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Scott M. McGinnis

Researcher at Harvard University

Publications -  63
Citations -  5671

Scott M. McGinnis is an academic researcher from Harvard University. The author has contributed to research in topics: Primary progressive aphasia & Dementia. The author has an hindex of 20, co-authored 52 publications receiving 5028 citations. Previous affiliations of Scott M. McGinnis include Brigham and Women's Hospital & University of Texas Health Science Center at San Antonio.

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Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness

TL;DR: Reciprocal changes involving subgenual cingulate and right prefrontal cortex occur with both transient and chronic changes in negative mood, suggesting that these regional interactions are obligatory and probably mediate the well-recognized relationships between mood and attention seen in both normal and pathological conditions.
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Regional metabolic effects of fluoxetine in major depression: serial changes and relationship to clinical response.

TL;DR: Chronic treatment and clinical response to fluoxetine was associated with a reciprocal pattern of subcortical and limbic decreases and cortical increases, which suggests a process of adaptation in specific brain regions over time in response to sustained serotonin reuptake inhibition.
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Differential limbic--cortical correlates of sadness and anxiety in healthy subjects: implications for affective disorders.

TL;DR: These findings are interpreted within a model in which sadness and anxiety are represented by segregated corticolimbic pathways, where a major role is played by selective dorsal cortical deactivations during sadness, and ventral cortical deactivateations in anxiety.
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Association of In Vivo [18F]AV-1451 Tau PET Imaging Results With Cortical Atrophy and Symptoms in Typical and Atypical Alzheimer Disease.

TL;DR: Results of tau PET imaging serve as a key biomarker that links a specific type of molecular Alzheimer disease neuropathologic condition with clinically significant neurodegeneration, which will likely catalyze additional efforts to develop disease-modifying therapeutics.