Sleep, inflammation, and perception of sad facial emotion: A laboratory-based study in older adults

Piber, Dominique; Eisenberger, Naomi I.; Olmstead, Richard G.; Cho, Hyong Jin; Breen, Elizabeth C.; Boyle, Chloe C.; Karmarkar, Ellora; Guzmán, María Dolores Martínez; Kim, Haesoo; Irwin, Michael R.

doi:10.1016/j.bbi.2020.06.011

Cited by 7 publications

(7 citation statements)

References 70 publications

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“…Whereas it is known that sleep disturbance is associated with subjective reports of negative affect, there are few empirical studies that have examined tasks of emotional processing, even though accurate face judgments may modulate emotional reactivity. We have previously found that sleep disturbance is associated with a delay in recognition of sad facial emotion in older adults ( Piber et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Sleep and Healthy Aging Research on Depression (SHARE-D) randomized controlled trial: Protocol overview of an experimental model of depression with insomnia, inflammation, and affect mechanisms in older adults

Irwin

Boyle

Cho

et al. 2023

Brain, Behavior, & Immunity - Health

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Section: Discussionmentioning

confidence: 99%

Sleep and Healthy Aging Research on Depression (SHARE-D) randomized controlled trial: Protocol overview of an experimental model of depression with insomnia, inflammation, and affect mechanisms in older adults

Irwin

Boyle

Cho

et al. 2023

Brain, Behavior, & Immunity - Health

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“…We evaluated five immune markers (interleukin‐6 [IL‐6], IL‐8, IL‐10, tumor necrosis factor α [TNF‐α], and interferon γ [IFN‐γ]) previously associated with cognition in cancer survivors 13,18–20,22–25 . Marker plasma levels were determined using an electrochemiluminescent immunoassay (MesoScale Discovery Custom Human Cytokine Proinflammatory Panel, Rockville, Maryland) 26 . Assays were performed in duplicate at a 2‐fold sample dilution with an extended eight‐point standard curve of serial 3‐fold dilutions.…”

Section: Methodsmentioning

confidence: 99%

“…13,[18][19][20][22][23][24][25] Marker plasma levels were determined using an electrochemiluminescent immunoassay (MesoScale Discovery Custom Human Cytokine Proinflammatory Panel, Rockville, Maryland). 26 Assays were performed in duplicate at a 2-fold sample dilution with an extended eight-point standard curve of serial 3-fold dilutions.…”

Section: Populationmentioning

confidence: 99%

Plasma levels of interleukin‐6 mediate neurocognitive performance in older breast cancer survivors: The Thinking and Living With Cancer study

Mandelblatt

Small

Zhou

et al. 2023

Cancer

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Background Immune activation/inflammation markers (immune markers) were tested to explain differences in neurocognition among older breast cancer survivors versus noncancer controls. Methods Women >60 years old with primary breast cancer (stages 0–III) (n = 400) were assessed before systemic therapy with frequency‐matched controls (n = 329) and followed annually to 60 months; blood was collected during annual assessments from 2016 to 2020. Neurocognition was measured by tests of attention, processing speed, and executive function (APE). Plasma levels of interleukin‐6 (IL‐6), IL‐8, IL‐10, tumor necrosis factor α (TNF‐α), and interferon γ were determined using multiplex testing. Mixed linear models were used to compare results of immune marker levels by survivor/control group by time and by controlling for age, racial/ethnic group, cognitive reserve, and study site. Covariate‐adjusted multilevel mediation analyses tested whether survivor/control group effects on cognition were explained by immune markers; secondary analyses examined the impact of additional covariates (e.g., comorbidity and obesity) on mediation effects. Results Participants were aged 60–90 years (mean, 67.7 years). Most survivors had stage I (60.9%) estrogen receptor–positive tumors (87.6%). Survivors had significantly higher IL‐6 levels than controls before systemic therapy and at 12, 24, and 60 months (p ≤ .001–.014) but there were no differences for other markers. Survivors had lower adjusted APE scores than controls (p < .05). Levels of IL‐6, IL‐10, and TNF‐α were related to APE, with IL‐6 explaining part of the relationship between survivor/control group and APE (p = .01). The magnitude of this mediation effect decreased but remained significant (p = .047) after the consideration of additional covariates. Conclusions Older breast cancer survivors had worse long‐term neurocognitive performance than controls, and this relationship was explained in part by elevated IL‐6.

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“…Plasma levels of TNF‐α, IL‐6, IL‐8, IL‐10 and IFN‐γ were evaluated using the Meso Scale Discovery MULTI‐SPOT Assay System (Rockville, MD 49 ). Plasma samples were assayed in duplicate on a custom 5‐plex from the Proinflammatory Panel 1 Human Kit.…”

Section: Methodsmentioning

confidence: 99%

Effects of ibudilast on central and peripheral markers of inflammation in alcohol use disorder: A randomized clinical trial

et al. 2022

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Ibudilast, a neuroimmune modulator, shows promise as a pharmacotherapy for alcohol use disorder (AUD). In vivo administration of ibudilast reduces the expression of pro‐inflammatory cytokines in animal models, but its effects on markers of inflammation in humans are unknown. This preliminary study examined the effect of ibudilast on peripheral and potential central markers of inflammation in individuals with AUD. This study also explored the predictive relationship of neurometabolite markers with subsequent drinking in the trial. Non‐treatment‐seeking individuals with an AUD (n = 52) were randomized to receive oral ibudilast (n = 24) or placebo (n = 28) for 2 weeks. Plasma levels of peripheral inflammatory markers were measured at baseline and after 1 and 2 weeks of medication. At study mid‐point, proton magnetic resonance spectroscopy was performed to measure potential neurometabolite markers of inflammation: choline‐compounds (Cho), myo‐inositol (MI) and creatine + phosphocreatine (Cr) in frontal and cingulate cortices from 43 participants (ibudilast: n = 20; placebo: n = 23). The treatment groups were compared on peripheral and central markers. Ibudilast‐treated participants had lower Cho in superior frontal white matter and nominally lower MI in pregenual anterior cingulate cortex. Ibudilast‐treated participants had nominally lower C‐reactive protein levels at visit 2 and nominally lower TNF‐α/IL‐10 ratios, relative to placebo. C‐reactive protein and Cho levels were correlated, controlling for medication. Superior frontal white matter Cho predicted drinking in the following week. Micro‐longitudinal ibudilast treatment may induce peripheral and putative central anti‐inflammatory responses in patients with AUD. The neurometabolite responses may be associated with reduction in drinking, suggesting an anti‐inflammatory component to the therapeutic action of ibudilast.

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Sleep, inflammation, and perception of sad facial emotion: A laboratory-based study in older adults

Cited by 7 publications

References 70 publications

Sleep and Healthy Aging Research on Depression (SHARE-D) randomized controlled trial: Protocol overview of an experimental model of depression with insomnia, inflammation, and affect mechanisms in older adults

Sleep and Healthy Aging Research on Depression (SHARE-D) randomized controlled trial: Protocol overview of an experimental model of depression with insomnia, inflammation, and affect mechanisms in older adults

Plasma levels of interleukin‐6 mediate neurocognitive performance in older breast cancer survivors: The Thinking and Living With Cancer study

Effects of ibudilast on central and peripheral markers of inflammation in alcohol use disorder: A randomized clinical trial

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