His primary scientific interests are in Alzheimer's disease, Neuroscience, Cell biology, Endocrinology and Internal medicine. His Alzheimer's disease research integrates issues from Neuropathology, Hippocampus and Neurodegeneration. His research investigates the connection between Neuroscience and topics such as Neurotrophin that intersect with problems in Tropomyosin receptor kinase B.
His research integrates issues of Messenger RNA, Cathepsin D, Biochemistry and Transcription factor in his study of Cell biology. Stephen D. Ginsberg usually deals with Endocrinology and limits it to topics linked to Downregulation and upregulation and Amyloid precursor protein secretase, Genetically modified mouse and Streptozotocin. His Basal forebrain study integrates concerns from other disciplines, such as Human brain and Cholinergic neuron.
Neuroscience, Internal medicine, Endocrinology, Alzheimer's disease and Basal forebrain are his primary areas of study. His biological study spans a wide range of topics, including Neurotrophin, Neurodegeneration and Gene expression profiling. His Neurodegeneration study combines topics from a wide range of disciplines, such as Neuropathology and Endosome.
His work carried out in the field of Alzheimer's disease brings together such families of science as Downregulation and upregulation and Immunology. His research in Downregulation and upregulation tackles topics such as Genetically modified mouse which are related to areas like Tauopathy. His study looks at the relationship between Basal forebrain and fields such as Cholinergic neuron, as well as how they intersect with chemical problems.
Stephen D. Ginsberg focuses on Neuroscience, Cell biology, Basal forebrain, Disease and Downregulation and upregulation. His Nucleus basalis study in the realm of Neuroscience interacts with subjects such as Population. His research in Cell biology intersects with topics in Microvesicles, Transcription factor, Regulation of gene expression, Genetically modified mouse and Tauopathy.
As a part of the same scientific study, Stephen D. Ginsberg usually deals with the Basal forebrain, concentrating on Cholinergic neuron and frequently concerns with Down syndrome, Choline acetyltransferase, CAMK2A, DYRK1A and Forebrain. His studies examine the connections between Neurodegeneration and genetics, as well as such issues in Cholinergic, with regards to Amyloid beta, Cerebral cortex and Gene expression profiling. The study incorporates disciplines such as Internal medicine and Endocrinology in addition to Neurodevelopmental disorder.
His primary areas of investigation include Neuroscience, Neurodegeneration, Cell biology, Downregulation and upregulation and Alzheimer's disease. Neuroscience is frequently linked to Amyloid beta in his study. The various areas that Stephen D. Ginsberg examines in his Neurodegeneration study include Mutation, Genetics and PPT1.
He has researched Cell biology in several fields, including Exosome, Messenger RNA, Brain-derived neurotrophic factor, Genetically modified mouse and Tauopathy. His study in Downregulation and upregulation is interdisciplinary in nature, drawing from both Cathepsin D, Neurotrophic factors, TFEB, Neurotrophin and Knockout mouse. His work on Senile plaques as part of general Alzheimer's disease research is frequently linked to Population, thereby connecting diverse disciplines of science.
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Cholinergic system during the progression of Alzheimer's disease: therapeutic implications.
Elliott J Mufson;Scott E Counts;Sylvia E Perez;Stephen D Ginsberg.
Expert Review of Neurotherapeutics (2008)
Expression profile of transcripts in Alzheimer's disease tangle-bearing CA1 neurons.
Stephen D. Ginsberg;Scott E. Hemby;Virginia M.‐Y. Lee;James H. Eberwine.
Annals of Neurology (2000)
Human cholinergic basal forebrain: chemoanatomy and neurologic dysfunction
Elliott J. Mufson;Stephen D. Ginsberg;Milos D. Ikonomovic;Steven T. DeKosky.
Journal of Chemical Neuroanatomy (2003)
Alzheimer’s-related endosome dysfunction in Down syndrome is Aβ-independent but requires APP and is reversed by BACE-1 inhibition
Ying Jiang;Kerry A. Mullaney;Corrinne M. Peterhoff;Shaoli Che.
Proceedings of the National Academy of Sciences of the United States of America (2010)
Down regulation of trk but not p75NTR gene expression in single cholinergic basal forebrain neurons mark the progression of Alzheimer's disease
Stephen D. Ginsberg;Shaoli Che;Joanne Wuu;Scott E. Counts.
Journal of Neurochemistry (2006)
Microarray Analysis of Hippocampal CA1 Neurons Implicates Early Endosomal Dysfunction During Alzheimer's Disease Progression
Stephen D. Ginsberg;Stephen D. Ginsberg;Melissa J. Alldred;Melissa J. Alldred;Scott E. Counts;Anne M. Cataldo.
Biological Psychiatry (2010)
Gene Expression Profile for Schizophrenia: Discrete Neuron Transcription Patterns in the Entorhinal Cortex
Scott E. Hemby;Stephen D. Ginsberg;Brian Brunk;Steven E. Arnold.
Archives of General Psychiatry (2002)
Mild cognitive impairment: pathology and mechanisms
Elliott J. Mufson;Lester Binder;Scott E. Counts;Steven T. DeKosky.
Acta Neuropathologica (2012)
Decreased brain-derived neurotrophic factor depends on amyloid aggregation state in transgenic mouse models of Alzheimer's disease
Shiyong Peng;Diego J. Garzon;Diego J. Garzon;Monica Marchese;William Klein.
The Journal of Neuroscience (2009)
Autophagy flux in CA1 neurons of Alzheimer hippocampus: Increased induction overburdens failing lysosomes to propel neuritic dystrophy.
Matteo Bordi;Martin J Berg;Panaiyur S Mohan;Corrinne M Peterhoff.
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