Professor, Neurology, UCSF School of Medicine

Neurology

Scott Zamvil works in the field of Neurology. He graduated from Stanford University School of Medicine. Stanford University School of Medicine is a top medical college. Stanford University School of Medicine is ranked 2 in research and 25 in primary care medicine He received awards:"CMS Meaningful Use Stage 1 Certification". Scott Zamvil is a published doctor and has 101 publications published. The lastest was: 'Astrocytes express elements of the class II endocytic pathway and process central nervous system autoantigen for presentation to encephalitogenic T cells.' He is registered with Medicare and accepts Medicare payments.

Publications

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• Vitamin D in clinically isolated syndrome: evidence for possible neuroprotection.
• Reduction of CD8(+) T lymphocytes in Multiple sclerosis patients treated with dimethyl fumarate.
• Does MOG Ig-positive AQP4-seronegative opticospinal inflammatory disease justify a diagnosis of NMO spectrum disorder?
• B-cell very late antigen-4 deficiency reduces leukocyte recruitment and susceptibility to central nervous system autoimmunity.
• Precision medicine in chronic disease management: The Multiple sclerosis BioScreen.
• Laquinimod, an upcoming oral immunomodulatory agent for treatment of Multiple sclerosis.
• MHC class II-dependent B cell APC function is required for induction of CNS autoimmunity independent of myelin-specific antibodies.
• Aquaporin 4-specific T cells in neuromyelitis optica exhibit a Th17 bias and recognize Clostridium ABC transporter.
• Laquinimod, a Quinoline-3-Carboxamide, Induces Type II Myeloid Cells That Modulate Central Nervous System Autoimmunity.
• B cells in Multiple sclerosis: connecting the dots.
• Combining statins with interferon beta in Multiple sclerosis: think twice, it might not be all right.
• Lymph node-derived donor encephalitogenic CD4+ T cells in C57BL/6 mice adoptive transfer experimental autoimmune encephalomyelitis highly express GM-CSF and T-bet.
• Proinflammatory role of aquaporin-4 in autoimmune neuroinflammation.
• Accelerated central nervous system autoimmunity in BAFF-receptor-deficient mice.
• Switching Multiple sclerosis patients with breakthrough disease to second-line therapy.
• Translational research in neurology and neuroscience 2010: Multiple sclerosis.
• Delivery of myelin peptides through the first line of defense, skin, to counter autoimmunity in Multiple sclerosis.
• B-cell activation influences T-cell polarization and outcome of anti-CD20 B-cell depletion in central nervous system autoimmunity.
• FTY720 and central memory: out of sight, out of mind.
• Natalizumab and progressive multifocal leukoencephalopathy: what are the causal factors and can it be avoided?
• Immunodominant T cell determinants of aquaporin-4, the autoantigen associated with neuromyelitis optica.
• Repetitive pertussis toxin promotes development of regulatory T cells and prevents central nervous system autoimmune disease.
• Depletion of B lymphocytes from cerebral perivascular spaces by rituximab.
• Glatiramer acetate increases IL-1 receptor antagonist but decreases T cell-induced IL-1beta in human monocytes and Multiple sclerosis.
• Decrease in the numbers of dendritic cells and CD4+ T cells in cerebral perivascular spaces due to natalizumab.
• Bench to bedside: tempering antigen-presenting cells in Multiple sclerosis.
• The immunogenicity of disease-modifying therapies for Multiple sclerosis: clinical implications for neurologists.
• Mechanism of action of glatiramer acetate in treatment of Multiple sclerosis.
• Statins--treatment option for central nervous system autoimmune disease?
• Neuroimmunotherapeutics comes of age.
• Type II monocytes modulate T cell-mediated central nervous system autoimmune disease.
• T effectors outfox T regulators in autoimmunity.
• Simvastatin regulates oligodendroglial process dynamics and survival.
• How to successfully apply animal studies in experimental allergic encephalomyelitis to research on Multiple sclerosis.
• Immunomodulatory synergy by combination of atorvastatin and glatiramer acetate in treatment of CNS autoimmunity.
• Isoprenoids determine Th1/Th2 fate in pathogenic T cells, providing a mechanism of modulation of autoimmunity by atorvastatin.
• Neutralizing antibodies to disease-modifying agents in the treatment of Multiple sclerosis.
• Statins as potential therapeutic agents in Multiple sclerosis.
• Diverse targets for intervention during inflammatory and neurodegenerative phases of Multiple sclerosis.
• The role of the MHC class II transactivator in class II expression and antigen presentation by astrocytes and in susceptibility to central nervous system autoimmune di...
• Cholesterol-lowering statins possess anti-inflammatory activity that might be useful for treatment of MS.
• Cutting edge: oral type I IFN-tau promotes a Th2 bias and enhances suppression of autoimmune encephalomyelitis by oral glatiramer acetate.
• Approved and future pharmacotherapy for Multiple sclerosis.
• Neither T-helper type 2 nor Foxp3+ regulatory T cells are necessary for therapeutic benefit of atorvastatin in treatment of central nervous system autoimmunity.
• T-cell clones specific for myelin basic protein induce chronic relapsing paralysis and demyelination.
• The T lymphocyte in experimental allergic encephalomyelitis.
• Lymphotoxin and tumor necrosis factor-alpha production by myelin basic protein-specific T cell clones correlates with encephalitogenicity.
• Localization of an encephalitogenic epitope for the SJL mouse in the N-terminal region of myelin basic protein.
• Therapy of autoimmune diseases with antibody to immune response gene products or to T-cell surface markers.
• Prevention of experimental encephalomyelitis with peptides that block interaction of T cells with major histocompatibility complex proteins.
• Polymorphic residues on the I-A beta chain modulate the stimulation of T cell clones specific for the N-terminal peptide of the autoantigen myelin basic protein.
• Involvement of distinct murine T-cell receptors in the autoimmune encephalitogenic response to nested epitopes of myelin basic protein.
