Author
Andrew P. Prescot
Other affiliations: McLean Hospital, Harvard University
Bio: Andrew P. Prescot is an academic researcher from University of Utah. The author has contributed to research in topics: Bipolar disorder & Anterior cingulate cortex. The author has an hindex of 22, co-authored 45 publications receiving 2077 citations. Previous affiliations of Andrew P. Prescot include McLean Hospital & Harvard University.
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University of California, San Diego1, McGill University2, Oregon Health & Science University3, Florida International University4, Yale University5, Washington University in St. Louis6, Virginia Commonwealth University7, University of Vermont8, University of Michigan9, Medical University of South Carolina10, National Institutes of Health11, SRI International12, University of Southern California13, McGovern Institute for Brain Research14, Harvard University15, Medical College of Wisconsin16, University of California, Irvine17, University of California, Los Angeles18, University of California, San Francisco19, University of Colorado Boulder20, University of Florida21, University of Maryland, Baltimore22, University of Massachusetts Boston23, University of Minnesota24, University of Pittsburgh25, University of Rochester26, University of Tennessee27, University of Utah28, University of Wisconsin–Milwaukee29, United States Department of Veterans Affairs30, Boston University31
TL;DR: The baseline neuroimaging processing and subject-level analysis methods used by the Adolescent Brain Cognitive Development Study are described to be a resource of unprecedented scale and depth for studying typical and atypical development.
431 citations
TL;DR: This is the first study to demonstrate that increased thalamic GABA levels are associated with improved mood and decreased anxiety, and the first time that a behavioral intervention (i.e., yoga postures) has been associated with a positive correlation between acute increases in thalamus GABA levels and improvements in mood and anxiety scales.
Abstract: Objectives: Yoga and exercise have beneficial effects on mood and anxiety. γ-Aminobutyric acid (GABA)-ergic activity is reduced in mood and anxiety disorders. The practice of yoga postures is associated with increased brain GABA levels. This study addresses the question of whether changes in mood, anxiety, and GABA levels are specific to yoga or related to physical activity. Methods: Healthy subjects with no significant medical/psychiatric disorders were randomized to yoga or a metabolically matched walking intervention for 60 minutes 3 times a week for 12 weeks. Mood and anxiety scales were taken at weeks 0, 4, 8, 12, and before each magnetic resonance spectroscopy scan. Scan 1 was at baseline. Scan 2, obtained after the 12-week intervention, was followed by a 60-minute yoga or walking intervention, which was immediately followed by Scan 3. Results: The yoga subjects (n = 19) reported greater improvement in mood and greater decreases in anxiety than the walking group (n = 15). There were positiv...
394 citations
University of California1, McGill University2, Oregon Health & Science University3, Florida International University4, Yale University5, University of Washington6, Virginia Commonwealth University7, University of Vermont8, University of Michigan9, Medical University of South Carolina10, National Institute on Drug Abuse11, SRI International12, Children's Hospital Los Angeles13, National Institutes of Health14, McGovern Institute for Brain Research15, Harvard University16, Medical College of Wisconsin17, University of Colorado Boulder18, University of Florida19, University of Maryland, Baltimore20, University of Massachusetts Amherst21, University of Minnesota22, University of Pittsburgh23, University of Rochester24, University of Tennessee25, University of Utah26, University of Wisconsin–Milwaukee27, Boston University28
TL;DR: The baseline neuroimaging processing and subject-level analysis methods used by the ABCD DAIC in the centralized processing and extraction of neuroanatomical and functional imaging phenotypes are described.
Abstract: The Adolescent Brain Cognitive Development (ABCD) Study is an ongoing, nationwide study of the effects of environmental influences on behavioral and brain development in adolescents. The ABCD Study is a collaborative effort, including a Coordinating Center, 21 data acquisition sites across the United States, and a Data Analysis and Informatics Center (DAIC). The main objective of the study is to recruit and assess over eleven thousand 9-10-year-olds and follow them over the course of 10 years to characterize normative brain and cognitive development, the many factors that influence brain development, and the effects of those factors on mental health and other outcomes. The study employs state-of-the-art multimodal brain imaging, cognitive and clinical assessments, bioassays, and careful assessment of substance use, environment, psychopathological symptoms, and social functioning. The data will provide a resource of unprecedented scale and depth for studying typical and atypical development. Here, we describe the baseline neuroimaging processing and subject-level analysis methods used by the ABCD DAIC in the centralized processing and extraction of neuroanatomical and functional imaging phenotypes. Neuroimaging processing and analyses include modality-specific corrections for distortions and motion, brain segmentation and cortical surface reconstruction derived from structural magnetic resonance imaging (sMRI), analysis of brain microstructure using diffusion MRI (dMRI), task-related analysis of functional MRI (fMRI), and functional connectivity analysis of resting-state fMRI.
276 citations
TL;DR: In this article, the authors examined the glutamine/glutamate ratio and levels of other metabolites in acute mania and schizophrenia in an exploratory study, and found that the elevated ratio is consistent with glutamatergic overactivity and/or defective neuronal-glial coupling.
249 citations
TL;DR: The findings indicate that the use of Cr as an internal reference in schizophrenia MRS research is problematic unless Cr levels are shown to be normal in the study population, and they add to the literature on bioenergetic abnormalities in schizophrenia.
