Pub Date : 2024-07-20DOI: 10.1016/j.bpsgos.2024.100366
Lucas Wahl, Arun Karim, Amy R. Hassett, Max van der Doe, Stephanie Dijkhuizen, Aleksandra Badura
Background
Current phenotyping approaches for murine autism models often focus on one selected behavioral feature, making the translation onto a spectrum of autistic characteristics in humans challenging. Furthermore, sex and environmental factors are rarely considered. Here, we aimed to capture the full spectrum of behavioral manifestations in 3 autism mouse models to develop a “behavioral fingerprint” that takes environmental and sex influences under consideration.
Methods
To this end, we employed a wide range of classical standardized behavioral tests and 2 multiparametric behavioral assays—the Live Mouse Tracker and Motion Sequencing—on male and female Shank2, Tsc1, and Purkinje cell–specific Tsc1 mutant mice raised in standard or enriched environments. Our aim was to integrate our high dimensional data into one single platform to classify differences in all experimental groups along dimensions with maximum discriminative power.
Results
Multiparametric behavioral assays enabled a more accurate classification of experimental groups than classical tests, and dimensionality reduction analysis demonstrated significant additional gains in classification accuracy, highlighting the presence of sex, environmental, and genotype differences in our experimental groups.
Conclusions
Together, our results provide a complete phenotypic description of all tested groups, suggesting that multiparametric assays can capture the entire spectrum of the heterogeneous phenotype in autism mouse models.
{"title":"Multiparametric Assays Capture Sex- and Environment-Dependent Modifiers of Behavioral Phenotypes in Autism Mouse Models","authors":"Lucas Wahl, Arun Karim, Amy R. Hassett, Max van der Doe, Stephanie Dijkhuizen, Aleksandra Badura","doi":"10.1016/j.bpsgos.2024.100366","DOIUrl":"10.1016/j.bpsgos.2024.100366","url":null,"abstract":"<div><h3>Background</h3><p>Current phenotyping approaches for murine autism models often focus on one selected behavioral feature, making the translation onto a spectrum of autistic characteristics in humans challenging. Furthermore, sex and environmental factors are rarely considered. Here, we aimed to capture the full spectrum of behavioral manifestations in 3 autism mouse models to develop a “behavioral fingerprint” that takes environmental and sex influences under consideration.</p></div><div><h3>Methods</h3><p>To this end, we employed a wide range of classical standardized behavioral tests and 2 multiparametric behavioral assays—the Live Mouse Tracker and Motion Sequencing—on male and female <em>Shank2</em>, <em>Tsc1</em>, and Purkinje cell–specific <em>Tsc1</em> mutant mice raised in standard or enriched environments. Our aim was to integrate our high dimensional data into one single platform to classify differences in all experimental groups along dimensions with maximum discriminative power.</p></div><div><h3>Results</h3><p>Multiparametric behavioral assays enabled a more accurate classification of experimental groups than classical tests, and dimensionality reduction analysis demonstrated significant additional gains in classification accuracy, highlighting the presence of sex, environmental, and genotype differences in our experimental groups.</p></div><div><h3>Conclusions</h3><p>Together, our results provide a complete phenotypic description of all tested groups, suggesting that multiparametric assays can capture the entire spectrum of the heterogeneous phenotype in autism mouse models.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 6","pages":"Article 100366"},"PeriodicalIF":4.0,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266717432400079X/pdfft?md5=aae6cbb8f3589d02645965481b4149ef&pid=1-s2.0-S266717432400079X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142040382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-15DOI: 10.1016/j.bpsgos.2024.100359
Ling-Sha Ju , Timothy Morey , Nikolaus Gravenstein , Barry Setlow , Christoph N. Seubert , Anatoly E. Martynyuk
Background
Having a sibling with autism spectrum disorder is a risk factor for autism spectrum disorder. We used a rat model in which the general anesthetic sevoflurane (SEVO) induces autism spectrum disorder–like neurodevelopmental abnormalities to test whether they can be transmitted via cohabitation.
