2015
DOI: 10.1590/2237-6089-2015-0007
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The role of inflammation in schizophrenia: an overview

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Cited by 5 publications
(7 citation statements)
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“…42 Second, CBF changes may be the result of changes in neurotransmitters (eg, dopamine 64,65 and GABA 66,67 ) and non-specific agents (eg, nitric oxide 68,69 ) in schizophrenia, because these chemicals also play a role in modulating vascular response. [70][71][72] Finally, CBF changes may be related to microvasculature alterations associated with neuroinflammation in schizophrenia, [73][74][75] resulting in imprecise regulation of CBF. 76 FCS depicts a whole-brain functional connectivity profile of each voxel from a global network perspective, [12][13][14][15] and reflects the role of each voxel in information transmission in the whole brain network.…”
Section: Discussionmentioning
confidence: 99%
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“…42 Second, CBF changes may be the result of changes in neurotransmitters (eg, dopamine 64,65 and GABA 66,67 ) and non-specific agents (eg, nitric oxide 68,69 ) in schizophrenia, because these chemicals also play a role in modulating vascular response. [70][71][72] Finally, CBF changes may be related to microvasculature alterations associated with neuroinflammation in schizophrenia, [73][74][75] resulting in imprecise regulation of CBF. 76 FCS depicts a whole-brain functional connectivity profile of each voxel from a global network perspective, [12][13][14][15] and reflects the role of each voxel in information transmission in the whole brain network.…”
Section: Discussionmentioning
confidence: 99%
“…Abnormal GABA interneurons in schizophrenia 66,67 may also contribute to neurovascular decoupling since normal GABA interneurons play an important role in modulating neurovascular coupling. 71,95 Additionally, other factors (eg, nitric oxide 68,69 and neuroinflammation [73][74][75][76] ) that affect vascular components (CBF) but not neuronal activity (FCS), could also result in neurovascular decoupling.…”
Section: Discussionmentioning
confidence: 99%
“…While fetal hypoxia has strong support as a risk factor for schizophrenia (Clarke et al, 2012;, it has also been proposed to mediate the effects of other OC Clarke et al, 2012). Research also indicate an association between schizophrenia and prenatal exposure to infection (Brown, 2006;Mittal et al, 2008b), to inflammation Chaves et al, 2015), to stress (Holloway et al, 2013;Khashan et al, 2008;Malaspina et al, 2008;van Os and Selten, 1998) and to diabetes (Cannon et al, 2002;Van Lieshout and Voruganti, 2008). Though the results diverge, a few studies find a relationship between risk of schizophrenia and a low birth weight, especially below 2500 g (Abel et al, 2010;, a low and high birth weight ) and a low gestational age Geddes et al, 1999;.…”
Section: Introductionmentioning
confidence: 99%
“…The repercussions of immune dysregulation on neuronal signaling, synapse organization, and brain connectivity are also significant ( 19 , 43 , 44 ). Williams et al.…”
Section: The Vulnerability-stress-inflammation Model Of Schizophreniamentioning
confidence: 99%