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Charles DeCarli

Researcher at University of California, Davis

Publications -  721
Citations -  77364

Charles DeCarli is an academic researcher from University of California, Davis. The author has contributed to research in topics: Dementia & Hyperintensity. The author has an hindex of 125, co-authored 614 publications receiving 65820 citations. Previous affiliations of Charles DeCarli include University of Southern California & French Institute of Health and Medical Research.

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Dissociable effects of Alzheimer disease and white matter hyperintensities on brain metabolism.

TL;DR: The dissociation of WMHs and cerebrospinal fluid β-amyloid in relation to regional glucose metabolism suggests that these pathologic conditions operate through different and independent pathways in AD that reflect dysfunction in different brain systems.
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Progression from normal cognition to mild cognitive impairment in a diverse clinic-based and community-based elderly cohort.

TL;DR: Predictors of conversion from NC to MCI in a racially and ethnically diverse sample drawn both from community and clinic recruitment sources are examined.
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Late life cognitive control deficits are accentuated by white matter disease burden

TL;DR: The results suggest that age-related goal maintenance impairments and associated dorsolateral prefrontal cortex dysfunction may partly reflect incipient white matter disease of interconnected cognitive networks.
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Gender differences in correlations of cerebral glucose matabolic rates in young normal adults

TL;DR: Gender differences in the pattern of functional neocortical interactions at the 'resting' state of healthy subjects using [18F]2-fluoro-2-deoxy-D-glucose are demonstrated.
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Relation between stage of disease and neurobehavioral measures in children with symptomatic HIV disease.

TL;DR: The relation between the CT brain-scan lesions and markers of HIV disease (both CD4 and p24) suggest that these CNS abnormalities are most likely associated with HIV-1 infection, and further support the hypothesis that the interaction between systemic disease progression and CNS manifestations is continuous rather than discrete.