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Medicine

D-Index
79
Citations
20140
World Ranking
17688
National Ranking
8828

Overview

Ann B. Moser is affiliated with the Kennedy Krieger Institute in the United States. Their research primarily focuses on biochemistry, genetics, and molecular biology, with significant contributions in medicine. The scientist's work spans subfields including molecular biology, physiology, clinical biochemistry, nutrition and dietetics, as well as endocrinology, diabetes, and metabolism.

Themes central to their research include peroxisome proliferator-activated receptors, metabolism and genetic disorders, adipose tissue and metabolism, vitamin K research studies, adrenal hormones and disorders, sphingolipid metabolism and signaling, and mitochondrial function and pathology.

Ann B. Moser has published extensively, with several relevant papers in recent years. These include:

  • X-linked adrenoleukodystrophy: Pathology, pathophysiology, diagnostic testing, newborn screening and therapies (2020), published in International Journal of Developmental Neuroscience
  • Loss- or Gain-of-Function Mutations in ACOX1 Cause Axonal Loss via Different Mechanisms (2020), published in Neuron
  • International Recommendations for the Diagnosis and Management of Patients With Adrenoleukodystrophy (2022), published in Neurology
  • MRI surveillance of boys with X-linked adrenoleukodystrophy identified by newborn screening: Meta-analysis and consensus guidelines (2020), published in Journal of Inherited Metabolic Disease
  • Nervonic Acid Attenuates Accumulation of Very Long-Chain Fatty Acids and is a Potential Therapy for Adrenoleukodystrophy (2022), published in Neurotherapeutics

The scientist has collaborated frequently with other researchers, including Nancy Braverman, Ali Fatemi, Gerald V. Raymond, Paul A. Watkins, and Florian Eichler. These collaborations have contributed to multiple studies and enhanced the scope of Moser's research.

Their published work appears regularly in several scientific venues, with recurring contributions to Neurotherapeutics, Annals of Neurology, bioRxiv (Cold Spring Harbor Laboratory), Molecular Genetics and Metabolism, and Genetics in Medicine Open.

Best Publications

  • Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease

    Zhiping Li;Shiqi Yang;Huizhi Lin;Jiawen Huang

  • Functions of plasmalogen lipids in health and disease.

    Nancy E. Braverman;Ann B. Moser

  • Peroxisome biogenesis disorders.

    Steven J. Steinberg;Gabriele Dodt;Gerald V. Raymond;Nancy E. Braverman

  • Mutations in the PTS1 receptor gene, PXR1, define complementation group 2 of the peroxisome biogenesis disorders

    Gabriele Dodt;Nancy Braverman;Candice Wong;Ann Moser

  • Human PEX7 encodes the peroxisomal PTS2 receptor and is responsible for rhizomelic chondrodysplasia punctata.

    Nancy Braverman;Gary Steel;Cassandra Obie;Ann Moser

  • Adrenoleukodystrophy Increased plasma content of saturated very long chain fatty acids

    Hugo W. Moser;Hugo W. Moser;Ann B. Moser;Karen K. Frayer;Winston Chen

  • Adrenoleukodystrophy: Incidence, new mutation rate, and results of extended family screening

    Lena Bezman;Ann B. Moser;Gerald V. Raymond;Piero Rinaldo

  • Plasma very long chain fatty acids in 3,000 peroxisome disease patients and 29,000 controls

    Ann B. Moser;Nancy Kreiter;Lena Bezman;Shou en Lu

  • Adrenoleukodystrophy: evidence for X linkage, inactivation, and selection favoring the mutant allele in heterozygous cells

    Barbara R. Migeon;Hugo W. Moser;Ann B. Moser;Joyce Axelman

  • A mouse model for X-linked adrenoleukodystrophy

    Jyh Feng Lu;Ann M. Lawler;Paul A. Watkins;James M. Powers

  • Hepatocyte transplantation in a 4-year-old girl with peroxisomal biogenesis disease: technique, safety, and metabolic follow-up.

    Etienne M. Sokal;Françoise Smets;Annick Bourgois;Lionel Van Maldergem

  • Mutations in the gene encoding 3β-hydroxysteroid-Δ8,Δ7-isomerase cause X-linked dominant Conradi-Hunermann syndrome

    Nancy Braverman;Paul Lin;Fabian F. Moebius;Cassandra Obie

  • Gene redundancy and pharmacological gene therapy: Implications for X-linked adrenoleukodystrophy

    Stephan Kemp;He Ming Wei;Jyh Feng Lu;Lelita T. Braiterman

  • Follow-up of 89 Asymptomatic Patients With Adrenoleukodystrophy Treated With Lorenzo's Oil

    Hugo W. Moser;Hugo W. Moser;Gerald V. Raymond;Shou En Lu;Larry R. Muenz

  • The inflammatory myelinopathy of adreno-leukodystrophy: cells, effector molecules, and pathogenetic implications.

    James M. Powers;Yan Liu;Ann B. Moser;Hugo W. Moser

  • Adrenoleukodystrophy: phenotypic variability and implications for therapy.

    H. W. Moser;A. B. Moser;K. D. Smith;A. Bergin

  • Phenotype of patients with peroxisomal disorders subdivided into sixteen complementation groups

    Ann B. Moser;Magnhild Rasmussen;Sakkubai Naidu;Paul A. Watkins

  • Neonatal adrenoleukodystrophy: new cases, biochemical studies, and differentiation from Zellweger and related peroxisomal polydystrophy syndromes

    R. I. Kelley;N. S. Datta;W. B. Dobyns;A. K. Hajra

  • Peroxisome biogenesis disorders in the Zellweger spectrum: An overview of current diagnosis, clinical manifestations, and treatment guidelines.

    Nancy E. Braverman;Gerald V. Raymond;William B. Rizzo;Ann B. Moser

  • Cerebral X-linked adrenoleukodystrophy in a girl with Xq27-Ter deletion.

    Eli Hershkovitz;Ginat Narkis;Zamir Shorer;Ann B. Moser

Frequent Co-Authors

Hugo W. Moser
Hugo W. Moser Kennedy Krieger Institute
Paul A. Watkins
Paul A. Watkins Kennedy Krieger Institute
Erik G. Puffenberger
Erik G. Puffenberger Clinic for Special Children
Michael F. Wangler
Michael F. Wangler Baylor College of Medicine
Richard I. Kelley
Richard I. Kelley Kennedy Krieger Institute
David Valle
David Valle Johns Hopkins University School of Medicine
Stephen Jay Gould
Stephen Jay Gould Harvard University
Aurora Pujol
Aurora Pujol Institut d'Investigació Biomédica de Bellvitge
Ronald J.A. Wanders
Ronald J.A. Wanders University of Amsterdam
Amiya K. Hajra
Amiya K. Hajra University of Michigan–Ann Arbor

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