Abstract: Total creatine (Cr) levels are widely used as an internal reference for the quantification of other metabolites in (1)H magnetic resonance spectroscopy (MRS). However, Cr plays an important role in brain energy metabolism, and its levels can be modulated by conditions of energy production and demand. Therefore, abnormal Cr levels in patient vs. control populations could confound the utility of this metabolite as an internal reference. We quantified Cr levels in 22 healthy controls, 15 acutely manic patients with bipolar disorder and 15 acutely ill patients with schizophrenia using (1)H MRS in the anterior cingulate cortex, and the parieto-occipital cortex at 4 Tesla. Patients with schizophrenia had a statistically significant reduction in Cr levels as compared with controls; bipolar disorder patients showed no difference in Cr as compared with controls. In addition, older age was associated with reductions in Cr in healthy controls, but not in patients with either disorder. These findings indicate that the use of Cr as an internal reference in schizophrenia MRS research is problematic unless Cr levels are shown to be normal in the study population. They also add to the literature on bioenergetic abnormalities in schizophrenia.
162 citations
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01 Jan 2013
TL;DR: In this article, the landscape of somatic genomic alterations based on multidimensional and comprehensive characterization of more than 500 glioblastoma tumors (GBMs) was described, including several novel mutated genes as well as complex rearrangements of signature receptors, including EGFR and PDGFRA.
Abstract: We describe the landscape of somatic genomic alterations based on multidimensional and comprehensive characterization of more than 500 glioblastoma tumors (GBMs). We identify several novel mutated genes as well as complex rearrangements of signature receptors, including EGFR and PDGFRA. TERT promoter mutations are shown to correlate with elevated mRNA expression, supporting a role in telomerase reactivation. Correlative analyses confirm that the survival advantage of the proneural subtype is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predictive biomarker for treatment response only in classical subtype GBM. Integrative analysis of genomic and proteomic profiles challenges the notion of therapeutic inhibition of a pathway as an alternative to inhibition of the target itself. These data will facilitate the discovery of therapeutic and diagnostic target candidates, the validation of research and clinical observations and the generation of unanticipated hypotheses that can advance our molecular understanding of this lethal cancer.
2,616 citations
University of British Columbia1, University of Toronto2, McGill University3, Dalhousie University4, University of Calgary5, University of Western Ontario6, Queen's University7, McMaster University8, University of São Paulo9, University of Pittsburgh10, Seoul National University11, University of Melbourne12, Deakin University13
TL;DR: The Canadian Network for Mood and Anxiety Treatments published guidelines for the management of bipolar disorder in 2005, with updates in 2007 and 2009, and this third update, in conjunction with the International Society for Bipolar Disorders, reviews new evidence and is designed to be used in conjunctionWith the previous publications.
Abstract: The Canadian Network for Mood and Anxiety Treatments published guidelines for the management of bipolar disorder in 2005, with updates in 2007 and 2009. This third update, in conjunction with the International Society for Bipolar Disorders, reviews new evidence and is designed to be used in conjunction with the previous publications.The recommendations for the management of acute mania remain largely unchanged. Lithium, valproate, and several atypical antipsychotic agents continue to be first-line treatments for acute mania. Monotherapy with asenapine, paliperidone extended release (ER), and divalproex ER, as well as adjunctive asenapine, have been added as first-line options.For the management of bipolar depression, lithium, lamotrigine, and quetiapine monotherapy, as well as olanzapine plus selective serotonin reuptake inhibitor (SSRI), and lithium or divalproex plus SSRI/bupropion remain first-line options. Lurasidone monotherapy and the combination of lurasidone or lamotrigine plus lithium or divalproex have been added as a second-line options. Ziprasidone alone or as adjunctive therapy, and adjunctive levetiracetam have been added as not-recommended options for the treatment of bipolar depression. Lithium, lamotrigine, valproate, olanzapine, quetiapine, aripiprazole, risperidone long-acting injection, and adjunctive ziprasidone continue to be first-line options for maintenance treatment of bipolar disorder. Asenapine alone or as adjunctive therapy have been added as third-line options.
1,369 citations
TL;DR: Understanding of the mechanisms by which stress and glucocorticoids affect glutamate transmission provides insights into normal brain functioning, as well as the pathophysiology and potential new treatments of stress-related neuropsychiatric disorders.
Abstract: Mounting evidence suggests that acute and chronic stress, especially the stress-induced release of glucocorticoids, induces changes in glutamate neurotransmission in the prefrontal cortex and the hippocampus, thereby influencing some aspects of cognitive processing. In addition, dysfunction of glutamatergic neurotransmission is increasingly considered to be a core feature of stress-related mental illnesses. Recent studies have shed light on the mechanisms by which stress and glucocorticoids affect glutamate transmission, including effects on glutamate release, glutamate receptors and glutamate clearance and metabolism. This new understanding provides insights into normal brain functioning, as well as the pathophysiology and potential new treatments of stress-related neuropsychiatric disorders.
1,121 citations
TL;DR: In conclusion, animal models demonstrate that the molecular basis of disruption is linked to specific defects in the development and function of interneurons — the cells that are responsible for establishing inhibitory circuits in the brain.
Abstract: The notion that the disruption of inhibitory circuits might underlie certain clinical features — notably cognitive impairment — in various neuropsychiatric disorders, including schizophrenia and autism, is receiving considerable attention. Focusing heavily on studies in animal models, Oscar Marin reviews the evidence indicating that the basis of such disruption is linked to specific defects in interneuron development and function.
991 citations
TL;DR: A new model of cortical dysfunction in schizophrenia is suggested in which PVBC inhibition is decreased to compensate for an upstream deficit in pyramidal cell excitation, but at a level insufficient to generate the gamma oscillation power required for high levels of cognitive control.
914 citations