Methods
Male rat pups from several litters were mixed and randomized to 3 new litter types: SEVO-exposed (SEVO), SEVO-unexposed (control), and equal numbers of SEVO-exposed and SEVO-unexposed (MIXED). After weaning, rats in experiment 1 were housed with littermates in SEVO, control, and MIXED (MIXED-exposed and MIXED-unexposed) pairs. In experiment 2, MIXED-exposed and MIXED-unexposed rats were paired with an unfamiliar naïve cagemate. Corticosterone levels, gene expression, central inflammatory markers (experiment 1), and behavior and corticosterone levels (experiment 2) were assessed in adulthood.
Results
In experiment 1, compared with control rats, SEVO rats exhibited abnormalities in the hypothalamic-pituitary-adrenal axis, inflammatory markers, oxytocin, arginine vasopressin, and DNA methylation systems. Almost all these measures in MIXED-exposed and MIXED-unexposed rats were statistically indistinguishable from and similar to those in SEVO or control rats, with most measures in MIXED rats being similar to those in SEVO rats. Experiment 2 showed that pairing with unfamiliar, naïve rats after weaning caused MIXED-unexposed and MIXED-exposed rats’ behavior to be no different from that of control and SEVO rats, respectively; however, the 2 groups of MIXED rats also did not differ from each other.
Conclusions
These findings suggest that neurodevelopmental abnormalities can be transmitted to otherwise healthy individuals through interactions during cohabitation; however, subsequent pairing with unfamiliar, naïve cohabitants may weaken this interaction effect.
{"title":"Effects of Cohabitation on Neurodevelopmental Outcomes in Rats Discordant for Neonatal Exposure to Sevoflurane","authors":"Ling-Sha Ju , Timothy Morey , Nikolaus Gravenstein , Barry Setlow , Christoph N. Seubert , Anatoly E. Martynyuk","doi":"10.1016/j.bpsgos.2024.100359","DOIUrl":"10.1016/j.bpsgos.2024.100359","url":null,"abstract":"<div><h3>Background</h3><p>Having a sibling with autism spectrum disorder is a risk factor for autism spectrum disorder. We used a rat model in which the general anesthetic sevoflurane (SEVO) induces autism spectrum disorder–like neurodevelopmental abnormalities to test whether they can be transmitted via cohabitation.</p></div><div><h3>Methods</h3><p>Male rat pups from several litters were mixed and randomized to 3 new litter types: SEVO-exposed (SEVO), SEVO-unexposed (control), and equal numbers of SEVO-exposed and SEVO-unexposed (MIXED). After weaning, rats in experiment 1 were housed with littermates in SEVO, control, and MIXED (MIXED-exposed and MIXED-unexposed) pairs. In experiment 2, MIXED-exposed and MIXED-unexposed rats were paired with an unfamiliar naïve cagemate. Corticosterone levels, gene expression, central inflammatory markers (experiment 1), and behavior and corticosterone levels (experiment 2) were assessed in adulthood.</p></div><div><h3>Results</h3><p>In experiment 1, compared with control rats, SEVO rats exhibited abnormalities in the hypothalamic-pituitary-adrenal axis, inflammatory markers, oxytocin, arginine vasopressin, and DNA methylation systems. Almost all these measures in MIXED-exposed and MIXED-unexposed rats were statistically indistinguishable from and similar to those in SEVO or control rats, with most measures in MIXED rats being similar to those in SEVO rats. Experiment 2 showed that pairing with unfamiliar, naïve rats after weaning caused MIXED-unexposed and MIXED-exposed rats’ behavior to be no different from that of control and SEVO rats, respectively; however, the 2 groups of MIXED rats also did not differ from each other.</p></div><div><h3>Conclusions</h3><p>These findings suggest that neurodevelopmental abnormalities can be transmitted to otherwise healthy individuals through interactions during cohabitation; however, subsequent pairing with unfamiliar, naïve cohabitants may weaken this interaction effect.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 6","pages":"Article 100359"},"PeriodicalIF":4.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000727/pdfft?md5=700f2ec060b6ea80ccbce99d9fbd9550&pid=1-s2.0-S2667174324000727-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141691464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/S2667-1743(24)00062-4
