Neuroimaging biomarkers for early drug development in schizophrenia.
TLDR
This review evaluates three potential neuroimaging biomarkers: hippocampal hyperactivity, gamma-band deficits, and default network abnormalities, which have shown initial promise as biomarkers of biological response in early studies of potential treatment strategies.About:
This article is published in Biological Psychiatry.The article was published on 2014-07-15 and is currently open access. It has received 44 citations till now.read more
Citations
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GABAergic mechanisms of hippocampal hyperactivity in schizophrenia
TL;DR: The post-mortem and animal studies are consistent with the neuroimaging finding of increased hippocampal activity in schizophrenia, which can explain some of the psychotic symptoms and cognitive deficits, and may guide the development of biomarkers and theDevelopment of new treatments for psychosis.
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γ-band abnormalities as markers of autism spectrum disorders.
Donald C. Rojas,Lisa B. Wilson +1 more
TL;DR: Although the utility of γ-band metrics as diagnostic biomarkers is currently limited, such changes in autism are also useful as endophenotypes, for evaluating potential neural mechanisms, and for use as surrogate markers of treatment response to interventions.
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Intrinsic Hippocampal Activity as a Biomarker for Cognition and Symptoms in Schizophrenia
Jason R. Tregellas,Jason Smucny,Josette G. Harris,Ann Olincy,Keeran Maharajh,Eugene Kronberg,Lindsay C. Eichman,Emma Lyons,Robert Freedman +8 more
TL;DR: Findings suggest that greater intrinsic hippocampal activity is a characteristic feature of schizophrenia that is broadly associated with cognitive dysfunction, and they support hippocampusal activity as a candidate biomarker for therapeutic development.
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Increased hippocampal CA1 cerebral blood volume in schizophrenia.
Pratik Talati,Swati Rane,Samet Kose,Jennifer Urbano Blackford,John C. Gore,Manus J. Donahue,Stephan Heckers +6 more
TL;DR: The results support the emerging hypothesis of increased hippocampal activity as a biomarker of schizophrenia and highlight the importance of subfield-level investigations.
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Neuroimaging Biomarkers in Schizophrenia.
Nina V. Kraguljac,William M. McDonald,Alik S. Widge,Carolyn I. Rodriguez,Mauricio Tohen,Charles B Nemeroff +5 more
TL;DR: In this article, the authors discuss a range of mechanistically plausible neuroimaging biomarker candidates, including dopamine hyperactivity, N-methyl-d-aspartate receptor hypofunction, hippocampal hyperactivity and immune dysregulation, dysconnectivity and cortical gray matter volume loss.
References
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A default mode of brain function.
Marcus E. Raichle,Ann Mary MacLeod,Abraham Z. Snyder,William J. Powers,Debra A. Gusnard,Gordon L. Shulman +5 more
TL;DR: A baseline state of the normal adult human brain in terms of the brain oxygen extraction fraction or OEF is identified, suggesting the existence of an organized, baseline default mode of brain function that is suspended during specific goal-directed behaviors.
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The Brain's Default Network Anatomy, Function, and Relevance to Disease
TL;DR: Past observations are synthesized to provide strong evidence that the default network is a specific, anatomically defined brain system preferentially active when individuals are not focused on the external environment, and for understanding mental disorders including autism, schizophrenia, and Alzheimer's disease.
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Functional connectivity in the resting brain: A network analysis of the default mode hypothesis
TL;DR: This study constitutes, to the knowledge, the first resting-state connectivity analysis of the default mode and provides the most compelling evidence to date for the existence of a cohesive default mode network.
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Mechanisms of Gamma Oscillations
György Buzsáki,Xiao Jing Wang +1 more
TL;DR: The cellular and synaptic mechanisms underlying gamma oscillations are reviewed and empirical questions and controversial conceptual issues are outlined, finding that gamma-band rhythmogenesis is inextricably tied to perisomatic inhibition.
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Cortical inhibitory neurons and schizophrenia
TL;DR: Convergent findings indicate that a deficiency in signalling through the TrkB neurotrophin receptor leads to reduced GABA synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia.