Kynurenine pathway metabolites are increased in inflammatory depression and decrease with omega-3 treatment Jesper Lindahl, Gustav Söderberg Veibäck, Klara Suneson, Wilma Blanking, Johanna Tjernberg, Darya Ståhl, Åsa Wiman, Filip Ventorp, Sophie Erhardt, Daniel Lindqvist Brain Behavior and Immunity Health, 2026 Activation of the kynurenine pathway (KP) with resulting accumulation of neuroactive metabolites may be a downstream pathophysiological mechanism in inflammatory depression. The aims of this study were to investigate KP metabolites in inflammatory depression compared to non-inflammatory depression and healthy controls, and whether these metabolites change with nutraceutical interventions with potential KP-modulating effects. We combined data from two antidepressant clinical trials: one with omega-3 polyunsaturated fatty acids (n-3 PUFAs) and one with a Limosilactobacillus reuteri probiotic supplement as the active intervention. Patients with Major Depressive Disorder (MDD) (n=170) were stratified at baseline according to high-sensitivity C-reactive protein (hs-CRP) levels into an inflammatory (hs-CRP ≥1 mg/L, n=127) and a non-inflammatory (hs-CRP <1 mg/L, n=43) group. We also included 80 non-depressed healthy controls (HC). We investigated between-group differences in KP metabolites at baseline, treatment-associated changes in these biomarkers and how they relate to clinical response. At baseline, the inflammatory depression group had significantly elevated levels of quinolinic acid (QUIN) (p<0.01), 3-hydroxykynurenine (3-HK) (p<0.05), and kynurenine (p<0.05) levels compared to both non-inflammatory depression and controls. N-3 PUFAs, but not probiotics or placebo, significantly decreased QUIN (p<0.05) and 3-HK (p<0.05). Higher baseline levels and a greater treatment-associated decrease of several KP metabolites were associated with a greater clinical response to n-3 PUFAs (p<0.05). In contrast, probiotic supplementation was not associated with significant changes in KP metabolites, and biomarker associations with treatment response were limited in this cohort. We found evidence of KP activation in MDD, but only in an inflammatory subgroup, suggesting that these biological alterations may be specific to a subset of patients with low-grade inflammation. These findings encourage further investigations into whether, and how, biomarkers of KP activation may predict antidepressant response. • MDD patients with low-grade inflammation had elevated kynurenine pathway metabolites. • N-3 PUFA supplementation reduced quinolinic acid, kynurenic acid and 3-hydroxykynurenine • Baseline activation of the kynurenine pathway was associated with n-3 PUFA treatment response • Decrease in kynurenine pathway metabolites was associated with n-3 PUFA treatment response
Turning to Service Users for the Understanding of Current and Future Mental Health Services in the Development Process of Research and Practice: A Qualitative Study Emmy Nilsson, Carina Tjörnstrand, Daniel Lindqvist, Jenny Wetterling, Annika Lexén, Ulrika Bejerholm Health Expectations, 2026 Background A person‐centred and recovery‐oriented approach is an integral part of modern mental health services founded on the experiential knowledge of service users. Their reflections as experts, grounded in their unique experience as service users, play a significant role in developing and improving the existing care. Experiential knowledge is therefore a means to enhance the relevance of research, inform the development of care, and bridge research and practice. Aim To understand service users' experiences of their current mental health services and explore reflections on the Flexible Assertive Community Treatment (FACT) model and its role in future practice. Methods A total of 17 experts participated in individual and dyadic in‐depth interviews. A reflexive thematic analysis was performed on the participants' experiences of current mental health services and on their reflections on a vignette describing an integrative, recovery‐oriented care and support model—FACT. Results The analysis resulted in three themes. The first theme, ‘Losing value and credibility as a person when becoming a service user’, reflected participants' experiences of being reduced to the signs and symptoms of their mental health problems. The second theme, ‘Navigating through the mental health maze’, describes participants view on the current mental health services, while the last theme, ‘Involving service users in their care and support would be empowering’, holds participants' views on the importance of greater involvement in future service design and delivery. Conclusions These results underscore the necessity for enhanced collaboration to empower and provide inclusive, tailored care and support, which the participants emphasised as essential for the future of mental health services. The participants reflected on certain structural concepts, such as hierarchy, caring culture, and financial strains, prior to the implementation of FACT, which need to be addressed before an adaptation of integrative, recovery‐oriented care and support models. Public and Service User Contribution The study planning and process involved stakeholders, including user organisations, Swedish Partnership for Mental Health (NSPH), Skåne and their sister organisation LIBRA Skåne, as well as managers and professionals of mental health services. One of the authors has own experience of mental illness and contributed greatly to the data analysis and the finalising of the manuscript, and two authors have experience as relatives.
