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Brian Patenaude

Researcher at Stanford University

Publications -  25
Citations -  6036

Brian Patenaude is an academic researcher from Stanford University. The author has contributed to research in topics: Major depressive disorder & Bayesian probability. The author has an hindex of 17, co-authored 25 publications receiving 5145 citations. Previous affiliations of Brian Patenaude include Veterans Health Administration & University of Oxford.

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Bayesian analysis of neuroimaging data in FSL.

TL;DR: How Bayesian techniques have made a significant impact in tackling problems such as neuroimaging problems, particularly in regards to the analysis tools in the FMRIB Software Library (FSL), is described.
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A Bayesian model of shape and appearance for subcortical brain segmentation

TL;DR: A fully-automated segmentation method that uses manually labelled image data to provide anatomical training information and is assessed both quantitatively, using Leave-One-Out testing on the 336 training images, and qualitatively,Using an independent clinical dataset involving Alzheimer's disease.
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Prefrontal cortical regulation of brainwide circuit dynamics and reward-related behavior

TL;DR: Optogenetic and brain imaging approaches reveal a causal brainwide dynamical mechanism for the hedonic-anhedonic transition and test the hypothesis that elevated medial prefrontal cortex (mPFC) excitability exerts suppressive control over the interactions between two distant subcortical regions: the dopaminergic midbrain and the striatum.
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An evaluation of four automatic methods of segmenting the subcortical structures in the brain.

TL;DR: Four novel methods of fully automated segmentation of subcortical structures using volumetric, spatial overlap and distance-based measures are evaluated and it is shown that all four methods perform on par with recently published methods.
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Combining shape and connectivity analysis: An MRI study of thalamic degeneration in Alzheimer's disease

TL;DR: MRI evidence of regional thalamic degeneration in AD is provided and it is suggested that ventral and dorsal-medial shape change in the thalamus in AD patients is likely to be driven by IML atrophy.