Selective effects of acute low-grade inflammation on human visual attention

Balter, L.J.; Bosch, Jos A.; Aldred, Sarah; Drayson, Mark T.; Zanten, Jet J.C.S. Veldhuijzen van; Higgs, Suzanne; Raymond, Jane E.; Mazaheri, Ali

doi:10.1016/j.neuroimage.2019.116098

Cited by 17 publications

(21 citation statements)

References 67 publications

(84 reference statements)

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“…While these analyses only considered structural MRI, additional complementary imaging approaches that examine cerebral perfusion ( 72 ), extracellular free-water ( 73 , 74 ) or fMRI connectivity networks (e.g. default mode ( 75 ), central executive ( 76 ) and visual networks ( 77 )) linked to these regions may improve our understand the pathophysiological effects of peripheral inflammation on microvascular dysfunction, neuroinflammation and functional connectivity.…”

Section: Discussionmentioning

confidence: 99%

Multivariate relationships between peripheral inflammatory marker subtypes and cognitive and brain structural measures in psychosis

Lizano

Lutz

et al. 2020

Mol Psychiatry

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Elevations in peripheral inflammatory markers have been reported in patients with psychosis. Whether this represents an inflammatory process defined by individual or subgroups of markers is unclear. Further, relationships between peripheral inflammatory marker elevations and brain structure, cognition, and clinical features of psychosis remain unclear. We hypothesized that a pattern of plasma inflammatory markers, and an inflammatory subtype established from this pattern, would be elevated across the psychosis spectrum and associated with cognition and brain structural alterations. Clinically stable psychosis probands (Schizophrenia spectrum, n=79; Psychotic Bipolar disorder, n=61) and matched healthy controls (HC, n=60) were assessed for 15 peripheral inflammatory markers, cortical thickness, subcortical volume, cognition, and symptoms. A combination of unsupervised exploratory factor analysis and hierarchical clustering was used to identify inflammation subtypes. Levels of IL6, TNFα, VEGF, and CRP were significantly higher in psychosis probands compared to HCs, and there were marker-specific differences when comparing diagnostic groups. Individual and/or inflammatory marker patterns were associated with neuroimaging, cognition, and symptom measures. A higher inflammation subgroup was defined by elevations in a group of 7 markers in 36% of Probands and 20% of HCs. Probands in the elevated inflammatory marker group performed significantly worse on cognitive measures of visuo-spatial working memory and response inhibition, displayed elevated hippocampal, amygdala, putamen and thalamus volumes, and evidence of gray matter thickening compared to the proband group with low inflammatory marker levels. These findings specify the nature of peripheral inflammatory marker alterations in psychotic disorders and establish clinical, neurocognitive and neuroanatomic associations with increased inflammatory activation in psychosis. The identification of a specific subgroup of patients with inflammatory alteration provides a potential means for targeting treatment with anti-inflammatory medications.

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Section: Discussionmentioning

confidence: 99%

Multivariate relationships between peripheral inflammatory marker subtypes and cognitive and brain structural measures in psychosis

Lizano

Lutz

et al. 2020

Mol Psychiatry

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“…Experimentally induced inflammation via administration of immune-activating agents, such as bacterial endotoxin or vaccination, also causes psychomotor slowing 7 , memory deficits 10 and alterations of social cognition 58,59 . However, the extant literature using experimental induction of inflammation so far provides little evidence of degraded selective attention 60 (reviewed in 61 ), suggesting the possibility of domain-specificity in the inflammation-cognition link.…”

Section: Introductionmentioning

confidence: 99%

Inflammation Mediates Body Weight and Ageing Effects on Psychomotor Slowing

Balter

Higgs

Aldred

et al. 2019

Sci Rep

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Inflammation (immune system activation) affects neuronal function and may have consequences for the efficiency and speed of functional brain processes. Indeed, unusually slow psychomotor speed, a measure predictive of behavioural performance and health outcomes, is found with obesity and ageing, two conditions also associated with chronic inflammation. Yet whether inflammation is the mediating factor remains unclear. Here, we assessed inflammation by indexing interleukin-6 level in blood and measured psychomotor speed as well as indices of selective visual attention in young (mean = 26 years) or old (mean = 71 years) adults (N = 83) who were either lean or currently significantly overweight (mean body mass index = 22.4 and 33.8, respectively). Inflammation was positively and significantly correlated with psychomotor speed, age, and body mass index but not with attention measures. Using mediation analyses we show for the first time that inflammation fully accounts for the significant psychomotor slowing found in those with high BMI. Moreover, we further show that age-related psychomotor slowing is partially mediated by inflammation. These findings support the proposal that reducing inflammation may mitigate weight- and age-related cognitive decline and thereby improve performance on daily tasks and health outcomes more generally.

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“…This result demonstrates that combined, alcohol and FPI injuries do not necessarily exacerbate the degree of in ammation, but rather prolong its persistence. However, failure to resolve this in ammation can lead to a chronic in ammatory state in the CNS and manifest debilitations in attention and cognition [38].…”

Section: Hemosiderin and Transferrin Bindingmentioning

confidence: 99%

Hemolytic Iron Regulation in Traumatic Brain Injury and Alcohol Use

Agas

Ravula

et al. 2022

Preprint

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Hemorrhage is often a major component of traumatic brain injury (TBI). Red blood cells (RBCs), accumulated at the hemorrhagic site, undergo hemolysis upon energy depletion. Hemolysis of RBCs is expected to release free iron into the central nervous system (CNS) which must be managed to prevent iron neurotoxicity. Here, we examine the hypothesis that chronic alcohol consumption, as a secondary stressor, may increase iron toxicity in a rat model of TBI by altering the iron management pathways. We found large accumulations of free iron at the site of hemorrhage with evidence of hemolytic activity. Our observations demonstrate that alcohol use can alter the three distinct iron management pathways: transferrin/hemosiderin binding, lipocalin 2/heme oxygenase 1/ferritin system, and possible microglial phagocytosis. Presence of alcohol prolonged the expression of lipocalin 2 as well as increased and sustained levels of ferritin, while the combined effects of alcohol and TBI elevated the levels of heme oxygenase 1 faster than TBI alone. The hippocampus, neocortex, ventricles, and around vessels near the site of impact appeared to be the prominent brain regions of induction. In addition, we provide evidence that microglia my also play a role in iron management through RBC phagocytosis.

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Selective effects of acute low-grade inflammation on human visual attention

Cited by 17 publications

References 67 publications

Multivariate relationships between peripheral inflammatory marker subtypes and cognitive and brain structural measures in psychosis

Multivariate relationships between peripheral inflammatory marker subtypes and cognitive and brain structural measures in psychosis

Inflammation Mediates Body Weight and Ageing Effects on Psychomotor Slowing

Hemolytic Iron Regulation in Traumatic Brain Injury and Alcohol Use

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