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15 results on '"Hudson, Kelsey E."'

2. Low Smoking Exposure, the Adolescent Brain, and the Modulating Role of CHRNA5 Polymorphisms

Author

Mann, Karl, Struve, Maren, Rietschel, Marcella, Spanagel, Rainer, Fauth-Bühler, Mira, Millenet, Sabina, Grimmer, Yvonne, Ivanov, Nikolay, Strache, Nicole, Rapp, Michael, Ströhle, Andreas, Reuter, Jan, Barbot, Alexis, Thyreau, Benjamin, Schwartz, Yannick, Lalanne, Christophe, Bricaud, Zuleima, Briand, Fanny Gollier, Lemaitre, Hervé, Massicotte, Jessica, Vulser, Helene, Pentillä, Jani, Galinowski, André, Jia, Tianye, Werts, Helen, Topper, Lauren, Reed, Laurence, Andrew, Chris, Mallik, Catherine, Ruggeri, Barbara, Nymberg, Charlotte, Smith, Lindsay, Loth, Eva, Havatzias, Stephanie, Stueber, Kerstin, Stringaris, Argyris, Constant, Patrick, Brühl, Ruediger, Ihlenfeld, Albrecht, Walaszek, Bernadeta, Hübner, Thomas, Müller, Kathrin, Ripke, Stephan, Rodehacke, Sarah, Mennigen, Eva, Schmidt, Dirk, Vetter, Nora, Ziesch, Veronika, Jones, Jennifer, Poline, Jean-Baptiste, Fadai, Tahmine, Yacubian, Juliana, Schneider, Sophia, Lawrence, Claire, Newman, Craig, Head, Kay, Heym, Nadja, Pausova, Zdenka, Tahmasebi, Amir, Chaarani, Bader, Kan, Kees-Jan, Mackey, Scott, Spechler, Philip A., Potter, Alexandra, Orr, Catherine, D’Alberto, Nicholas, Hudson, Kelsey E., Banaschewski, Tobias, Bokde, Arun L.W., Bromberg, Uli, Büchel, Christian, Cattrell, Anna, Conrod, Patricia J., Desrivières, Sylvane, Flor, Herta, Frouin, Vincent, Gallinat, Jürgen, Gowland, Penny, Heinz, Andreas, Ittermann, Bernd, Martinot, Jean-Luc, Nees, Frauke, Papadopoulos-Orfanos, Dimitri, Paus, Tomáš, Poustka, Luise, Smolka, Michael N., Walter, Henrik, Whelan, Robert, Higgins, Stephen T., Schumann, Gunter, Althoff, Robert R., Stein, Elliot A., and Garavan, Hugh

Published
2019
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4. Cannabis use in early adolescence: Evidence of amygdala hypersensitivity to signals of threat

Author

Spechler, Philip A., Orr, Catherine A., Chaarani, Bader, Kan, Kees-Jan, Mackey, Scott, Morton, Aaron, Snowe, Mitchell P., Hudson, Kelsey E., Althoff, Robert R., Higgins, Stephen T., Cattrell, Anna, Flor, Herta, Nees, Frauke, Banaschewski, Tobias, Bokde, Arun L.W., Whelan, Robert, Büchel, Christian, Bromberg, Uli, Conrod, Patricia, Frouin, Vincent, Papadopoulos, Dimitri, Gallinat, Jurgen, Heinz, Andreas, Walter, Henrik, Ittermann, Bernd, Gowland, Penny, Paus, Tomáš, Poustka, Luise, Martinot, Jean-Luc, Artiges, Eric, Smolka, Michael N., Schumann, Gunter, and Garavan, Hugh

Published
2015
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10. Low smoking-exposure, the adolescent brain, and the modulating role of CHRNA5 polymorphisms

Author

Chaarani, Bader, Kan, Kees-Jan, Mackey, Scott, Spechler, Philip A., Potter, Alexandra, Orr, Catherine, D'Alberto, Nicholas, Hudson, Kelsey E., Banaschewski, Tobias, Bokde, Arun L.W., Bromberg, Uli, Cattrell, Anna, Conrod, Patricia J., Flor, Herta, Frouin, Vincent, Gowland, Penny, Heinz, Andreas, Ittermann, Bernd, Martinot, Jean-Luc, Nees, Frauke, Papadopoulos-Orfanos, Dimitri, Poustka, Luise, Smolka, Michael N., Walter, Henrik, Whelan, Robert, Higgins, Stephen T., Schumann, Gunter, Althoff, Robert R., Stein, Elliot A., and Garavan, Hugh

Subjects
Low smoking exposure, fMRI, Genetics, Neuroimaging, adolescents, Grey matter volume
Abstract