Medical students’ perspectives on learning challenging patient communication through simulated patients: insights mirrored by teachers Sten Erici, Sofie Westling, Daniel Lindqvist, Mats B. Lindström, Samuel Edelbring Medical Teacher, 2026 INTRODUCTION: Future physicians must develop the necessary knowledge and skills to effectively manage challenging patient communication. To design linked meaningful learning activities, perspectives from students and teachers need to be taken into account as well as students' previous knowledge. Aiming to better understand how this knowledge can be acquired through patient simulation, we examined students' perceptions, mirrored in teachers' reflections, and how these relate to the medical curriculum. METHODS: Data were collected from students and teachers during the ninth semester of a medical program in Sweden. A narrative survey and individual interviews were conducted. Using thematic analysis, we analyzed nineteen student surveys, five student interviews, and four teacher interviews to explore perceptions of learning. The student themes were then used to identify corresponding subthemes in the teacher data through a mirroring process. RESULTS: Self-knowledge was identified as a crucial skill in order to effectively convey empathy in challenging patient communications. Patient simulation was described as a valuable learning activity which, however, lacked integration with adjacent learning activities in the medical program. Learning progression was hindered by a disconnect between communication-related learning activities and those focused on medical knowledge. CONCLUSION: Both self-knowledge and medical knowledge are perceived as essential for learning how to manage challenging patient communication. Our findings suggest that the learning of patient communication and medical knowledge should be integrated in the curriculum and reinforced across various settings. Patient simulation is a valuable method for developing self-knowledge and communication skills.
Positive correlation between plasma and cerebrospinal fluid galectin-3 in suicide attempters Annamaria Bontidean, Daniel Lindqvist, Cécile Grudet, Lena Brundin, Tomas Deierborg, Filip Ventorp World Journal of Biological Psychiatry, 2026 Objectives Both depression and suicidal behaviour have been associated with neuroinflammation. Galectin-3 (Gal-3), a protein involved in microglial activation, has been linked to pro-inflammatory cytokines and the severity of depressive symptoms. The extent to which peripheral levels of Gal-3 reflect neuroinflammation is unknown, as is the relationship between Gal-3 and suicidality.Methods Blood and CSF samples were collected from recent suicide attempters and healthy controls. CSF levels of cytokines interleukin (IL)-8, IL-1β, IL-6, and tumour necrosis factor-alpha (TNF-α) were available from a subset of the suicide attempters. The Montgomery-Åsberg Depression Rating Scale (MADRS) was used for the assessment of depression symptom severity.Results We found a strong positive correlation between Gal-3 levels in plasma and CSF (r = 0.77, p < 0.001, n = 22). There were no significant differences in Gal-3 between suicide attempters and controls in plasma (n = 16 and 23, respectively) or CSF (n = 13 and 18, respectively). Among suicide attempters, we found a negative correlation between Gal-3 and IL-8 in CSF (r = −0.40, p = 0.01, n = 39). Gal-3 did not correlate significantly with any of the other cytokines.Conclusions Peripheral Gal-3 levels seem to reflect Gal-3 in the central nervous system. Results from this small-scale study do not support the role of Gal-3 in the pathophysiology of suicidal behaviour.
