D-Index & Metrics Best Publications

D-Index & Metrics

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 93 Citations 41,093 184 World Ranking 936 National Ranking 576

Research.com Recognitions

Awards & Achievements

2008 - Fellow of the American Association for the Advancement of Science (AAAS)

1997 - Metlife Foundation Award for Medical Research in Alzheimer's Disease

1997 - Potamkin Prize for Research in Pick's, Alzheimer's, and Related Diseases, American Academy of Neurology

1997 - Sedgwick Memorial Medal, American Public Health Association

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • DNA

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:

  • Gene
  • Enzyme
  • DNA

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.

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.

Best Publications

Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo

David R. Borchelt;Gopal Thinakaran;Christopher B. Eckman;Christopher B. Eckman;Michael K. Lee.
Neuron (1996)

1833 Citations

APP processing and synaptic function.

Flavio Kamenetz;Taisuke Tomita;Helen Hsieh;Helen Hsieh;Guy Seabrook.
Neuron (2003)

1792 Citations

An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria

Philip C Wong;Carlos A Pardo;David R Borchelt;Michael K Lee.
Neuron (1995)

1582 Citations

ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions

L. I. Bruijn;M. W. Becher;M. K. Lee;K. L. Anderson.
Neuron (1997)

1416 Citations

Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins

David R Borchelt;Tamara Ratovitski;Judy van Lare;Michael K Lee.
Neuron (1997)

1410 Citations

Evidence that beta-amyloid protein in Alzheimer's disease is not derived by normal processing.

S. S. Sisodia;E. H. Koo;K. Beyreuther;A. Unterbeck.
Science (1990)

1324 Citations

ENDOPROTEOLYSIS OF PRESENILIN 1 AND ACCUMULATION OF PROCESSED DERIVATIVES IN VIVO

Gopal Thinakaran;David R Borchelt;Michael K Lee;Hilda H Slunt.
Neuron (1996)

1245 Citations

AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss.

Helen Hsieh;Helen Hsieh;Jannic Boehm;Chihiro Sato;Takeshi Iwatsubo.
Neuron (2006)

1133 Citations

Beta-amyloid precursor protein cleavage by a membrane-bound protease.

Sangram S. Sisodia.
Proceedings of the National Academy of Sciences of the United States of America (1992)

1017 Citations

Environmental Enrichment Reduces Aβ Levels and Amyloid Deposition in Transgenic Mice

Orly Lazarov;John Robinson;Ya Ping Tang;Ilana S. Hairston.
Cell (2005)

1015 Citations

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