Author
Jody Tanabe
Other affiliations: United States Department of Veterans Affairs, Nathan Kline Institute for Psychiatric Research, University of California, San Francisco ...read more
Bio: Jody Tanabe is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Smooth pursuit & Hyperintensity. The author has an hindex of 35, co-authored 88 publications receiving 4593 citations. Previous affiliations of Jody Tanabe include United States Department of Veterans Affairs & Nathan Kline Institute for Psychiatric Research.
Papers published on a yearly basis
Papers
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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
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TL;DR: Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes, but may be partially indexed by the severity of WMSH.
Abstract: Article abstract Background: The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial. Objectives: To determine whether cognitive impairment in SIVD 1) correlates with measures of ischemic brain injury or brain atrophy, and/or 2) is due to concomitant AD. Methods: Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment—normal cognition (NC+L, n = 32), mild cognitive impairment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group with probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i.e., hippocampal, cortical gray matter, and CSF volumes). Results: Among the three lacune groups, severity of cognitive impairment correlated with atrophy of the hippocampus and cortical gray matter, but not with any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, partially independent, atrophic process associated with ventricular dilation, cortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cases showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probable AD group gave evidence of only one atrophic process, reflected in the severity of hippocampal atrophy. Comparison of regional neocortical gray matter volumes showed sparing of the primary motor and visual cortices in the probable AD group, but relatively uniform atrophy in the D+L group. Conclusions: Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there is evidence for partial independence between these two atrophic processes. Hippocampal atrophy may result from a mixture of ischemic and degenerative pathologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.
396 citations
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TL;DR: The findings suggest that the interference effects of these two tasks are caused by different types of conflict but both invoke similar sources of top-down modulation.
351 citations
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TL;DR: The results support a hypothesis that defects in ventral medial frontal processing lead to impaired decisions that involve risk and reductions in right prefrontal activity during decision‐making appear to be modulated by the presence of gambling problems.
Abstract: Objective: Poor decision-making is a hallmark of addiction, whether to substances or activities. Performance on a widely used test of decision-making, the Iowa Gambling Task (IGT), can discriminate controls from persons with ventral medial frontal lesions, substance-dependence, and pathological gambling. Positron emission tomography (PET) studies indicate that substance-dependent individuals show altered prefrontal activity on the task. Here we adapted the IGT to an fMRI setting to test the hy- pothesis that defects in ventral medial and prefrontal processing are associated with impaired decisions that involve risk but may differ depending on whether substance dependence is comorbid with gam- bling problems. Method: 18 controls, 14 substance-dependent individuals (SD), and 16 SD with gam- bling problems (SDPG) underwent fMRI while performing a modified version of the IGT. Result: Group differences were observed in ventral medial frontal, right frontopolar, and superior frontal cortex dur- ing decision-making. Controls showed the greatest activity, followed by SDPG, followed by SD. Conclu- sion: Our results support a hypothesis that defects in ventral medial frontal processing lead to impaired decisions that involve risk. Reductions in right prefrontal activity during decision-making appear to be modulated by the presence of gambling problems and may reflect impaired working memory, stimulus reward valuation, or cue reactivity in substance-dependent individuals. Hum Brain Mapp 28:1276-1286, 2007. V C 2007 Wiley-Liss, Inc.
289 citations
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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
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9,362 citations
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TL;DR: Functional neuroimaging studies conducted in the past decade that have expanded the understanding of the involvement of the PFC in drug addiction are focused on.
Abstract: The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
2,008 citations
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TL;DR: This is one of the first studies, in children or adults, to explore: (a) how memory requirements interact with spatial compatibility and (b) spatial incompatibility effects both with stimulus-specific rules (Simon task) and with higher-level, conceptual rules.
1,803 citations
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TL;DR: It is demonstrated that negative affect, pain and cognitive control activate an overlapping region of the dorsal cingulate — the anterior midcingulate cortex (aMCC), which constitutes a hub where information about reinforcers can be linked to motor centres responsible for expressing affect and executing goal-directed behaviour.
Abstract: It has been argued that emotion, pain and cognitive control are functionally segregated in distinct subdivisions of the cingulate cortex. However, recent observations encourage a fundamentally different view. Imaging studies demonstrate that negative affect, pain and cognitive control activate an overlapping region of the dorsal cingulate — the anterior midcingulate cortex (aMCC). Anatomical studies reveal that the aMCC constitutes a hub where information about reinforcers can be linked to motor centres responsible for expressing affect and executing goal-directed behaviour. Computational modelling and other kinds of evidence suggest that this intimacy reflects control processes that are common to all three domains. These observations compel a reconsideration of the dorsal cingulate's contribution to negative affect and pain.
1,714 citations
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TL;DR: An overview of the criteria used in the diagnosis of Alzheimer disease is provided, highlighting how this disease is related to, but distinct from, normal aging.
Abstract: The global prevalence of dementia is estimated to be as high as 24 million, and is predicted to double every 20 years through to 2040, leading to a costly burden of disease. Alzheimer disease (AD) is the leading cause of dementia and is characterized by a progressive decline in cognitive function, which typically begins with deterioration in memory. Before death, individuals with this disorder have usually become dependent on caregivers. The neuropathological hallmarks of the AD brain are diffuse and neuritic extracellular amyloid plaques-which are frequently surrounded by dystrophic neurites-and intracellular neurofibrillary tangles. These hallmark pathologies are often accompanied by the presence of reactive microgliosis and the loss of neurons, white matter and synapses. The etiological mechanisms underlying the neuropathological changes in AD remain unclear, but are probably affected by both environmental and genetic factors. Here, we provide an overview of the criteria used in the diagnosis of AD, highlighting how this disease is related to, but distinct from, normal aging. We also summarize current information relating to AD prevalence, incidence and risk factors, and review the biomarkers that may be used for risk assessment and in diagnosis.
1,496 citations