Association between prenatal exposure to Crohn's disease and offspring psychiatric regulatory disturbances Samson Nivins, Elin Skott, MaiBritt Giacobini, Daniel Lindqvist, Mika Gissler, Klas Sjöberg, Catharina Lavebratt Acta Obstetricia Et Gynecologica Scandinavica, 2025 Sir, We thank Khawar et al. for their Letter “Reconsidering the association between maternal Crohn's disease and offspring psychiatric outcomes” published in Acta Obstetricia et Gynecologica Scandinavica,1 raising concerns regarding our study “Offspring exposure to Crohn's disease during pregnancy and association with psychiatric regulatory disturbances in childhood.”2 Khawar et al. propose that corticosteroid exposure may explain the associations we detected between Crohn's disease (CD) and offspring sleeping disorder, incontinence, and feeding disorders. Corticosteroids, commonly prescribed during CD flares, cross the placenta and have been associated with adverse neurodevelopmental risks. Although our original models adjusted for grouped anti-inflammatory-medication use in maternal CD (ATC codes A07E (intestinal anti-inflammatory agents), H02A (corticosteroids for systemic use), L04A (immunosuppressants) [yes/no]) dispensed either within (i) 3 months before pregnancy (B3)/trimester one (T1) or (ii) T2–T3, we acknowledge that corticosteroids might constitute distinct pharmacological exposures. To address this, we conducted post-hoc sensitivity analyses adjusting for corticosteroid medication (H02A) during these periods. Corticosteroids were dispensed to 11.7% of mothers with CD and were associated with mildly increased risks of sleeping disorders (HRB3–T1 = 1.67 (1.30–2.15), HRT2–T3 = 2.02 (1.55–2.63)), incontinence (HRB3–T1 = 1.20 (1.00–1.44), HRT2–T3 = 1.29 (1.05–1.59)), and other feeding disorders (HRB3–T1 = 1.46 (1.12–1.90), HRT2–T3 = 1.68 (1.23–2.29)). However, the adjustment for corticosteroid medication did not attenuate the effect sizes of the reported associations2 between maternal CD and offspring sleeping disorders, incontinence, or other feeding disorders. We refer to Gastroenterology Rep review,3 supporting continued use of most IBD therapies during pregnancy, citing low-risk profile for fetal neurodevelopment and emphasizing the importance of maternal disease control. Khawar et al. suggest that the associations we observed between CD exposure and childhood sleeping, incontinence, and feeding disorders may reflect genetic predisposition. They cite GWAS findings,4, 5 indicating that polygenic-risk scores for CD are associated with neurobiological pathways regulating sleep, appetite, and hypothalamic signaling. We agree that shared genetic mechanisms warrant further investigation. However, our population-based epidemiological study was without access to genetic data and was designed to explore associations between maternal CD and specific, often understudied, childhood psychiatric outcomes. We clearly stated that the study did not allow causal claims. We also adjusted for maternal psychiatric diagnoses before delivery, which partially accounts for familial psychiatric vulnerability. Therefore, we are concerned that Khawar et al. may have misunderstood the scope and conclusions of our study. Khawar et al. further cite a Danish registry study by Jølving et al.,6 that found no increased risk of certain long-term morbidities, including certain psychiatric disorders, in offspring of mothers with IBD. We appreciate this reference, but the outcomes assessed, such as schizophrenia, anxiety, and personality disorders, differ meaningfully from early-onset regulatory disorders (sleeping, incontinence and feeding disturbances) associated with CD in our study. Thus, the outcomes in Jølving et al.,6 are not directly comparable with ours, raising concerns about the appropriateness of using that study to challenge the generalizability of ours. Further research is needed to disentangle the roles of in-utero environmental exposure and genetic predisposition in neurodevelopment. Still, our population-based findings, supported by sensitivity analyses, provide valuable insights into associations between maternal CD and early psychiatric regulatory outcomes. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
Add-on probiotics for inflammatory depression – A double-blind randomized placebo-controlled trial Gustav Söderberg Veibäck, Jesper Lindahl, Klara Suneson, Johanna Tjernberg, Darya Ståhl, Rikard Landberg, Marie Asp, Amanda Kjellberg, Fabian Falknäs, Klas Sjöberg, Catharina Lavebratt, Owen M. Wolkowitz, Daniel Lindqvist Brain Behavior and Immunity, 2025 Previous treatment studies have suggested an antidepressant effect of adjunctive probiotics, but more high-quality Randomized Controlled Trials (RCTs) are needed before clinical implementation. The mechanisms underlying putative antidepressant effects of probiotics are not understood, but one possibility is that they are mediated via short-chain fatty acids (SCFAs) − neuroactive bacterial metabolites with anti-inflammatory properties. The main aim of this study was to test the adjunctive antidepressant efficacy of a Lactobacillus probiotic in depressed patients with concomitant systemic low-grade inflammation, and to test the relationship between treatment response and short-chain fatty acids (SCFAs) in blood and feces. In this 8-week double-blind RCT, patients with major depressive disorder (MDD), BMI ≥ 25 kg/m 2 and high-sensitivity C-reactive protein (hs-CRP) ≥ 1 mg/L were randomized to receive either a Limosilactobacillus reuteri (L. reuteri) probiotic supplement or placebo added to their regular and stable treatment. Primary outcomes were change in the Montgomery-Åsberg Depression Rating Scale (MADRS) total score and “inflammatory depressive symptoms” defined as a composite score of Patient Health Questionnaire-9 items related to sleep disturbance, energy levels, and appetite disturbance. Secondary outcomes included anxiety symptoms, anhedonia, insomnia, fatigue and gastrointestinal symptoms. SCFAs were analyzed in blood and feces pre- and post-intervention. In a modified intention-to-treat analysis including all patients with at least one post-baseline visit (n = 75), there were no significant effects of probiotics relative to placebo on any of the primary or secondary outcomes (all p > 0.25). Lower baseline levels, and a greater treatment-associated increase, of fecal formic acid was significantly associated with a decrease in MADRS score in the probiotics group (p < 0.01). While we did not observe an overall antidepressant effect of add-on L. reuteri probiotic for overweight depressed patients with systemic low-grade inflammation, we found preliminary evidence for anti-inflammatory formic acid as a biomarker, and possibly a mediator, of treatment response.
A plasma protein profile of antidepressant response to omega-3 fatty acids Jesper Lindahl, Miranda Stiernborg, Filip Ventorp, Klara Suneson, Gustav Söderberg Veibäck, Johanna Tjernberg, Darya Ståhl, Marie Hjärn, Catharina Lavebratt, Daniel Lindqvist Progress in Neuro Psychopharmacology and Biological Psychiatry, 2025 BACKGROUND: Previous studies suggest an antidepressant effect of omega-3 fatty acids (n-3 PUFAs). This effect may be larger in patients with low-grade inflammation, defined as mild elevations of high sensitivity C-reactive protein or other commonly used inflammatory markers. The antidepressant mechanisms of n-3 PUFAs are not fully understood but may involve modulation of immunometabolic processes and neurotrophic effects. Here we investigated inflammatory and cardiometabolic biomarkers in patients with major depressive disorder (MDD) and controls, how these biomarkers change with n-3 PUFA treatment, and their association with antidepressant response. METHODS: Ninety-four MDD patients were treated with 2.2 g eicosapentaenoic acid, 400 mg docosahexaenoic acid, and 800 mg other omega-3 fatty acids per day, added to stable antidepressant treatment for 8 weeks. Inflammatory and cardiometabolic plasma markers were assayed in MDD patients, before and after n-3 PUFA treatment, and in healthy controls (n = 76) using proximity extension assay technology. Treatment response was defined as ≥50 % reduction on the 17-item Hamilton Depression Rating Scale. Partial least squares discriminant analysis identified plasma proteins with differential levels between patients, controls, responders, and non-responders. RESULTS: After adjusting for relevant covariates and multiple comparisons, baseline levels of several biomarkers associated with immunometabolic functions and neurotrophic processes differed significantly between MDD patients and controls and between n-3 PUFA responders and non-responders. Some of these biomarkers, related to cell-cell communication and neurotrophy, increased significantly with treatment. CONCLUSION: These findings provide new insights into the antidepressant mechanisms of n-3 PUFAs. Consistent with previous reports, we found evidence of pre-treatment immune activation in responders compared to non-responders, which could be used to personalize antidepressant n-3 PUFA treatment.
Offspring exposure to Crohn's disease during pregnancy and association with milder psychiatric regulatory disturbances in childhood Elin Skott, Gustav Söderberg, MaiBritt Giacobini, Samson Nivins, Xinxia Chen, Daniel Lindqvist, Mika Gissler, Klas Sjöberg, Catharina Lavebratt Acta Obstetricia Et Gynecologica Scandinavica, 2025 IntroductionPrenatal exposure to inflammatory states has been suggested to influence offspring neurodevelopment. The aim was to investigate if offspring exposure to maternal Inflammatory bowel disorder (IBD), or specifically the IBD disorder Crohn's disease, during gestation is associated with neurodevelopmental or psychiatric disorders in childhood.Material and MethodsWe conducted a population‐based registry study in Finland. All live births from 1996 until 2014 in Finland were included and followed up until December 2018. Exposure was maternal IBD or Crohn's disease. Outcome was a broad range of neurodevelopmental and psychiatric disorders in offspring. Cox proportional hazards regression was applied to assess association. Sensitivity analyses included assessing, for example, exposure to severe episode of IBD or Crohn's disease, the outcome psychotropic medication for the children, and influence from perinatal risk factors.ResultsOf the participants (N = 1 105 997), 0.55% (N = 6067) were exposed to maternal IBD 0.18% (N = 1959) to maternal Crohn's disease. Among the children exposed to IBD or the subgroup Crohn's disease, 6.3% or 7.3%, respectively, had received an outcome diagnosis during the follow‐up. There were higher risks for Sleeping disorders HR = 1.77 (95% CI, 1.13–2.78), Other feeding disorders HR = 1.83 (95% CI, 1.19, 2.19), and Incontinence HR = 1.42 (95% CI, 1.02–1.97) in children exposed to maternal Crohn's disease compared to unexposed children. This was supported by even higher point risk estimates for Incontinence HR = 2.43 (95% CI, 1.34–4.38) and Other feeding disorders HR = 2.83 (95% CI, 1.35–5.91) in offspring where the mother was hospitalized for Crohn's disease during pregnancy. Furthermore, there was a higher risk of dispensed antipsychotic, anxiolytic, hypnotic, and/or sedative medications for children with maternal Crohn's disease HR = 1.38 (95% CI, 1.03–1.85). These associations were not explained by cesarean section, preterm birth, or small birth size.ConclusionsOffspring exposed to maternal Crohn's disease during pregnancy had modestly higher risks of early sleeping, continence, and feeding disturbances. The exposure had no detectable association with any of the other psychiatric disorders studied.