{"title":"Subscribers Page","authors":"","doi":"10.1016/S2667-1743(24)00062-4","DOIUrl":"10.1016/S2667-1743(24)00062-4","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100349"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000624/pdfft?md5=dcb361af4d3c269a9f865eb2e74e8f05&pid=1-s2.0-S2667174324000624-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/S2667-1743(24)00064-8
{"title":"Guide for Authors","authors":"","doi":"10.1016/S2667-1743(24)00064-8","DOIUrl":"10.1016/S2667-1743(24)00064-8","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100351"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000648/pdfft?md5=8e33f4496acd15507ecfb2b321bacf5e&pid=1-s2.0-S2667174324000648-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/S2667-1743(24)00061-2
{"title":"Editorial Board Page","authors":"","doi":"10.1016/S2667-1743(24)00061-2","DOIUrl":"10.1016/S2667-1743(24)00061-2","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100348"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000612/pdfft?md5=4f6f0078669bf5335ccc8a2e1a3d4c61&pid=1-s2.0-S2667174324000612-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/j.bpsgos.2024.100335
Sanne J.H. van Rooij
{"title":"Targeting the Hippocampus in the Context of Trauma","authors":"Sanne J.H. van Rooij","doi":"10.1016/j.bpsgos.2024.100335","DOIUrl":"10.1016/j.bpsgos.2024.100335","url":null,"abstract":"","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100335"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266717432400048X/pdfft?md5=5ad797f21fe297e1ba10d663f2c2993a&pid=1-s2.0-S266717432400048X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01DOI: 10.1016/j.bpsgos.2024.100330
Hestia Moningka , Liam Mason
Background
Dysregulated reward processing and mood instability are core features of bipolar disorder that have largely been considered separately, with contradictory findings. We sought to test a mechanistic account that emphasizes an excessive tendency in bipolar disorder to enter recursive cycles in which reward perception is biased by signals that the environment may be changing for the better or worse.
Methods
Participants completed a probabilistic reward task with functional magnetic resonance imaging. Using an influential computational model, we ascertained whether participants with bipolar disorder (n = 21) showed greater striatal tracking of momentum-biased reward prediction errors (RPEs) than matched control participants (n = 21). We conducted psychophysiological interaction analyses to quantify the degree to which each group modulated functional connectivity between the ventral striatum and left anterior insula in response to fluctuations in momentum.
Results
In participants with bipolar disorder, but not control participants, the momentum-biased RPE model accounted for significant additional variance in striatal activity beyond a standard model of veridical RPEs. Compared with control participants, participants with bipolar disorder exhibited lower insular-striatal functional connectivity modulated by momentum-biased RPEs, an effect that was more pronounced as a function of current manic symptoms.
Conclusions
Consistent with existing theory, we found evidence that bipolar disorder is associated with a tendency for momentum to excessively bias striatal tracking of RPEs. We identified impaired insular-striatal connectivity as a possible locus for this propensity. We argue that computational psychiatric approaches that examine momentary shifts in reward and mood dynamics have strong potential for yielding new mechanistic insights and intervention targets.
