What is he best known for?
The fields of study he is best known for:
His primary scientific interests are in Amyotrophic lateral sclerosis, Cell biology, Neuroscience, SOD1 and Molecular biology.
His Amyotrophic lateral sclerosis study integrates concerns from other disciplines, such as Genetically modified mouse, Transgene, Mutation, Anatomy and Motor neuron.
His studies examine the connections between Genetically modified mouse and genetics, as well as such issues in Pathology, with regards to Astrogliosis.
His studies deal with areas such as Cyclin-dependent kinase and Intermediate filament, Cytoskeleton as well as Cell biology.
His Neuroscience research includes elements of Innate immune system, Neurodegeneration and Microglia.
His SOD1 study introduces a deeper knowledge of Superoxide dismutase.
His most cited work include:
- Bone Marrow-Derived Microglia Play a Critical Role in Restricting Senile Plaque Formation in Alzheimer's Disease (958 citations)
- Wild-type nonneuronal cells extend survival of SOD1 mutant motor neurons in ALS mice. (952 citations)
- Innate immunity: the missing link in neuroprotection and neurodegeneration? (605 citations)
What are the main themes of his work throughout his whole career to date?
His primary areas of study are Amyotrophic lateral sclerosis, Genetically modified mouse, Cell biology, SOD1 and Molecular biology.
His Amyotrophic lateral sclerosis study combines topics in areas such as Motor neuron, Neuroscience, Immunology and Neurodegeneration.
In Motor neuron, Jean-Pierre Julien works on issues like Anatomy, which are connected to Degenerative disease.
Jean-Pierre Julien interconnects Peripherin, Neuroinflammation, Microglia and Pathogenesis in the investigation of issues within Genetically modified mouse.
His research in Cell biology focuses on subjects like Protein subunit, which are connected to Phosphorylation.
He usually deals with SOD1 and limits it to topics linked to Antibody and Disease.
He most often published in these fields:
- Amyotrophic lateral sclerosis (42.02%)
- Genetically modified mouse (31.51%)
- Cell biology (30.25%)
What were the highlights of his more recent work (between 2013-2021)?
- Amyotrophic lateral sclerosis (42.02%)
- Genetically modified mouse (31.51%)
- Cell biology (30.25%)
In recent papers he was focusing on the following fields of study:
The scientist’s investigation covers issues in Amyotrophic lateral sclerosis, Genetically modified mouse, Cell biology, SOD1 and Pathology.
His Amyotrophic lateral sclerosis research is within the category of Disease.
His research integrates issues of Inflammation and Gliosis in his study of Genetically modified mouse.
His biological study spans a wide range of topics, including Intermediate filament, Cytoskeleton, Mutant and Mitochondrial DNA.
His SOD1 study necessitates a more in-depth grasp of Superoxide dismutase.
His studies in Superoxide dismutase integrate themes in fields like Immunology and Neuroprotection.
Between 2013 and 2021, his most popular works were:
- Exosome secretion is a key pathway for clearance of pathological TDP-43. (133 citations)
- The Src/c-Abl pathway is a potential therapeutic target in amyotrophic lateral sclerosis (104 citations)
- Adeno-associated virus-mediated delivery of a recombinant single-chain antibody against misfolded superoxide dismutase for treatment of amyotrophic lateral sclerosis (85 citations)
In his most recent research, the most cited papers focused on:
Jean-Pierre Julien mainly investigates Amyotrophic lateral sclerosis, SOD1, Immunology, Neuroscience and UBQLN2.
His research in Amyotrophic lateral sclerosis intersects with topics in Protein aggregation, Neurodegeneration, Molecular biology, Neuroinflammation and Neuromuscular junction.
His study on SOD1 is covered under Pathology.
His study brings together the fields of Superoxide dismutase and Immunology.
His Superoxide dismutase course of study focuses on Heat shock protein and Genetically modified mouse.
The study incorporates disciplines such as Frontotemporal lobar degeneration, Microglia and Cell biology in addition to Lipopolysaccharide.
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