What is he best known for?
The fields of study he is best known for:
- Gene
- Neuron
- Internal medicine
Lynn A. Raymond mainly focuses on Neuroscience, Excitotoxicity, NMDA receptor, Huntingtin and Glutamate receptor.
His Neuroscience study integrates concerns from other disciplines, such as Synaptic plasticity, Huntington's disease and Neurotransmission.
His Excitotoxicity research is within the category of Internal medicine.
His studies deal with areas such as Biophysics, Programmed cell death and Endocrinology as well as NMDA receptor.
Lynn A. Raymond has researched Huntingtin in several fields, including Molecular biology, Neurodegeneration, Neuroprotection and Cell biology.
His biological study spans a wide range of topics, including Biochemistry, Mutant and Polyglutamine tract.
His most cited work include:
- Cleavage at the caspase-6 site is required for neuronal dysfunction and degeneration due to mutant huntingtin. (562 citations)
- Increased sensitivity to N-methyl-D-aspartate receptor-mediated excitotoxicity in a mouse model of Huntington's disease. (551 citations)
- A Calcium-Dependent Feedback Mechanism Participates in Shaping Single NMDA Miniature EPSCs (423 citations)
What are the main themes of his work throughout his whole career to date?
Lynn A. Raymond focuses on Neuroscience, NMDA receptor, Huntingtin, Excitotoxicity and Huntington's disease.
The concepts of his Neuroscience study are interwoven with issues in Glutamate receptor and Synaptic plasticity.
The NMDA receptor study combines topics in areas such as Endocrinology and Programmed cell death.
His Huntingtin research integrates issues from Molecular biology, Genetically modified mouse, Neurodegeneration and Cell biology.
His Excitotoxicity study integrates concerns from other disciplines, such as Electrophysiology, Neuroprotection and Protein kinase A.
Lynn A. Raymond has included themes like Clinical trial, Endocannabinoid system and Pathogenesis in his Huntington's disease study.
He most often published in these fields:
- Neuroscience (48.85%)
- NMDA receptor (31.30%)
- Huntingtin (31.30%)
What were the highlights of his more recent work (between 2017-2021)?
- Neuroscience (48.85%)
- Excitatory postsynaptic potential (16.03%)
- Glutamate receptor (26.72%)
In recent papers he was focusing on the following fields of study:
His main research concerns Neuroscience, Excitatory postsynaptic potential, Glutamate receptor, Huntington's disease and Synapse.
His Neuroscience study incorporates themes from NMDA receptor and Neurodegeneration, Disease.
Lynn A. Raymond studies Excitotoxicity which is a part of NMDA receptor.
His research in Excitatory postsynaptic potential intersects with topics in Synaptic plasticity, AMPA receptor and Cell biology.
He combines subjects such as Endoplasmic reticulum and Neurotransmission with his study of Glutamate receptor.
His Huntington's disease study combines topics in areas such as Wild type, Mutant and Patch clamp.
Between 2017 and 2021, his most popular works were:
- Huntingtin suppression restores cognitive function in a mouse model of Huntington’s disease (44 citations)
- Alterations in synaptic function and plasticity in Huntington disease. (31 citations)
- Impairment and Restoration of Homeostatic Plasticity in Cultured Cortical Neurons From a Mouse Model of Huntington Disease. (19 citations)
In his most recent research, the most cited papers focused on:
- Gene
- Neuron
- Internal medicine
His primary areas of study are Neuroscience, Huntington's disease, Glutamate receptor, AMPA receptor and Synaptic plasticity.
His research integrates issues of Mutation, Neurodegeneration and Synaptic scaling in his study of Neuroscience.
His Mutation research is multidisciplinary, incorporating elements of Huntingtin, Mutant, Limbic system, Disease and Cortex.
The study incorporates disciplines such as Neurochemical, Hippocampus, Neurotransmission and Dopamine in addition to Glutamate receptor.
His AMPA receptor study frequently draws connections between adjacent fields such as Excitatory postsynaptic potential.
His study in Gliosis is interdisciplinary in nature, drawing from both Synapse, Synaptic cleft and Postsynaptic density.
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