{"title":"Misperceiving Momentum: Computational Mechanisms of Biased Striatal Reward Prediction Errors in Bipolar Disorder","authors":"Hestia Moningka , Liam Mason","doi":"10.1016/j.bpsgos.2024.100330","DOIUrl":"10.1016/j.bpsgos.2024.100330","url":null,"abstract":"<div><h3>Background</h3><p>Dysregulated reward processing and mood instability are core features of bipolar disorder that have largely been considered separately, with contradictory findings. We sought to test a mechanistic account that emphasizes an excessive tendency in bipolar disorder to enter recursive cycles in which reward perception is biased by signals that the environment may be changing for the better or worse.</p></div><div><h3>Methods</h3><p>Participants completed a probabilistic reward task with functional magnetic resonance imaging. Using an influential computational model, we ascertained whether participants with bipolar disorder (<em>n</em> = 21) showed greater striatal tracking of momentum-biased reward prediction errors (RPEs) than matched control participants (<em>n</em> = 21). We conducted psychophysiological interaction analyses to quantify the degree to which each group modulated functional connectivity between the ventral striatum and left anterior insula in response to fluctuations in momentum.</p></div><div><h3>Results</h3><p>In participants with bipolar disorder, but not control participants, the momentum-biased RPE model accounted for significant additional variance in striatal activity beyond a standard model of veridical RPEs. Compared with control participants, participants with bipolar disorder exhibited lower insular-striatal functional connectivity modulated by momentum-biased RPEs, an effect that was more pronounced as a function of current manic symptoms.</p></div><div><h3>Conclusions</h3><p>Consistent with existing theory, we found evidence that bipolar disorder is associated with a tendency for momentum to excessively bias striatal tracking of RPEs. We identified impaired insular-striatal connectivity as a possible locus for this propensity. We argue that computational psychiatric approaches that examine momentary shifts in reward and mood dynamics have strong potential for yielding new mechanistic insights and intervention targets.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 4","pages":"Article 100330"},"PeriodicalIF":4.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000430/pdfft?md5=fec0e6195a7b2242719484cff2576524&pid=1-s2.0-S2667174324000430-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141623582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-29DOI: 10.1016/j.bpsgos.2024.100357
Yanli Lin , Marne L. White , Deanna Wu , Natee Viravan , Todd S. Braver
Background
Mindfulness has long been theorized to benefit emotion regulation, but despite the ubiquity of the claim, there is little empirical evidence demonstrating how mindfulness modulates the neurophysiology of emotion processing. The current study aimed to fill this gap in knowledge by leveraging a novel research approach capable of discretizing mindfulness into distinct states of open monitoring (OM) and focused attention (FA) to distinguish their influence on multimodal subjective and objective measures of emotion processing.
Methods
Utilizing a fully within-participant picture viewing state induction protocol (N = 30), we compared the effects of OM and FA, rigorously contrasted against an active control, on the visually evoked late positive potential (LPP), a neural index of motivated attention. Bayesian mixed modeling was used to distinguish OM versus FA effects on the early and late sustained LPP while evaluating the influence of subjective arousal ratings as a within-participant moderator of the state inductions.
Results
When negative picture trials were retrospectively rated as more subjectively arousing, the OM induction reduced the late sustained LPP response, whereas the FA induction enhanced the LPP.
Conclusions
Acute manipulation of OM and FA states may reduce and enhance motivated attention to aversive stimuli during conditions of high subjective arousal, respectively. Functional distinctions between different mindfulness states on emotion processing may be most dissociable after accounting for within-participant variability in how stimuli are appraised. These results support the future potential of the state induction protocol for parsing the neural affective mechanisms that underlie mindfulness training programs and interventions.
{"title":"Distinct Mindfulness States Produce Dissociable Effects on Neural Markers of Emotion Processing: Evidence From the Late Positive Potential","authors":"Yanli Lin , Marne L. White , Deanna Wu , Natee Viravan , Todd S. Braver","doi":"10.1016/j.bpsgos.2024.100357","DOIUrl":"10.1016/j.bpsgos.2024.100357","url":null,"abstract":"<div><h3>Background</h3><p>Mindfulness has long been theorized to benefit emotion regulation, but despite the ubiquity of the claim, there is little empirical evidence demonstrating how mindfulness modulates the neurophysiology of emotion processing. The current study aimed to fill this gap in knowledge by leveraging a novel research approach capable of discretizing mindfulness into distinct states of open monitoring (OM) and focused attention (FA) to distinguish their influence on multimodal subjective and objective measures of emotion processing.</p></div><div><h3>Methods</h3><p>Utilizing a fully within-participant picture viewing state induction protocol (<em>N</em> = 30), we compared the effects of OM and FA, rigorously contrasted against an active control, on the visually evoked late positive potential (LPP), a neural index of motivated attention. Bayesian mixed modeling was used to distinguish OM versus FA effects on the early and late sustained LPP while evaluating the influence of subjective arousal ratings as a within-participant moderator of the state inductions.</p></div><div><h3>Results</h3><p>When negative picture trials were retrospectively rated as more subjectively arousing, the OM induction reduced the late sustained LPP response, whereas the FA induction enhanced the LPP.</p></div><div><h3>Conclusions</h3><p>Acute manipulation of OM and FA states may reduce and enhance motivated attention to aversive stimuli during conditions of high subjective arousal, respectively. Functional distinctions between different mindfulness states on emotion processing may be most dissociable after accounting for within-participant variability in how stimuli are appraised. These results support the future potential of the state induction protocol for parsing the neural affective mechanisms that underlie mindfulness training programs and interventions.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100357"},"PeriodicalIF":4.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000703/pdfft?md5=aee0b80cfe093e2bc520c3ceb00ea55e&pid=1-s2.0-S2667174324000703-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141950436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-29DOI: 10.1016/j.bpsgos.2024.100356
Jee Hyung Pyo , Sae Saem Han , Min-Ji Kim , Young Kyung Moon , Su Jin Lee , Chaemin Lee , AhRam Lee , Shinn-Won Lim , Doh Kwan Kim
Background
Inflammation has been postulated as a mediating factor in the development of Alzheimer’s disease (AD) pathology. We investigated candidate inflammatory markers related to conversion to AD among patients with depression.
