What is he best known for?
The fields of study he is best known for:
His primary scientific interests are in Amyloid precursor protein, Molecular biology, Presenilin, Cell biology and Neuroscience.
His Amyloid precursor protein study is concerned with Alzheimer's disease in general.
The Molecular biology study combines topics in areas such as Complementary DNA, Messenger RNA, Gene, Transfection and Epitope.
His research integrates issues of Genetics and Transgene in his study of Presenilin.
Sangram S. Sisodia combines subjects such as Secretion, Amyotrophic lateral sclerosis, Mutant, SOD1 and Amyloid with his study of Cell biology.
The concepts of his Neuroscience study are interwoven with issues in Ion channel linked receptors and Disease.
His most cited work include:
- Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo (1356 citations)
- APP processing and synaptic function. (1315 citations)
- An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria (1271 citations)
What are the main themes of his work throughout his whole career to date?
Sangram S. Sisodia focuses on Presenilin, Cell biology, Neuroscience, Amyloid precursor protein and Biochemistry.
Sangram S. Sisodia has included themes like Amyloid precursor protein secretase, Transgene, Mutant, Molecular biology and Membrane protein in his Presenilin study.
His Cell biology research is multidisciplinary, relying on both Receptor, In vitro, Cell culture and Secretion.
His study in Neuroscience is interdisciplinary in nature, drawing from both Alzheimer's disease, Dementia and Disease.
His study in Amyloid precursor protein is interdisciplinary in nature, drawing from both Senile plaques and Amyloid.
His research in Biochemistry tackles topics such as APH-1 which are related to areas like PEN-2 and Gamma-secretase complex.
He most often published in these fields:
- Presenilin (33.45%)
- Cell biology (29.01%)
- Neuroscience (27.30%)
What were the highlights of his more recent work (between 2009-2021)?
- Presenilin (33.45%)
- Biochemistry (19.80%)
- Cell biology (29.01%)
In recent papers he was focusing on the following fields of study:
Sangram S. Sisodia mostly deals with Presenilin, Biochemistry, Cell biology, Amyloid precursor protein secretase and Neuroscience.
His research in Presenilin intersects with topics in Neurogenesis, Wild type, Mutant and Transgene.
Within one scientific family, Sangram S. Sisodia focuses on topics pertaining to APH-1 under Biochemistry, and may sometimes address concerns connected to Biophysics.
He has included themes like Mutation, RNA, Genetically modified mouse and Zebrafish in his Cell biology study.
He is exploring Amyloid precursor protein secretase as part of his Amyloid precursor protein and Alzheimer's disease and Amyloid precursor protein secretase studies.
His Neuroscience research includes elements of Metaplasticity, Synaptic scaling and Neurodegeneration.
Between 2009 and 2021, his most popular works were:
- Trafficking and Proteolytic Processing of APP (620 citations)
- Heterogeneity of CNS myeloid cells and their roles in neurodegeneration (470 citations)
- Amyloid beta from axons and dendrites reduces local spine number and plasticity (251 citations)
In his most recent research, the most cited papers focused on:
His primary areas of investigation include Presenilin, Amyloid precursor protein secretase, Alzheimer's disease, Amyloidosis and Neuroscience.
His Presenilin research is multidisciplinary, incorporating perspectives in Biochemistry, Transgene and Cell biology.
His work investigates the relationship between Biochemistry and topics such as APH-1 that intersect with problems in BACE1-AS, Biochemistry of Alzheimer's disease and P3 peptide.
His Amyloid precursor protein secretase study results in a more complete grasp of Amyloid precursor protein.
His Amyloid precursor protein study integrates concerns from other disciplines, such as Phenotype and Transgenic Model.
His study looks at the intersection of Alzheimer's disease and topics like Receptor with Genetically modified mouse, Intracellular, Molecular biology, Senile plaques and Plasma protein binding.
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