His primary areas of investigation include Neuroscience, Alzheimer's disease, Cognitive decline, Cholinergic and Neurotrophin. Scott E. Counts studies Basal forebrain, a branch of Neuroscience. His Alzheimer's disease research is multidisciplinary, incorporating elements of Neuropathology and Dementia, Prodromal Stage.
His Cognitive decline research is multidisciplinary, incorporating perspectives in Progressive disease, Temporal cortex, Autopsy and Degenerative disease. The Cholinergic portion of his research involves studies in Endocrinology and Internal medicine. In his study, Gene knockdown, Neuroprotection, Neurotrophic factors and Brain-derived neurotrophic factor is strongly linked to Cell biology, which falls under the umbrella field of Neurotrophin.
Scott E. Counts mainly focuses on Neuroscience, Alzheimer's disease, Cholinergic, Internal medicine and Basal forebrain. His research integrates issues of Gene expression, Downregulation and upregulation, Neurodegeneration, Disease and Synaptophysin in his study of Neuroscience. The various areas that he examines in his Alzheimer's disease study include Temporal cortex, Receptor, Cognitive decline, Hippocampus and Degenerative disease.
In his research, Tropomyosin receptor kinase B and Cell biology is intimately related to Neurotrophin, which falls under the overarching field of Cholinergic. While the research belongs to areas of Internal medicine, he spends his time largely on the problem of Endocrinology, intersecting his research to questions surrounding Nerve growth factor and Frontal lobe. His Basal forebrain research includes themes of Galanin and Neuron.
Scott E. Counts focuses on Alzheimer's disease, Neuroscience, Amyloid, Hippocampus and Hippocampal formation. His Alzheimer's disease research incorporates elements of Nucleus basalis and Cognitive decline. Neuroplasticity and Gene expression is closely connected to Disease in his research, which is encompassed under the umbrella topic of Neuroscience.
His study on Amyloid also encompasses disciplines like
Alzheimer's disease, Postsynaptic potential, Cognitive decline, Hippocampus and Neuroscience are his primary areas of study. His studies in Alzheimer's disease integrate themes in fields like Progressive disease and Regulation of gene expression. His Progressive disease research incorporates themes from Neuropathology, Autopsy and Dementia, Prodromal Stage.
His Prodromal Stage study improves the overall literature in Pathology. His Synaptophysin research extends to Postsynaptic potential, which is thematically connected. He integrates many fields in his works, including Memory impairment, Dendritic spine and Hippocampal formation.
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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)
Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity
Vincenzo Sorrentino;Mario Romani;Laurent Mouchiroud;John S. Beck.
Nature (2017)
The role of nerve growth factor receptors in cholinergic basal forebrain degeneration in prodromal Alzheimer disease.
Scott E. Counts;Elliott J. Mufson.
Journal of Neuropathology and Experimental Neurology (2005)
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)
Mild cognitive impairment: pathology and mechanisms
Elliott J. Mufson;Lester Binder;Scott E. Counts;Steven T. DeKosky.
Acta Neuropathologica (2012)
Light and electron microscopic localization of presenilin-1 in primate brain.
James J. Lah;Craig J. Heilman;Norman R. Nash;Howard D. Rees.
The Journal of Neuroscience (1997)
Differential expression of synaptic proteins in the frontal and temporal cortex of elderly subjects with mild cognitive impairment.
Scott E. Counts;Muhammad Nadeem;Shivanand P. Lad;Joanne Wuu.
Journal of Neuropathology and Experimental Neurology (2006)
Reduction of cortical TrkA but not p75(NTR) protein in early-stage Alzheimer's disease.
Scott E. Counts;Muhammad Nadeem;Joanne Wuu;Stephen D. Ginsberg.
Annals of Neurology (2004)
Locus coeruleus cellular and molecular pathology during the progression of Alzheimer’s disease
Sarah C. Kelly;Bin He;Sylvia E. Perez;Stephen D. Ginsberg;Stephen D. Ginsberg.
Acta neuropathologica communications (2017)
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