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Michael J. Minzenberg

Researcher at Semel Institute for Neuroscience and Human Behavior

Publications -  88
Citations -  7064

Michael J. Minzenberg is an academic researcher from Semel Institute for Neuroscience and Human Behavior. The author has contributed to research in topics: Cognition & Schizophrenia. The author has an hindex of 37, co-authored 83 publications receiving 6359 citations. Previous affiliations of Michael J. Minzenberg include Icahn School of Medicine at Mount Sinai & University of California, San Francisco.

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Meta-analysis of 41 Functional Neuroimaging Studies of Executive Function in Schizophrenia

TL;DR: Healthy adults and schizophrenic patients activate a qualitatively similar neural network during executive task performance, consistent with the engagement of a general-purpose cognitive control network, with critical nodes in the dorsolateral PFC and ACC.
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Modafinil: A Review of Neurochemical Actions and Effects on Cognition

TL;DR: Overall, modafinil is an excellent candidate agent for remediation of cognitive dysfunction in neuropsychiatric disorders and shows initial promise for a variety of off-label indications in psychiatry.
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Cognitive Control Deficits in Schizophrenia: Mechanisms and Meaning

TL;DR: This model provides a theoretical link between cellular abnormalities, functional disturbances in local circuit function, altered inter-regional cortical connectivity, and symptom presentation in the disorder and discusses recent advances in the neuropharmacology of cognition.
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GABA Concentration Is Reduced in Visual Cortex in Schizophrenia and Correlates with Orientation-Specific Surround Suppression

TL;DR: The results suggest that a neocortical GABA deficit in subjects with schizophrenia leads to impaired cortical inhibition and that GABAergic synaptic transmission in visual cortex plays a critical role in OSSS.
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Fronto-limbic dysfunction in response to facial emotion in borderline personality disorder: an event-related fMRI study.

TL;DR: The authors found that adults with borderline personality disorder exhibit changes in fronto-limbic activity in the processing of fear stimuli, with exaggerated amygdala response and impaired emotion-modulation of ACC activity.