© 2019 Background: Studying the neural consequences of tobacco smoking during adolescence, including those associated with early light use, may help expose the mechanisms that underlie the transition from initial use to nicotine dependence in adulthood. However, only a few studies in adolescents exist, and they include small samples. In addition, the neural mechanism, if one exists, that links nicotinic receptor genes to smoking behavior in adolescents is still unknown. Methods: Structural and diffusion tensor magnetic resonance imaging data were acquired from a large sample of 14-year-old adolescents who completed an extensive battery of neuropsychological, clinical, personality, and drug-use assessments. Additional assessments were conducted at 16 years of age. Results: Exposure to smoking in adolescents, even at low doses, is linked to volume changes in the ventromedial prefrontal cortex and to altered neuronal connectivity in the corpus callosum. The longitudinal analyses strongly suggest that these effects are not preexisting conditions in those who progress to smoking. There was a genetic contribution wherein the volume reduction effects were magnified in smokers who were carriers of the high-risk genotype of the alpha 5 nicotinic receptor subunit gene, rs16969968. Conclusions: These findings give insight into a mechanism involving genes, brain structure, and connectivity underlying why some adolescents find nicotine especially addictive.

Published
2019

11. Low Smoking Exposure, the Adolescent Brain, and the Modulating Role of CHRNA5 Polymorphisms

Author

Chaarani, Bader, primary, Kan, Kees-Jan, additional, Mackey, Scott, additional, Spechler, Philip A., additional, Potter, Alexandra, additional, Orr, Catherine, additional, D’Alberto, Nicholas, additional, Hudson, Kelsey E., additional, Banaschewski, Tobias, additional, Bokde, Arun L.W., additional, Bromberg, Uli, additional, Büchel, Christian, additional, Cattrell, Anna, additional, Conrod, Patricia J., additional, Desrivières, Sylvane, additional, Flor, Herta, additional, Frouin, Vincent, additional, Gallinat, Jürgen, additional, Gowland, Penny, additional, Heinz, Andreas, additional, Ittermann, Bernd, additional, Martinot, Jean-Luc, additional, Nees, Frauke, additional, Papadopoulos-Orfanos, Dimitri, additional, Paus, Tomáš, additional, Poustka, Luise, additional, Smolka, Michael N., additional, Walter, Henrik, additional, Whelan, Robert, additional, Higgins, Stephen T., additional, Schumann, Gunter, additional, Althoff, Robert R., additional, Stein, Elliot A., additional, Garavan, Hugh, additional, Mann, Karl, additional, Struve, Maren, additional, Rietschel, Marcella, additional, Spanagel, Rainer, additional, Fauth-Bühler, Mira, additional, Millenet, Sabina, additional, Grimmer, Yvonne, additional, Ivanov, Nikolay, additional, Strache, Nicole, additional, Rapp, Michael, additional, Ströhle, Andreas, additional, Reuter, Jan, additional, Barbot, Alexis, additional, Thyreau, Benjamin, additional, Schwartz, Yannick, additional, Lalanne, Christophe, additional, Bricaud, Zuleima, additional, Briand, Fanny Gollier, additional, Lemaitre, Hervé, additional, Massicotte, Jessica, additional, Vulser, Helene, additional, Pentillä, Jani, additional, Galinowski, André, additional, Jia, Tianye, additional, Werts, Helen, additional, Topper, Lauren, additional, Reed, Laurence, additional, Andrew, Chris, additional, Mallik, Catherine, additional, Ruggeri, Barbara, additional, Nymberg, Charlotte, additional, Smith, Lindsay, additional, Loth, Eva, additional, Havatzias, Stephanie, additional, Stueber, Kerstin, additional, Stringaris, Argyris, additional, Constant, Patrick, additional, Brühl, Ruediger, additional, Ihlenfeld, Albrecht, additional, Walaszek, Bernadeta, additional, Hübner, Thomas, additional, Müller, Kathrin, additional, Ripke, Stephan, additional, Rodehacke, Sarah, additional, Mennigen, Eva, additional, Schmidt, Dirk, additional, Vetter, Nora, additional, Ziesch, Veronika, additional, Jones, Jennifer, additional, Poline, Jean-Baptiste, additional, Fadai, Tahmine, additional, Yacubian, Juliana, additional, Schneider, Sophia, additional, Lawrence, Claire, additional, Newman, Craig, additional, Head, Kay, additional, Heym, Nadja, additional, Pausova, Zdenka, additional, and Tahmasebi, Amir, additional

Published
2019
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13. Cross-Disorder Cognitive Impairments in Youth Referred for Neuropsychiatric Evaluation

Author

Doyle, Alysa E., primary, Vuijk, Pieter J., additional, Doty, Nathan D., additional, McGrath, Lauren M., additional, Willoughby, Brian L., additional, O’Donnell, Ellen H., additional, Wilson, H. Kent, additional, Colvin, Mary K., additional, Toner, Deanna C., additional, Hudson, Kelsey E., additional, Blais, Jessica E., additional, Ditmars, Hillary L., additional, Faraone, Stephen V., additional, Seidman, Larry J., additional, and Braaten, Ellen B., additional

Published
2017
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14. The initiation of cannabis use in adolescence is predicted by sex‐specific psychosocial and neurobiological features.