Efficacy and safety of varenicline and bupropion, in combination and alone, for alcohol use disorder: a randomized, double-blind, placebo-controlled multicentre trial Bo Söderpalm, Helga Lidö, Johan Franck, Anders Håkansson, Daniel Lindqvist, Markus Heilig, Joar Guterstam, Markus Samuelson, Barbro Askerup, Cecilia Wallmark-Nilsson, Andrea de Bejczy Lancet Regional Health Europe, 2025 Background: Alcohol use disorder (AUD) is associated with an enormous burden of disease and cost to society. The dopamine deficiency hypothesis posits that negative reinforcement generated by a low brain dopamine state drives ethanol intake. Here, we evaluated the efficacy and safety of combined administration of two dopamine-enhancing drugs, varenicline (a partial nicotinic acetylcholine receptor agonist) and bupropion (a weak dopamine-reuptake inhibitor) on alcohol intake in AUD. Methods: Participants aged 25-70 years with moderate-to-severe AUD (defined as ≥4/11 Diagnostic and Statistical Manual of Mental Disorders [DSM]-5 criteria) were enrolled in this randomized, double-blind, placebo-controlled trial, done at four outpatient clinics in Sweden. Participants were randomly assigned (block size 8) 1:1:1:1 to Placebo + Placebo, Varenicline + Bupropion, Varenicline + Placebo, or Placebo + Bupropion. After a 1-week titration period, Varenicline was taken as 1 mg orally twice per day and bupropion as 150 mg orally twice per day for 12 weeks. Participants, investigators, and all study personnel were unaware of treatment allocation. The two primary outcomes were phosphatidylethanol in blood (B-PEth) and self-reported percentage heavy drinking days (%HDD), assessed over a steady state 10-week-period (from start of week 2 to end of week 11). Modified intention-to-treat (mITT) and per protocol analyses (PP) were performed using a sequential hierarchical statistical method. This registered study (EudraCT 2018-000048-24; clinicaltrials.govNCT04167306) is completed. Findings: Between March 4, 2019, and December 14, 2022, 384 participants were randomly assigned: Placebo + Placebo = 97, Varenicline + Bupropion = 100, Varenicline + Placebo = 96, Placebo + Bupropion = 91. 72% participants were male (277/384) and 28% female (107/384), median age 57 (13) years. In the mITT analyses, Varenicline + Bupropion reduced B-PEth (Cohen's d [d] = 0·39, p = 0·004) and %HDD (d = 0·31, p = 0·008) vs Placebo + Placebo. Varenicline + Placebo also reduced B-PEth (d = 0·30, p = 0·005) and %HDD (d = 0·36, p = 0·023) vs Placebo + Placebo. For both primary endpoints, differences between the Varenicline + Bupropion and Varenicline + Placebo groups were not statistically significant (B-PEth: d = 0·022, p = 0·97, %HDD: d = 0·027, p = 0·76), precluding further comparisons according to the statistical hierarchy. In PP analyses, both primary outcomes were reduced with Varenicline + Bupropion (d = 0·43 [B-PEth]; d = 0·41 [%HDD]) and Varenicline + Placebo (d = 0·29 [B-PEth]; d = 0·34 [%HDD]) compared with Placebo + Placebo. Nausea, the only safety concern, was more common in the Varenicline + Placebo group than in the Placebo + Placebo group (49/96 vs 11/97, p < 0·0001) and of longer median duration (45 (70) vs 10 (14·5) days, p = 0·001). Nausea incidence was lower in the Varenicline + Bupropion group vs Varenicline + Placebo (36/100 vs 49/96, p = 0·048) and of shorter median duration (16·5 (39·3) vs 45 (70) days, p = 0·010). Interpretation: Two brain dopamine elevating treatments (Varenicline + Bupropion; Varenicline + Placebo) reduce alcohol consumption compared with placebo alone. Effect sizes were largest when Varenicline and Bupropion were combined and compliance was high (PP-population). Bupropion reduced Varenicline-induced nausea. Varenicline + Bupropion or other mild dopamine enhancers should be further explored for treatment of AUD. Funding: This study was funded primarily by the Swedish Research Council.
