His primary areas of investigation include Microglia, Inflammation, Cell biology, Internal medicine and Alzheimer's disease. His Microglia research is multidisciplinary, incorporating elements of Proinflammatory cytokine, Receptor, Phagocytosis and Neuroscience. The study incorporates disciplines such as Neuroprotection and Pathology in addition to Inflammation.
His work in Cell biology addresses issues such as Senile plaques, which are connected to fields such as Coated vesicle. His work in Internal medicine tackles topics such as Endocrinology which are related to areas like Peroxisome proliferator-activated receptor. Gary E. Landreth combines subjects such as Apolipoprotein E, Neurodegeneration and Amyloid with his study of Alzheimer's disease.
Gary E. Landreth mainly investigates Neuroscience, Microglia, Cell biology, Disease and Internal medicine. His research integrates issues of TREM2, Neurodegeneration and MAPK/ERK pathway in his study of Neuroscience. His biological study spans a wide range of topics, including Alzheimer's disease, Receptor and Amyloid.
Gary E. Landreth has researched Alzheimer's disease in several fields, including Apolipoprotein E and Amyloid beta. His work on Signal transduction, Phosphorylation and Tyrosine kinase as part of his general Cell biology study is frequently connected to Cellular differentiation, thereby bridging the divide between different branches of science. His research in Internal medicine intersects with topics in Endocrinology and Pioglitazone.
Gary E. Landreth focuses on Neuroscience, Microglia, Neuroinflammation, TREM2 and Cognitive decline. His work in the fields of Neuroscience, such as Hippocampus, overlaps with other areas such as Autism. His Microglia research integrates issues from Receptor, Immune system and Amyloid.
The various areas that Gary E. Landreth examines in his Neuroinflammation study include Agonist, Alzheimer's disease, Pharmacology and Pathogenesis. The Agonist study combines topics in areas such as Cerebral arteries, Apolipoprotein E, Proinflammatory cytokine and Ischemia. His Inflammation study combines topics from a wide range of disciplines, such as Phagocytosis, Extracellular, Secretion, Neuroprotection and Pathology.
His primary scientific interests are in Neuroscience, TREM2, Microscopy, Autism and MAPK/ERK pathway. His study in Neuroscience is interdisciplinary in nature, drawing from both Receptor and Microglia. His TREM2 research includes themes of Neuroinflammation and Neurodegeneration.
His Microscopy study combines topics in areas such as Single Molecule Imaging, Point spread, Optical phenomena and Adaptive optics. His Autism investigation overlaps with Kinase, Neurogenesis, Intellectual disability, Copy-number variation and Chromosomal Deletion. His MAPK/ERK pathway research is multidisciplinary, incorporating perspectives in Mitogen-activated protein kinase, Corticogenesis, Central nervous system and Intracellular.
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Inflammation and Alzheimer's disease.
H Akiyama;S Barger;S Barnum;B Bradt.
Neurobiology of Aging (2000)
Neuroinflammation in Alzheimer's disease
Michael T Heneka;Monica J Carson;Joseph El Khoury;Gary E Landreth.
Lancet Neurology (2015)
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.
The Journal of Neuroscience (2001)
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 Journal of Neuroscience (2000)
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.
The Journal of Neuroscience (1999)
A Cell Surface Receptor Complex for Fibrillar β-Amyloid Mediates Microglial Activation
Maria E. Bamberger;Meera E. Harris;Douglas R. McDonald;Jens Husemann.
The Journal of Neuroscience (2003)
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.
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.
The Journal of Neuroscience (2003)
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