Methods
A longitudinal study was conducted with older women with depression who were at least 55 years of age, with a mean follow-up period of 5.73 years. At baseline, 9 inflammatory cytokines were measured using the immunoreactivity method. During follow-up, patients with depression who complained of cognitive impairment were evaluated and diagnosed with AD conversion. Association of the cytokines with conversion to AD was analyzed using multivariable Cox proportional hazards regression with adjusting covariates. For clinical applicability, the optimal cutoff value was determined using the minimum p value approach for the conversion to AD and was used to plot an AD-free survival curve.
Results
Among 132 participants, 34 patients with depression (25.76%) developed AD during their follow-up period. Higher levels of interleukin (IL) 1β at baseline (hazard ratio = 3.30 [95% CI, 1.11–9.78], p = .031) and lower levels of IL-10 (p < .001) were significantly associated with an increased risk of progression to AD. The survival curve plotted by the cutoff value of ≥0.25 pg/mL for IL-1β and ≤0.15 pg/mL for IL-10 suggested adjusted hazard ratios of 8.96 (95% CI, 3.48–23.09; p < .001) for IL-1β and 10.99 (p < .001) for IL-10, respectively.
Conclusions
This study demonstrated that IL-1β and IL-10 were associated with conversion to AD among patients with late-life depression, suggesting their potential as predictive markers of the transition to AD from depression.
{"title":"Potential Inflammatory Markers Related to the Conversion to Alzheimer’s Disease in Female Patients With Late-Life Depression","authors":"Jee Hyung Pyo , Sae Saem Han , Min-Ji Kim , Young Kyung Moon , Su Jin Lee , Chaemin Lee , AhRam Lee , Shinn-Won Lim , Doh Kwan Kim","doi":"10.1016/j.bpsgos.2024.100356","DOIUrl":"10.1016/j.bpsgos.2024.100356","url":null,"abstract":"<div><h3>Background</h3><p>Inflammation has been postulated as a mediating factor in the development of Alzheimer’s disease (AD) pathology. We investigated candidate inflammatory markers related to conversion to AD among patients with depression.</p></div><div><h3>Methods</h3><p>A longitudinal study was conducted with older women with depression who were at least 55 years of age, with a mean follow-up period of 5.73 years. At baseline, 9 inflammatory cytokines were measured using the immunoreactivity method. During follow-up, patients with depression who complained of cognitive impairment were evaluated and diagnosed with AD conversion. Association of the cytokines with conversion to AD was analyzed using multivariable Cox proportional hazards regression with adjusting covariates. For clinical applicability, the optimal cutoff value was determined using the minimum <em>p</em> value approach for the conversion to AD and was used to plot an AD-free survival curve.</p></div><div><h3>Results</h3><p>Among 132 participants, 34 patients with depression (25.76%) developed AD during their follow-up period. Higher levels of interleukin (IL) 1β at baseline (hazard ratio = 3.30 [95% CI, 1.11–9.78], <em>p</em> = .031) and lower levels of IL-10 (<em>p</em> < .001) were significantly associated with an increased risk of progression to AD. The survival curve plotted by the cutoff value of ≥0.25 pg/mL for IL-1β and ≤0.15 pg/mL for IL-10 suggested adjusted hazard ratios of 8.96 (95% CI, 3.48–23.09; <em>p</em> < .001) for IL-1β and 10.99 (<em>p</em> < .001) for IL-10, respectively.</p></div><div><h3>Conclusions</h3><p>This study demonstrated that IL-1β and IL-10 were associated with conversion to AD among patients with late-life depression, suggesting their potential as predictive markers of the transition to AD from depression.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100356"},"PeriodicalIF":4.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000697/pdfft?md5=993afd834df8b58554a2a64cfa6aa50b&pid=1-s2.0-S2667174324000697-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141962466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-29DOI: 10.1016/j.bpsgos.2024.100358
Yana Schwarze , Johanna Voges , Alexander Schröder , Sven Dreeßen , Oliver Voß , Sören Krach , Frieder Michel Paulus , Klaus Junghanns , Lena Rademacher
Background
There is evidence that the processing of acute stress is altered in alcohol use disorder (AUD), but little is known about how this is manifested simultaneously across different stress parameters and which neural processes are involved. The current study examined physiological and affective responses to stress and functional connectivity in AUD.
