2008 - Fellow of the American Association for the Advancement of Science (AAAS)
1997 - Potamkin Prize for Research in Pick's, Alzheimer's, and Related Diseases, American Academy of Neurology
1997 - Metlife Foundation Award for Medical Research in Alzheimer's Disease
1997 - Sedgwick Memorial Medal, American Public Health Association
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.
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.
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.
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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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.
APP processing and synaptic function.
Flavio Kamenetz;Taisuke Tomita;Helen Hsieh;Helen Hsieh;Guy Seabrook.
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.
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.
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.
ENDOPROTEOLYSIS OF PRESENILIN 1 AND ACCUMULATION OF PROCESSED DERIVATIVES IN VIVO
Gopal Thinakaran;David R Borchelt;Michael K Lee;Hilda H Slunt.
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.
AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss.
Helen Hsieh;Jannic Boehm;Chihiro Sato;Takeshi Iwatsubo.
Environmental Enrichment Reduces Aβ Levels and Amyloid Deposition in Transgenic Mice
Orly Lazarov;John Robinson;Ya Ping Tang;Ilana S. Hairston.
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)
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