Author

Spechler, Philip A., Allgaier, Nicholas, Chaarani, Bader, Whelan, Robert, Watts, Richard, Orr, Catherine, Albaugh, Matthew D., D'Alberto, Nicholas, Higgins, Stephen T., Hudson, Kelsey E., Mackey, Scott, Potter, Alexandra, Banaschewski, Tobias, Bokde, Arun L. W., Bromberg, Uli, Büchel, Christian, Cattrell, Anna, Conrod, Patricia J., Desrivières, Sylvane, and Flor, Herta

Subjects
MARIJUANA, ADOLESCENCE, OPIOID receptors, BINGE drinking, FEATURE selection
Abstract

Cannabis use initiated during adolescence might precipitate negative consequences in adulthood. Thus, predicting adolescent cannabis use prior to any exposure will inform the aetiology of substance abuse by disentangling predictors from consequences of use. In this prediction study, data were drawn from the IMAGEN sample, a longitudinal study of adolescence. All selected participants (n = 1,581) were cannabis‐naïve at age 14. Those reporting any cannabis use (out of six ordinal use levels) by age 16 were included in the outcome group (N = 365, males n = 207). Cannabis‐naïve participants at age 14 and 16 were included in the comparison group (N = 1,216, males n = 538). Psychosocial, brain and genetic features were measured at age 14 prior to any exposure. Cross‐validated regularized logistic regressions for each use level by sex were used to perform feature selection and obtain prediction error statistics on independent observations. Predictors were probed for sex‐ and drug‐specificity using post‐hoc logistic regressions. Models reliably predicted use as indicated by satisfactory prediction error statistics, and contained psychosocial features common to both sexes. However, males and females exhibited distinct brain predictors that failed to predict use in the opposite sex or predict binge drinking in independent samples of same‐sex participants. Collapsed across sex, genetic variation on catecholamine and opioid receptors marginally predicted use. Using machine learning techniques applied to a large multimodal dataset, we identified a risk profile containing psychosocial and sex‐specific brain prognostic markers, which were likely to precede and influence cannabis initiation. [ABSTRACT FROM AUTHOR]

Published
2019
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15. Cross-Disorder Cognitive Impairments in Youth Referred for Neuropsychiatric Evaluation.

Author

Doyle, Alysa E., Vuijk, Pieter J., Doty, Nathan D., McGrath, Lauren M., Willoughby, Brian L., O'Donnell, Ellen H., Wilson, H. Kent, Colvin, Mary K., Toner, Deanna C., Hudson, Kelsey E., Blais, Jessica E., Ditmars, Hillary L., Faraone, Stephen V., Seidman, Larry J., and Braaten, Ellen B.

Subjects
MILD cognitive impairment, MENTAL health of youth, NEUROBEHAVIORAL disorders, COMORBIDITY, EXECUTIVE function
Abstract

Objectives: Studies suggest that impairments in some of the same domains of cognition occur in different neuropsychiatric conditions, including those known to share genetic liability. Yet, direct, multi-disorder cognitive comparisons are limited, and it remains unclear whether overlapping deficits are due to comorbidity. We aimed to extend the literature by examining cognition across different neuropsychiatric conditions and addressing comorbidity. Methods: Subjects were 486 youth consecutively referred for neuropsychiatric evaluation and enrolled in the Longitudinal Study of Genetic Influences on Cognition. First, we assessed general ability, reaction time variability (RTV), and aspects of executive functions (EFs) in youth with non-comorbid forms of attention-deficit/hyperactivity disorder (ADHD), mood disorders and autism spectrum disorder (ASD), as well as in youth with psychosis. Second, we determined the impact of comorbid ADHD on cognition in youth with ASD and mood disorders. Results: For EFs (working memory, inhibition, and shifting/flexibility), we observed weaknesses in all diagnostic groups when participants' own ability was the referent. Decrements were subtle in relation to published normative data. For RTV, weaknesses emerged in youth with ADHD and mood disorders, but trend-level results could not rule out decrements in other conditions. Comorbidity with ADHD did not impact the pattern of weaknesses for youth with ASD or mood disorders but increased the magnitude of the decrement in those with mood disorders. Conclusions: Youth with ADHD, mood disorders, ASD, and psychosis show EF weaknesses that are not due to comorbidity. Whether such cognitive difficulties reflect genetic liability shared among these conditions requires further study. [ABSTRACT FROM AUTHOR]

Published
2018
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