Methods
Salivary cortisol samples, pulse rate, and affect ratings were collected on 2 days from 34 individuals with moderate or severe AUD during early abstinence and 34 control participants. On one of the days, stress was induced, and on the other day, a nonstressful control task was performed. Following the intervention, participants underwent functional magnetic resonance imaging to assess functional connectivity, with a focus on cortical and subcortical seed regions previously reported to be involved in AUD and/or stress.
Results
For pulse rate and cortisol, stress responses were blunted in AUD, whereas the affective response was stronger. Neuroimaging analyses revealed stress-related group differences in functional connectivity, involving the connectivity of striatal seeds with the posterior default mode network, cerebellum, and midcingulate cortex and of the posterior default mode network seed with the striatum and thalamus.
Conclusions
The results suggest a dissociation between subjectively experienced distress and the physiological stress response in AUD as well as stress-related alterations in functional connectivity. These findings highlight the complex interplay between chronic alcohol use and acute stress regulation, offering valuable considerations for the development of therapeutic strategies.
{"title":"Altered Physiological, Affective, and Functional Connectivity Responses to Acute Stress in Patients With Alcohol Use Disorder","authors":"Yana Schwarze , Johanna Voges , Alexander Schröder , Sven Dreeßen , Oliver Voß , Sören Krach , Frieder Michel Paulus , Klaus Junghanns , Lena Rademacher","doi":"10.1016/j.bpsgos.2024.100358","DOIUrl":"10.1016/j.bpsgos.2024.100358","url":null,"abstract":"<div><h3>Background</h3><p>There is evidence that the processing of acute stress is altered in alcohol use disorder (AUD), but little is known about how this is manifested simultaneously across different stress parameters and which neural processes are involved. The current study examined physiological and affective responses to stress and functional connectivity in AUD.</p></div><div><h3>Methods</h3><p>Salivary cortisol samples, pulse rate, and affect ratings were collected on 2 days from 34 individuals with moderate or severe AUD during early abstinence and 34 control participants. On one of the days, stress was induced, and on the other day, a nonstressful control task was performed. Following the intervention, participants underwent functional magnetic resonance imaging to assess functional connectivity, with a focus on cortical and subcortical seed regions previously reported to be involved in AUD and/or stress.</p></div><div><h3>Results</h3><p>For pulse rate and cortisol, stress responses were blunted in AUD, whereas the affective response was stronger. Neuroimaging analyses revealed stress-related group differences in functional connectivity, involving the connectivity of striatal seeds with the posterior default mode network, cerebellum, and midcingulate cortex and of the posterior default mode network seed with the striatum and thalamus.</p></div><div><h3>Conclusions</h3><p>The results suggest a dissociation between subjectively experienced distress and the physiological stress response in AUD as well as stress-related alterations in functional connectivity. These findings highlight the complex interplay between chronic alcohol use and acute stress regulation, offering valuable considerations for the development of therapeutic strategies.</p></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 5","pages":"Article 100358"},"PeriodicalIF":4.0,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667174324000715/pdfft?md5=829d23d3959b36a21224f1f93edf4cbc&pid=1-s2.0-S2667174324000715-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141950421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号