Sotabase

Career

· Teaching Experience, MIT Department of Chemistry2012–
· BSE in Electrical and Biomedical Engineering, Duke University
· Master in Supply Chain Management, Massachusetts Institute of Technology
· Master's in Physics, Massachusetts Institute of Technology
· PhD Candidate in Biomaterials, Nanotechnology, Chemical Engineering, Massachusetts Institute of Technology
· PhD in Chemical Engineering, Massachusetts Institute of Technology
· PhD in Cognitive Science, Massachusetts Institute of Technology
· PhD in Physics, Massachusetts Institute of Technology
· Postdoctoral Researcher, MIT Department of Brain and Cognitive Sciences
· Graduate Student, MIT Department of Chemistry
· Intelligence Observatory Research Scientist, MIT Quest for Intelligence

Publications (192)

An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria
Neuron · 1995
1,517
cited
Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo
Neuron · 1996
1,470
cited
Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase
2004
1,399
cited
ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions
Neuron · 1997
1,361
cited
Endoproteolysis of Presenilin 1 and Accumulation of Processed Derivatives In Vivo
Neuron · 1996
1,069
cited
Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins
Neuron · 1997
1,063
cited
Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase.
Human Molecular Genetics · 2004
790
cited
Altered Reactivity of Superoxide Dismutase in Familial Amyotrophic Lateral Sclerosis
Science · 1996
746
cited
Human α-synuclein-harboring familial Parkinson's disease-linked Ala-53 → Thr mutation causes neurodegenerative disease with α-synuclein aggregation in transgenic mice
Proceedings of the National Academy of Sciences of the United States of America · 2002
738
cited
Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity.
Proceedings of the National Academy of Sciences of the United States of America · 1994
632
cited
Age-Dependent Emergence and Progression of a Tauopathy in Transgenic Mice Overexpressing the Shortest Human Tau Isoform
Neuron · 1999
589
cited
Parkinson's Disease α-Synuclein Transgenic Mice Develop Neuronal Mitochondrial Degeneration and Cell Death
Journal of Neuroscience · 2006
563
cited
Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations.
Proceedings of the National Academy of Sciences of the United States of America · 2005
468
cited
Lysine 63-linked ubiquitination promotes the formation and autophagic clearance of protein inclusions associated with neurodegenerative diseases.
Human Molecular Genetics · 2008
461
cited
Neurofilaments are obligate heteropolymers in vivo
Journal of Cell Biology · 1993
408
cited
A mutant neurofilament subunit causes massive, selective motor neuron death: Implications for the pathogenesis of human motor neuron disease
Neuron · 1994
390
cited
Assessment of normal and mutant human presenilin function in Caenorhabditis elegans.
Proceedings of the National Academy of Sciences of the United States of America · 1996
390
cited
Human alpha-synuclein-harboring familial Parkinson's disease-linked Ala-53 --> Thr mutation causes neurodegenerative disease with alpha-synuclein aggregation in transgenic mice.
Proceedings of the National Academy of Sciences of the United States of America · 2002
366
cited
Mutations associated with amyotrophic lateral sclerosis convert superoxide dismutase from an antiapoptotic gene to a proapoptotic gene: studies in yeast and neural cells.
Proceedings of the National Academy of Sciences of the United States of America · 1995
355
cited
Endoplasmic Reticulum Stress Is Important for the Manifestations of α-Synucleinopathy In Vivo
Journal of Neuroscience · 2012
334
cited
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