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Medicine

D-Index
108
Citations
52474
World Ranking
5923
National Ranking
3172

Overview

Gary E. Landreth is affiliated with Indiana University in the United States. Their research primarily focuses on medicine and neuroscience, with significant contributions in neurology, physiology, immunology, molecular biology, and radiology related to brain imaging.

The scientist's work addresses several core topics, including:

  • Neuroinflammation and Neurodegeneration Mechanisms
  • Alzheimer's disease research and treatments
  • Immune cells in cancer
  • Tryptophan and brain disorders
  • Neurological Disease Mechanisms and Treatments
  • Advanced Fluorescence Microscopy Techniques
  • Inflammation biomarkers and pathways

Gary E. Landreth has contributed publications to frequent venues, such as:

  • Alzheimer's & Dementia
  • bioRxiv (Cold Spring Harbor Laboratory)
  • Neurobiology of Disease
  • Research Square (Research Square)
  • Nature Methods

The following are notable recent papers authored or co-authored by Gary E. Landreth, including publication year and venue:

  • Neuroinflammation in Alzheimer disease, 2024, Nature reviews. Immunology
  • Microglia depletion rapidly and reversibly alters amyloid pathology by modification of plaque compaction and morphologies, 2020, Neurobiology of Disease
  • CNS-Native Myeloid Cells Drive Immune Suppression in the Brain Metastatic Niche through Cxcl10, 2020, Cell
  • Three-dimensional nanoscopy of whole cells and tissues with in situ point spread function retrieval, 2020, Nature Methods
  • INPP5D expression is associated with risk for Alzheimer's disease and induced by plaque-associated microglia, 2021, Neurobiology of Disease

Frequent collaborators include:

  • Adrian L. Oblak
  • Andy P. Tsai
  • Peter Bor-Chian Lin
  • Bruce T. Lamb
  • Miguel Moutinho

Best Publications

  • Neuroinflammation in Alzheimer's disease

    Michael T Heneka;Monica J Carson;Joseph El Khoury;Gary E Landreth

  • Inflammation and Alzheimer's disease.

    H Akiyama;S Barger;S Barnum;B Bradt

  • ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models.

    Paige E. Cramer;John R. Cirrito;Daniel W. Wesson;Daniel W. Wesson;C. Y. Daniel Lee

  • ApoE Promotes the Proteolytic Degradation of Aβ

    Qingguang Jiang;C.Y. Daniel Lee;Shweta Mandrekar;Brandy Wilkinson

  • β-Amyloid Stimulation of Microglia and Monocytes Results in TNFα-Dependent Expression of Inducible Nitric Oxide Synthase and Neuronal Apoptosis

    Colin K. Combs;J. Colleen Karlo;Shih Chu Kao;Gary E. Landreth

  • Inflammatory Mechanisms in Alzheimer's Disease: Inhibition of β-Amyloid-Stimulated Proinflammatory Responses and Neurotoxicity by PPARγ Agonists

    Colin K. Combs;Derrick E. Johnson;J. Colleen Karlo;Steven B. Cannady

  • The National Alzheimer's Coordinating Center (NACC) database: the Uniform Data Set.

    Duane L. Beekly;Erin M. Ramos;William W. Lee;Woodrow D. Deitrich

  • Cellular and Molecular Mechanisms of Glial Scarring and Progressive Cavitation: In Vivo and In Vitro Analysis of Inflammation-Induced Secondary Injury after CNS Trauma

    Michael T. Fitch;Catherine Doller;Colin K. Combs;Gary E. Landreth

  • A Cell Surface Receptor Complex for Fibrillar β-Amyloid Mediates Microglial Activation

    Maria E. Bamberger;Meera E. Harris;Douglas R. McDonald;Jens Husemann

  • Acute treatment with the PPARγ agonist pioglitazone and ibuprofen reduces glial inflammation and Aβ1–42 levels in APPV717I transgenic mice

    Michael T Heneka;Magdalena Sastre;Lucia Dumitrescu-Ozimek;Anne Hanke

  • TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models

    Taylor R. Jay;Crystal M Miller;Paul J Cheng;Leah C Graham

  • The role of microglia in amyloid clearance from the AD brain.

    C. Y. Daniel Lee;Gary E. Landreth

  • Anti-Inflammatory Drug Therapy Alters β-Amyloid Processing and Deposition in an Animal Model of Alzheimer's Disease

    Qiao Yan;Jianhua Zhang;Hantao Liu;Safura Babu-Khan

  • CD14 and Toll-Like Receptors 2 and 4 Are Required for Fibrillar Aβ-Stimulated Microglial Activation

    Erin G. Reed-Geaghan;Julie C. Savage;Amy G. Hise;Gary E. Landreth

  • Microglial Phagocytosis Induced by Fibrillar β-Amyloid and IgGs Are Differentially Regulated by Proinflammatory Cytokines

    Jessica Koenigsknecht-Talboo;Gary E. Landreth

  • A Toll-like receptor 2 ligand stimulates Th2 responses in vivo, via induction of extracellular signal-regulated kinase mitogen-activated protein kinase and c-Fos in dendritic cells.

    Stephanie Dillon;Anshu Agrawal;Thomas Van Dyke;Gary Landreth

  • Antineoplastic effects of peroxisome proliferatoractivated receptor γ agonists

    Christian Grommes;Gary E Landreth;Michael T Heneka

  • Microglial Phagocytosis of Fibrillar β-Amyloid through a β1 Integrin-Dependent Mechanism

    Jessica Koenigsknecht;Gary Landreth

  • Inflammation, microglia, and Alzheimer's disease.

    Brent Cameron;Gary E. Landreth

  • Identification of Microglial Signal Transduction Pathways Mediating a Neurotoxic Response to Amyloidogenic Fragments of β-Amyloid and Prion Proteins

    Colin K. Combs;Derrick E. Johnson;Steve B. Cannady;Timothy M. Lehman

Frequent Co-Authors

Bruce T. Lamb
Bruce T. Lamb Indiana University
Michael T. Heneka
Michael T. Heneka University Hospital Bonn
Richard M. Ransohoff
Richard M. Ransohoff Harvard University
Douglas L. Feinstein
Douglas L. Feinstein University of Illinois at Chicago
Jari Koistinaho
Jari Koistinaho University of Helsinki
Jerry Silver
Jerry Silver Case Western Reserve University
Daniel W. Wesson
Daniel W. Wesson University of Florida
Donald A. Wilson
Donald A. Wilson Nathan Kline Institute for Psychiatric Research
Yunlong Liu
Yunlong Liu Indiana University
David M. Holtzman
David M. Holtzman Washington University in St. Louis

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