Publications by authors named "C F Curtis"

Perception, working memory, and long-term memory each evoke neural responses in visual cortex. While previous neuroimaging research on the role of visual cortex in memory has largely emphasized similarities between perception and memory, we hypothesized that responses in visual cortex would differ depending on the origins of the inputs. Using fMRI, we quantified spatial tuning in visual cortex while participants (both sexes) viewed, maintained in working memory, or retrieved from long-term memory a peripheral target.

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Decades of macaque research established the importance of prefrontal cortex for working memory. Surprisingly, recent human neuroimaging studies demonstrated that the contents of working memory can be decoded from primary visual cortex (V1). However the necessity of this mnemonic information remains unknown and contentious.

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Exposure to toxic organic chemicals such as β-methylamino-L-alanine (BMAA) and glyphosate has been associated with neurodegenerative diseases (NDDs), including amyotrophic lateral sclerosis (ALS), Parkinson's Disease (PD), and Alzheimer's Disease (AD). We explored the utility of BMAA and glyphosate's metabolite aminomethylphosphonic acid (AMPA) for serving as potential markers of NDDs by comparing levels of wastewater-borne BMAA and AMPA with regional U.S.

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In the nonhuman primate, discrete parts of premotor frontal and parietal cortex appear to code for movements of different effectors. However, the evidence regarding homologous effector selectivity within the human brain remains inconclusive. Here, we measured neural activity in the human brain using functional magnetic resonance imaging while participants remembered a target location and planned either saccades or reaches that matched the rich kinematics used in seminal monkey studies.

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Psoriasis is a common, debilitating immune-mediated skin disease. Genetic studies have identified biological mechanisms of psoriasis risk, including those targeted by effective therapies. However, the genetic liability to psoriasis is not fully explained by variation at robustly identified risk loci.

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