Cerebrospinal fluid platelet-derived growth factor receptor-beta is negatively correlated with depressive symptom severity in suicide attempters A. Bontidean, D. Lindqvist, C. Grudet, L. Träskman-Bendz, L. Brundin, F. Ventorp Journal of Affective Disorders Reports, 2025 • Low CSF PDGFR-β levels are associated with more severe depressive symptoms in suicide attempters. • PDGFR-β may indicate depression severity, independent of blood-brain barrier integrity. • Blood-brain barrier dysfunction may play a role in suicidality and depression. Depression and suicidal behavior have been linked to increased blood-brain barrier (BBB) permeability. Platelet-derived growth factor receptor beta (PDGFR-β) is widely expressed in pericytes and promotes BBB integrity. Here, we investigated cerebrospinal fluid (CSF) levels of PDGFR-β in suicide attempters and healthy controls and correlated PDGFR-β to depression symptom severity. We measured levels of PDGFR-β in CSF from recent suicide attempters using electrochemiluminescence immunoassays. PDGFR-β was correlated to CSF/serum albumin ratio (Qalb), an established BBB integrity biomarker, and symptom severity according to the Montgomery-Åsberg Depression Rating Scale (MADRS). There was a significant negative correlation between PDGFR-β and total MADRS score in suicide attempters ( r =-0.47, p = 0.003, n = 38). PDGFR-β did not correlate significantly with Qalb ( r = 0.179, p = 0.268, n = 40). Although PDGFR-β levels may not reflect BBB integrity, low CSF levels of this biomarker were associated with more severe depressive symptoms. We hypothesize that this may be due to mechanisms unrelated to BBB integrity including the effects of PDGFR-β on neurogenesis and cellular proliferation.
Circulating cell-free mitochondrial DNA levels and glucocorticoid sensitivity in a cohort of male veterans with and without combat-related PTSD Zachary N. Blalock, Gwyneth W. Y Wu, Daniel Lindqvist, Caroline Trumpff, Janine D. Flory, Jue Lin, Victor I. Reus, Ryan Rampersaud, Rasha Hammamieh, Aarti Gautam, SBPBC, Kerry J. Ressler, Ruoting Yang, Seid Muhie, Bernie J. Daigle, Linda M. Bierer, Leroy Hood, Kai Wang, Inyoul Lee, Kelsey R. Dean, Pramod R. Somvanshi, Francis J. Doyle, Charles R. Marmar, Marti Jett, Rachel Yehuda, Owen M. Wolkowitz, Synthia H. Mellon Translational Psychiatry, 2024
The researcher's guide to selecting biomarkers in mental health studies Josine E. Verhoeven, Owen M. Wolkowitz, Isaac Barr Satz, Quinn Conklin, Femke Lamers, Catharina Lavebratt, Jue Lin, Daniel Lindqvist, Stefanie E. Mayer, Philippe A. Melas, Yuri Milaneschi, Martin Picard, Ryan Rampersaud, Natalie Rasgon, Kathryn Ridout, Gustav Söderberg Veibäck, Caroline Trumpff, Audrey R. Tyrka, Kathleen Watson, Gwyneth Winnie Y. Wu, Ruoting Yang, Anthony S. Zannas, Laura K. M. Han, Kristoffer N. T. Månsson Bioessays, 2024
An inflamed subtype of difficult-to-treat depression Klara Suneson, Cécile Grudet, Filip Ventorp, Johan Malm, Marie Asp, Åsa Westrin, Daniel Lindqvist Progress in Neuro Psychopharmacology and Biological Psychiatry, 2023
