-66 receptor prevents raphespinal and rubrospinal axon regeneration and limits functional recovery from spinal cord injury.
- A neutralizing anti-Nogo66 receptor monoclonal antibody reverses inhibition of neurite outgrowth by central nervous system myelin.
- Nogo receptor antagonism promotes stroke recovery by enhancing axonal plasticity.
- A new role for Nogo as a regulator of vascular remodeling.
- Fibroblast growth factor-inducible-14 is induced in axotomized neurons and promotes neurite outgrowth.
- Nogo-C is sufficient to delay nerve regeneration.
- Delayed systemic Nogo-66 receptor antagonist promotes recovery from spinal cord injury.
- Axon regeneration in young adult mice lacking Nogo-A/B.
- Rho kinase inhibition enhances axonal regeneration in the injured CNS.
- Truncated soluble Nogo receptor binds Nogo-66 and blocks inhibition of axon growth by myelin.
- Regenerating nerves follow the road more traveled.
- Myelin-associated glycoprotein as a functional ligand for the Nogo-66 receptor.
- Modulation of axonal regeneration in neurodegenerative Disease: focus on Nogo.
- Localization of Nogo-A and Nogo-66 receptor proteins at sites of axon-myelin and synaptic contact.
- Small proline-rich repeat protein 1A is expressed by axotomized neurons and promotes axonal outgrowth.
- Parkinson's Disease: nigral receptor changes support peptidergic role in nigrostriatal modulation.
- Nogo-66 receptor antagonist peptide (NEP1-40) administration promotes functional recovery and axonal growth after lateral funiculus injury in the adult rat.
- Inosine alters gene expression and axonal projections in neurons contralateral to a cortical infarct and improves skilled use of the impaired limb.
- Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity.
- Axon regeneration in the peripheral and central nervous systems.
- Functional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice.
- Nogo: a molecular determinant of axonal growth and regeneration.
- Semaphorin-mediated axonal guidance via Rho-related G proteins.
- Plexina1 autoinhibition by the plexin sema domain.
- Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration.
- Repulsive factors and axon regeneration in the CNS.
- Rho GTPases and axonal growth cone collapse.
- Molecular basis of semaphorin-mediated axon guidance.
- Semaphorin3A enhances endocytosis at sites of receptor-F-actin colocalization during growth cone collapse.
- Dendrites go up, axons go down.
- Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein.
- Brain-derived neurotrophic factor induces excitotoxic sensitivity in cultured embryonic rat spinal motor neurons through activation of the phosphatidylinositol 3-kinas...
- G(o) protein-dependent survival of primary accessory olfactory neurons.
- Plexin-neuropilin-1 complexes form functional semaphorin-3A receptors.
- Sequence-specific cleavage of Huntingtin mRNA by catalytic DNA.
- Growth cone neuropilin-1 mediates collapsin-1/Sema III facilitation of antero- and retrograde axoplasmic transport.
- Isolation of receptor clones by expression screening in Xenopus oocytes.
- A PDZ protein regulates the distribution of the transmembrane semaphorin, M-SemF.
Schools
Johns Hopkins University School of Medicine
Massachusetts General Hospital
Procedures Preformed
- EEG (Electroencephalogram)
Conditions Treated
- Dementia
- Huntington's Disease
- Sleep Apnea
Doctors Specialties
- Neurology
Accepted Insurances
Education
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Massachusetts General Hospital -
Johns Hopkins University School of Medicine
Hospital
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Yale-New Haven Hospital
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1083695381 |
| Last Name Of The Provider | STRITTMATTER |
| First Name Of The Provider | STEPHEN |
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