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Open AccessJournal ArticleDOI

The Role of Genes, Stress, and Dopamine in the Development of Schizophrenia.

TLDR
A model is presented of how genes and environmental factors may sensitize the dopamine system so that it is vulnerable to acute stress, leading to progressive dysregulation and the onset of psychosis.
About
This article is published in Biological Psychiatry.The article was published on 2017-01-01 and is currently open access. It has received 410 citations till now. The article focuses on the topics: Dopaminergic & Dopamine receptor D3.

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Citations
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Dopamine: Functions, Signaling, and Association with Neurological Diseases

TL;DR: The aspects of dopamine as a catecholaminergic neurotransmitter and dopamine signaling pathways elicited through dopamine receptor activation in normal brain function are summarized and the potential involvement of these signaling pathways in evoking the onset and progression of some diseases in the nervous system are described.
Journal ArticleDOI

30 Years on: How the Neurodevelopmental Hypothesis of Schizophrenia Morphed Into the Developmental Risk Factor Model of Psychosis

TL;DR: The neurodevelopment hypothesis of schizophrenia morphed into the developmental risk factor model of psychosis and integrated new evidence concerning dysregulated striatal dopamine as the final step on the pathway linking risk factors to psychotic symptoms.
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Defining the Locus of Dopaminergic Dysfunction in Schizophrenia: A Meta-analysis and Test of the Mesolimbic Hypothesis

TL;DR: In individuals with schizophrenia dopaminergic dysfunction is greater in dorsal compared to limbic subdivisions of the striatum, which is inconsistent with the mesolimbic hypothesis and identifies the dorsal striatum as a target for novel treatment development.
Journal ArticleDOI

Auditory verbal hallucinations and continuum models of psychosis: A systematic review of the healthy voice-hearer literature

TL;DR: Overall the results of the present systematic review support a continuum view rather than a diagnostic model, but cannot distinguish between ‘quasi’ and ‘fully’ dimensional models.
References
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Journal ArticleDOI

Stress weakens prefrontal networks: molecular insults to higher cognition

TL;DR: Understanding of stress signaling pathways by genetic insults likely contributes to PFC deficits in schizophrenia, while age-related insults initiate interacting vicious cycles that increase vulnerability to Alzheimer's degeneration.
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NMDA receptor hypofunction produces concomitant firing rate potentiation and burst activity reduction in the prefrontal cortex

TL;DR: Using ensemble recording in freely moving rats, it is found that NMDA antagonist treatment, at doses that impaired working memory, potentiated the firing rate of most prefrontal cortex neurons, which provides a physiological basis for the NMDA receptor deficiency model of schizophrenia and may clarify the nature of cortical dysfunction in this disease.
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Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice.

TL;DR: Exposure to prenatal immune challenge and peripubertal stress induces synergistic pathological effects on adult behavioral functions and neurochemistry and it is demonstrated that the prenatal insult markedly increases the vulnerability of the pubescent offspring to brain immune changes in response to stress.
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Linking neurodevelopmental and synaptic theories of mental illness through DISC1

TL;DR: The disrupted in schizophrenia 1 (DISC1) gene was originally discovered at the breakpoint of an inherited chromosomal translocation, which segregates with major mental illnesses.
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Microglial Activity in People at Ultra High Risk of Psychosis and in Schizophrenia: An [11C]PBR28 PET Brain Imaging Study

TL;DR: It is suggested that neuroinflammation is linked to the risk of psychosis and related disorders, as well as the expression of subclinical symptoms, in participants at ultra high risk for psychosis.
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