S
Sangram S. Sisodia
Researcher at University of Chicago
Publications - 260
Citations - 41379
Sangram S. Sisodia is an academic researcher from University of Chicago. The author has contributed to research in topics: Presenilin & Amyloid precursor protein. The author has an hindex of 97, co-authored 253 publications receiving 39419 citations. Previous affiliations of Sangram S. Sisodia include Heidelberg University & Howard Hughes Medical Institute.
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Journal ArticleDOI
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,Frances Davenport,Tamara Ratovitsky,Cristian Mihail Prada,Grace Kim,Sophia Seekins,Debra Yager,Hilda H. Slunt,Rong Wang,Mary Seeger,Allan I. Levey,Sam Gandy,Neal G. Copeland,Nancy A. Jenkins,Donald L. Price,Steven G. Younkin,Steven G. Younkin,Sangram S. Sisodia +21 more
TL;DR: These studies provide compelling support for the view that one mechanism by which these mutant PS1 cause AD is by increasing the extracellular concentration of Abeta peptides terminating at 42(43), species that foster Abeta deposition.
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APP processing and synaptic function.
Flavio Kamenetz,Taisuke Tomita,Helen Hsieh,Helen Hsieh,Guy R. Seabrook,David R. Borchelt,Takeshi Iwatsubo,Sangram S. Sisodia,Roberto Malinow,Roberto Malinow +9 more
TL;DR: It is shown that neuronal activity modulates the formation and secretion of Abeta peptides in hippocampal slice neurons that overexpress APP, and it is proposed that activity-dependent modulation of endogenous Abeta production may normally participate in a negative feedback that could keep neuronal hyperactivity in check.
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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,Neal G. Copeland,Nancy A. Jenkins,Sangram S. Sisodia,Don W. Cleveland,Don W. Cleveland,Donald L. Price +9 more
TL;DR: Mutations in Cu/Zn superoxide dismutase cause a subset of cases of familial amyotrophic lateral sclerosis, and four lines of mice accumulating one of these mutant proteins (G37R) develop severe, progressive motor neuron disease.
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ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions
Lucie Bruijn,Mark W. Becher,Michael K. Lee,K. L. Anderson,Nancy A. Jenkins,Neal G. Copeland,Sangram S. Sisodia,Jeffrey D. Rothstein,David R. Borchelt,Donald L. Price,Don W. Cleveland +10 more
TL;DR: It is reported here that even low levels of another mutant, G85R, cause motor neuron disease characterized by an extremely rapid clinical progression, without changes in SOD1 activity.
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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,Vicki Gonzales,Nancy A. Jenkins,Neal G. Copeland,Donald L. Price,Sangram S. Sisodia +8 more
TL;DR: Transgenic animals that coexpress a FAD-linked human PS1 variant (A246E) and a chimeric mouse/human APP harboring mutations linked to Swedish FAD kindreds (APP swe) develop numerous amyloid deposits much earlier than age-matched mice expressing APP swe and wild-type Hu PS1 or APP swe alone.