Multi-omic biomarker identification and validation for diagnosing warzone-related post-traumatic stress disorder Kelsey R. Dean, , Rasha Hammamieh, Synthia H. Mellon, Duna Abu-Amara, Janine D. Flory, Guia Guffanti, Kai Wang, Bernie J. Daigle, Aarti Gautam, Inyoul Lee, Ruoting Yang, Lynn M. Almli, F. Saverio Bersani, Nabarun Chakraborty, Duncan Donohue, Kimberly Kerley, Taek-Kyun Kim, Eugene Laska, Min Young Lee, Daniel Lindqvist, Adriana Lori, Liangqun Lu, Burook Misganaw, Seid Muhie, Jennifer Newman, Nathan D. Price, Shizhen Qin, Victor I. Reus, Carole Siegel, Pramod R. Somvanshi, Gunjan S. Thakur, Yong Zhou, Leroy Hood, Kerry J. Ressler, Owen M. Wolkowitz, Rachel Yehuda, Marti Jett, Francis J. Doyle, Charles Marmar Molecular Psychiatry, 2020
Effect of Combat Exposure and Posttraumatic Stress Disorder on Telomere Length and Amygdala Volume Jee In Kang, Susanne G. Mueller, Gwyneth W.Y. Wu, Jue Lin, Peter Ng, Rachel Yehuda, Janine D. Flory, Duna Abu-Amara, Victor I. Reus, Aarti Gautam, Rasha Hammamieh, Francis J. Doyle, Marti Jett, Charles R. Marmar, Synthia H. Mellon, Owen M. Wolkowitz, Leroy Hood, Kerry J. Ressler, Daniel Lindqvist, Ji Hoon Cho, Michelle Coy, Frank Desarnaud, Francesco Saverio Bersani, Silvia Fossati, Allison Hoke, Raina Kumar, Meng Li, Iouri Makotkine, Stacy-Ann Miller, Linda Petzold, Laura Price, Meng Qian, Kelsey Scherler, Seshamalini Srinivasan, Anna Suessbrick, Li Tang, Xiaogang Wu, David Baxter, Esther Blessing, Kelsey R. Dean, Bernie J. Daigle, Guia Guffanti, Kai Wang, Lynn M. Almli, F. Nabarun Chakraborty, Duncan Donohue, Kimberly Kerley, Taek-Kyun Kim, Eugene Laska, Inyoul Lee, Min Young Lee, Adriana Lori, Liangqun Lu, Burook Misganaw, Seid Muhie, Jennifer Newman, Nathan Price, Shizhen Qin, Carole Siegel, Pramod R. Somvanshi, Gunjan S. Thakur, Young Zhou, Ruoting Yang Biological Psychiatry Cognitive Neuroscience and Neuroimaging, 2020
Vitamin D and inflammation in major depressive disorder Cécile Grudet, Owen M. Wolkowitz, Synthia H. Mellon, Johan Malm, Victor I. Reus, Lena Brundin, Brenton M. Nier, Firdaus S. Dhabhar, Christina M. Hough, Åsa Westrin, Daniel Lindqvist Journal of Affective Disorders, 2020
Improvement in indices of cellular protection after psychological treatment for social anxiety disorder Kristoffer N. T. Månsson, Daniel Lindqvist, Liu L. Yang, Cecilia Svanborg, Josef Isung, Gustav Nilsonne, Lise Bergman-Nordgren, Samir El Alaoui, Erik Hedman-Lagerlöf, Martin Kraepelien, Jens Högström, Gerhard Andersson, Carl-Johan Boraxbekk, Håkan Fischer, Catharina Lavebratt, Owen M. Wolkowitz, Tomas Furmark Translational Psychiatry, 2019
Metabolomic analysis of male combat veterans with post traumatic stress disorder Synthia H. Mellon, F. Saverio Bersani, Daniel Lindqvist, Rasha Hammamieh, Duncan Donohue, Kelsey Dean, Marti Jett, Rachel Yehuda, Janine Flory, Victor I. Reus, Linda M. Bierer, Iouri Makotkine, Duna Abu Amara, Clare Henn Haase, Michelle Coy, Francis J. Doyle, Charles Marmar, Owen M. Wolkowitz Plos One, 2019
The vermiform appendix impacts the risk of developing Parkinson’s disease Bryan A. Killinger, Zachary Madaj, Jacek W. Sikora, Nolwen Rey, Alec J. Haas, Yamini Vepa, Daniel Lindqvist, Honglei Chen, Paul M. Thomas, Patrik Brundin, Lena Brundin, Viviane Labrie Science Translational Medicine, 2018