• Multiple discrete encephalitogenic epitopes of the autoantigen myelin basic protein include a determinant for I-E class II-restricted T cells.
• Characterization of a major encephalitogenic T cell epitope in SJL/J mice with synthetic oligopeptides of myelin basic protein.
• Limited heterogeneity of T cell receptors from lymphocytes mediating autoimmune encephalomyelitis allows specific immune intervention.
• Predominant expression of a T cell receptor V beta gene subfamily in autoimmune encephalomyelitis.
• Comparison of antigen specificity, class II major histocompatibility complex restriction, and in vivo behavior of myelin basic protein-specific T cell lines and clones...
• T cell specificity for class II (I-A) and the encephalitogenic N-terminal epitope of the autoantigen myelin basic protein.
• T-cell epitope of the autoantigen myelin basic protein that induces encephalomyelitis.
• Encephalitogenic T cell clones specific for myelin basic protein. An unusual bias in antigen recognition.
• Single nucleotide polymorphisms in MHC2TA, the gene encoding the MHC class II transactivator (CIITA).
• Malignant glioma cells use MHC class II transactivator (CIITA) promoters III and IV to direct IFN-gamma-inducible CIITA expression and can function as nonprofessional ...
• Requirement for endocytic antigen processing and influence of invariant chain and H-2M deficiencies in CNS autoimmunity.
• Specific immunotherapy: one size does not fit all.
• Pathogenesis, diagnosis, and treatment of acute disseminated encephalomyelitis.
• Highlights from the Fifth International Congress of the International Society of Neuroimmunology.
• Differential expression of B7 co-stimulatory molecules by astrocytes correlates with T cell activation and cytokine production.
• Astrocytes express elements of the class II endocytic pathway and process central nervous system autoantigen for presentation to encephalitogenic T cells.
• Pathogenesis and treatment of central nervous system demyelinating disease.
• Prior exposure to superantigen can inhibit or exacerbate autoimmune encephalomyelitis: T-cell repertoire engaged by the autoantigen determines clinical outcome.
• Effect of oral beta interferon on subsequent immune responsiveness.
• T cell receptor (TCR) usage determines disease susceptibility in experimental autoimmune encephalomyelitis: studies with TCR V beta 8.2 transgenic mice.
• B7-1 and B7-2 costimulatory molecules activate differentially the Th1/Th2 developmental pathways: application to autoimmune disease therapy.
• Reciprocal expression of co-stimulatory molecules, B7-1 and B7-2, on murine T cells following activation.
• ''Lupus-prone'' mice are susceptible to organ-specific autoimmune disease, experimental allergic encephalomyelitis.
• The HMG-CoA reductase inhibitor, atorvastatin, promotes a Th2 bias and reverses paralysis in central nervous system autoimmune disease.
• Transcriptional analysis of targets in Multiple sclerosis.
• The potential therapeutic role of statins in central nervous system autoimmune disorders.
• Statins and their potential targets in Multiple sclerosis therapy.
• Efficient technique for immortalization of murine microglial cells relevant for studies in murine models of Multiple sclerosis.
• Statins as potential therapeutic agents in neuroinflammatory disorders.
• MRI lesion volume heterogeneity in primary progressive MS in relation with axonal damage and brain atrophy.
• [Statins for treatment of CNS diseases. Status report from research and clinical practice].
• Mitoxantrone as a potential therapy for primary progressive Multiple sclerosis.
• Are statins a treatment option for Multiple sclerosis?
• Therapeutic considerations for disease progression in Multiple sclerosis: evidence, experience, and future expectations.
• Evaluation of HMG-CoA reductase inhibitors for Multiple sclerosis: opportunities and obstacles.
• Virtues and pitfalls of EAE for the development of therapies for Multiple sclerosis.
• A neuropeptide in immune-mediated inflammation, Y?
• Statin therapy and autoimmune disease: from protein prenylation to immunomodulation.
• Drug Insight: using statins to treat neuroinflammatory disease.
• Statins in the treatment of central nervous system autoimmune disease.
• Inhibition of naive Th1 CD4+ T cells by glatiramer acetate in Multiple sclerosis.
• Pharmacological treatment of early Multiple sclerosis.
• Spotlight on statins.
• Combination therapies for Multiple sclerosis: scientific rationale, clinical trials, and clinical practice.
• Statins and demyelination.
• Autoimmune demyelinating disease.
• Glatiramer acetate treatment does not modify the clinical course of (NZB x BXSB)F1 lupus murine model.
• Genotype-Phenotype correlations in Multiple sclerosis: HLA genes influence disease severity inferred by 1HMR spectroscopy and MRI measures.

Schools

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• Stanford University

Conditions Treated

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• Headache
• Multiple Sclerosis (MS)

Doctors Specialties

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• Neurology

Accepted Insurances

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Awards

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• CMS Meaningful Use Stage 1 Certification

Education

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• Stanford University School of Medicine

Hospital

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• San Francisco General Hospital and Trauma Center
• UCSF Medical Center

Drug Facts

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NPI NUMBER		1720139348
NPPES Provider LastName		ZAMVIL
NPPES Provider FirstName		SCOTT
NPPES Provider ZIPCode		941430001
NPPES Provider State		CA
Specialty Description		Neurology
Total Claim Count		98.0
Distinct Opioid Count		0.0
Opioid Claim Count		0.0
Percent Opioid Claims		0.0

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Medicare Facts

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National Provider Identifier [NPI]	1720139348
Last Name Of The Provider	ZAMVIL
First Name Of The Provider	SCOTT
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