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Robert H. Paul

Researcher at University of Missouri–St. Louis

Publications -  260
Citations -  10590

Robert H. Paul is an academic researcher from University of Missouri–St. Louis. The author has contributed to research in topics: Neurocognitive & Cognition. The author has an hindex of 59, co-authored 247 publications receiving 9253 citations. Previous affiliations of Robert H. Paul include University of Missouri & Washington University in St. Louis.

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Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety

TL;DR: Findings are consistent with the correlation of depression and anxiety, yet suggest that partially differentiated gene–brain cognition pathways to these syndromes can be identified, even in a nonclinical sample, and may aid establishing an evidence base for more tailored intervention strategies.
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Cognitive Aging, Executive Function, and Fractional Anisotropy: A Diffusion Tensor MR Imaging Study

TL;DR: A relationship between FA and a measure of executive function-a core cognitive component that is a key feature of cognitive aging is demonstrated and proposed that that FA may provide an early means for the detection of age-related cognitive change.
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Obesity is associated with reduced white matter integrity in otherwise healthy adults.

TL;DR: Findings suggest a possible role for adiposity in WM dysfunction and associated cognitive deficits, and an interaction between obesity and aging processes on certain WM tracts in otherwise healthy adults.
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Independent Effects of HIV, Aging, and HAART on Brain Volumetric Measures

TL;DR: HIV associated volumetric reductions within the amygdala, caudate, and corpus callosum occurs despite HAART, and HIV and aging independently increase brain vulnerability.
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Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer's disease model.

TL;DR: It is demonstrated that a mAb specific for the human microglial receptor TREM2 induces microglia proliferation, ameliorates Aβ-induced pathology in a mouse model of Alzheimer’s disease, and can be given safely in a first-in-human phase I clinical trial.