Oxidative stress, inflammation and treatment response in major depression Daniel Lindqvist, Firdaus S. Dhabhar, S. Jill James, Christina M. Hough, Felipe A. Jain, F. Saverio Bersani, Victor I. Reus, Josine E. Verhoeven, Elissa S. Epel, Laura Mahan, Rebecca Rosser, Owen M. Wolkowitz, Synthia H. Mellon Psychoneuroendocrinology, 2017
Increased pro-inflammatory milieu in combat related PTSD – A new cohort replication study Daniel Lindqvist, Firdaus S. Dhabhar, Synthia H. Mellon, Rachel Yehuda, S. Marlene Grenon, Janine D. Flory, Linda M. Bierer, Duna Abu-Amara, Michelle Coy, Iouri Makotkine, Victor I. Reus, F. Saverio Bersani, Charles R. Marmar, Owen M. Wolkowitz Brain Behavior and Immunity, 2017
Association of dimensional psychological health measures with telomere length in male war veterans Francesco S. Bersani, Daniel Lindqvist, Synthia H. Mellon, Elissa S. Epel, Rachel Yehuda, Janine Flory, Clare Henn-Hasse, Linda M. Bierer, Iouri Makotkine, Duna Abu-Amara, Michelle Coy, Victor I. Reus, Jue Lin, Elizabeth H. Blackburn, Charles Marmar, Owen M. Wolkowitz Journal of Affective Disorders, 2016
Mitochondrial DNA copy number is reduced in male combat veterans with PTSD Francesco Saverio Bersani, Claire Morley, Daniel Lindqvist, Elissa S. Epel, Martin Picard, Rachel Yehuda, Janine Flory, Linda M. Bierer, Iouri Makotkine, Duna Abu-Amara, Michelle Coy, Victor I. Reus, Jue Lin, Elizabeth H. Blackburn, Charles Marmar, Owen M. Wolkowitz, Synthia H. Mellon Progress in Neuro Psychopharmacology and Biological Psychiatry, 2016
Increased CSF biomarkers of angiogenesis in Parkinson disease Shorena Janelidze, Daniel Lindqvist, Veronica Francardo, Sara Hall, Henrik Zetterberg, Kaj Blennow, Charles H. Adler, Thomas G. Beach, Geidy E. Serrano, Danielle van Westen, Elisabet Londos, M. Angela Cenci, Oskar Hansson Neurology, 2015
Parkinson's Disease Case Ascertainment in the EPIC Cohort: The NeuroEPIC4PD Study Valentina Gallo, Carol Brayne, Lars Forsgren, Roger A. Barker, Jesper Petersson, Oskar Hansson, Daniel Lindqvist, Claudio Ruffmann, Lianna Ishihara, Robert Luben, Larraitz Arriola, Alberto Bergareche, Diana Gavrila, Maria Elena Erro, Nicola Vanacore, Carlotta Sacerdote, Bas Bueno-de-Mesquita, Roel Vermeulen, Meinie Seelen, Sabina Sieri, Giovanna Masala, Silvia Ramat, Andreas Kyrozis, Antonia Thricopolou, Salvatore Panico, Amalia Mattiello, Rudolf Kaaks, Birgit Teucher, Verena Katzke, Manja Kloss, Lisa Curry, Federico Calboli, Elio Riboli, Paolo Vineis, Lefkos Middleton Neurodegenerative Diseases, 2015
Proinflammatory milieu in combat-related PTSD is independent of depression and early life stress Daniel Lindqvist, Owen M. Wolkowitz, Synthia Mellon, Rachel Yehuda, Janine D. Flory, Clare Henn-Haase, Linda M. Bierer, Duna Abu-Amara, Michelle Coy, Thomas C. Neylan, Iouri Makotkine, Victor I. Reus, Xiaodan Yan, Nicole M. Taylor, Charles R. Marmar, Firdaus S. Dhabhar Brain Behavior and Immunity, 2014
Connecting inflammation with glutamate agonism in suicidality Sophie Erhardt, Chai K Lim, Klas R Linderholm, Shorena Janelidze, Daniel Lindqvist, Martin Samuelsson, Kristina Lundberg, Teodor T Postolache, Lil Träskman-Bendz, Gilles J Guillemin, Lena Brundin Neuropsychopharmacology, 2013