2010 - Fellow of the American Association for the Advancement of Science (AAAS)
Mark P. Mattson mainly focuses on Internal medicine, Endocrinology, Cell biology, Neuroscience and Oxidative stress. In his research, Growth cone is intimately related to Neuron, which falls under the overarching field of Internal medicine. His work carried out in the field of Endocrinology brings together such families of science as Ryanodine receptor, Genetically modified mouse and Neurodegeneration.
He interconnects Excitotoxicity, Apoptosis and Programmed cell death in the investigation of issues within Cell biology. His Neuroscience research is multidisciplinary, incorporating perspectives in Glutamate receptor, Neurotrophic factors and Alzheimer's disease. His Oxidative stress study incorporates themes from Molecular biology, Ceramide, Homocysteine and Reactive oxygen species.
Mark P. Mattson spends much of his time researching Neuroscience, Internal medicine, Cell biology, Endocrinology and Glutamate receptor. His Neuroscience research is multidisciplinary, incorporating elements of Synaptic plasticity and Neurotrophic factors. His studies in Neurotrophic factors integrate themes in fields like Neurogenesis and Neurotrophin.
His Cell biology research includes themes of Apoptosis, Biochemistry and Programmed cell death. The study incorporates disciplines such as Alzheimer's disease, Calcium, Neuroprotection and Amyloid in addition to Endocrinology. His Glutamate receptor study integrates concerns from other disciplines, such as NMDA receptor, Neurotoxicity and Neuron.
Mark P. Mattson focuses on Neuroscience, Internal medicine, Endocrinology, Cell biology and Disease. His Neuroscience study deals with Synaptic plasticity intersecting with Long-term potentiation. Specifically, his work in Endocrinology is concerned with the study of Oxidative stress.
Mark P. Mattson studies Mitochondrion which is a part of Cell biology. As a member of one scientific family, Mark P. Mattson mostly works in the field of Mitochondrion, focusing on Neurodegeneration and, on occasion, Neuroprotection. As a part of the same scientific study, he usually deals with the Neuroplasticity, concentrating on Neurogenesis and frequently concerns with Neural stem cell and Glutamate receptor.
The scientist’s investigation covers issues in Neuroscience, Cell biology, Disease, Mitophagy and Internal medicine. His Neuroscience research is multidisciplinary, relying on both Synaptic plasticity, Bioenergetics and Neurodegeneration. Mark P. Mattson has included themes like Cell, Neuroinflammation, DNA repair and NAD+ kinase in his Cell biology study.
His Mitophagy study also includes
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
Daniel J. Klionsky;Kotb Abdelmohsen;Akihisa Abe;Joynal Abedin.
Autophagy (2016)
Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
Daniel J. Klionsky;Kotb Abdelmohsen;Akihisa Abe;Joynal Abedin.
Autophagy (2016)
Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction
Salvatore Oddo;Antonella Caccamo;Jason D. Shepherd;M. Paul Murphy.
Neuron (2003)
Pathways towards and away from Alzheimer's disease
Mark P. Mattson.
Nature (2004)
beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity
Mark P. Mattson;Bin Cheng;Dave Davis;Karin Bryant.
The Journal of Neuroscience (1992)
Apoptosis in neurodegenerative disorders.
Mark P. Mattson.
Nature Reviews Molecular Cell Biology (2000)
Self-Propagating, Molecular-Level Polymorphism in Alzheimer's {beta}-Amyloid Fibrils
Aneta T. Petkova;Richard D. Leapman;Zhihong Guo;Wai Ming Yau.
Science (2005)
A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease.
K Hensley;J M Carney;M P Mattson;M Aksenova.
Proceedings of the National Academy of Sciences of the United States of America (1994)
Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives
Mark P. Mattson.
Physiological Reviews (1997)
Mitochondrial Manganese Superoxide Dismutase Prevents Neural Apoptosis and Reduces Ischemic Brain Injury: Suppression of Peroxynitrite Production, Lipid Peroxidation, and Mitochondrial Dysfunction
Jeffrey N. Keller;Mark S. Kindy;Fredrick W. Holtsberg;Daret K. St. Clair.
The Journal of Neuroscience (1998)
Profile was last updated on December 6th, 2021.
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