Pub Date : 2024-07-24DOI: 10.1016/j.bionps.2024.100104
Maxwell Z. Price , Richard L. Price
Treatment-resistant depression, defined as a failure of at least two oral antidepressants of adequate dose and duration in the current episode, is a debilitating condition with low rates of response and remission. Intranasal esketamine is the first medication approved by regulatory authorities for difficult to treat depressive episodes that builds directly on the discovery of the rapid antidepressant effects of intravenously administered racemic ketamine. Approved in the United States in 2019, and subsequently, in many countries worldwide, intranasal esketamine is indicated in conjunction with any new or previously taken oral antidepressant medication of the clinician’s choosing for treatment-resistant depression in adults. It is also indicated for the treatment of major depressive disorder in adults with acute suicidal ideation or behavior who may or may not be treatment-naive or have treatment-resistant depression. This article outlines the case for the efficacy, safety profile, and feasibility of acute, short-term intranasal esketamine followed by the long-term continuation of intranasal esketamine versus long-term off-label intravenous ketamine in treatment-resistant depression. The article further suggests biomarkers to predict response that warrant further study.
{"title":"Benefits and risks of esketamine nasal spray continuation in treatment-resistant depression","authors":"Maxwell Z. Price , Richard L. Price","doi":"10.1016/j.bionps.2024.100104","DOIUrl":"10.1016/j.bionps.2024.100104","url":null,"abstract":"<div><p>Treatment-resistant depression, defined as a failure of at least two oral antidepressants of adequate dose and duration in the current episode, is a debilitating condition with low rates of response and remission. Intranasal esketamine is the first medication approved by regulatory authorities for difficult to treat depressive episodes that builds directly on the discovery of the rapid antidepressant effects of intravenously administered racemic ketamine. Approved in the United States in 2019, and subsequently, in many countries worldwide, intranasal esketamine is indicated in conjunction with any new or previously taken oral antidepressant medication of the clinician’s choosing for treatment-resistant depression in adults. It is also indicated for the treatment of major depressive disorder in adults with acute suicidal ideation or behavior who may or may not be treatment-naive or have treatment-resistant depression. This article outlines the case for the efficacy, safety profile, and feasibility of acute, short-term intranasal esketamine followed by the long-term continuation of intranasal esketamine versus long-term off-label intravenous ketamine in treatment-resistant depression. The article further suggests biomarkers to predict response that warrant further study.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"11 ","pages":"Article 100104"},"PeriodicalIF":0.0,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000224/pdfft?md5=7b709245c38a99a3e9739bf4b7bbdc2f&pid=1-s2.0-S2666144624000224-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141852688","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 : 2024-07-24DOI: 10.1016/j.bionps.2024.100103
Weiyi Xie , Man Wang , Hui Yun Li , Pingqiao Wang , Clifton Robert Emery , Siuman Ng
Prenatal emotional distress is common in pregnant women. Altered emotional distress can occur from the very beginning to the end of pregnancy. Heart rate variability (HRV) has recently become considered to be a potentially reliable psychophysiological stress biomarker in adults. In the current study, we evaluated ultra-short-term HRV (1-minute measurement) as a psychophysiological biomarker by examining the association between HRV parameters and self-reported prenatal emotional distress among pregnant women (N = 230) across three trimesters of pregnancy.
Results
Prenatal emotional distress was associated with a lower root mean square of successive differences between normal heartbeats (RMSSD), NN50, and SDNN Index among pregnant women who are in the second trimester. For women in the first and third trimester of pregnancy, prenatal emotional distress was not significantly correlated with any HRV indicators.
Limitations
The cross-sectional nature of our results limits the directional expression and assessment of the relationships, and longitudinal studies that target the recruitment of more pregnant women with subtypes of emotional distress issues are also needed.
Conclusions
Time-domain parameters of low HRV (associated with reduced parasympathetic activity) can potentially serve as an efficient psychophysiological biomarker for prenatal emotional distress in the second trimester of pregnancy. However, the time-domain HRV indicators in pregnant women in the first and third trimesters may be affected by other physiological and psychological fluctuations, thus decreasing the HRV biomarker’s efficiency in predicting their prenatal emotional distress.
{"title":"An emotional distress biomarker in pregnant women: Ultra-short-term heart rate variability","authors":"Weiyi Xie , Man Wang , Hui Yun Li , Pingqiao Wang , Clifton Robert Emery , Siuman Ng","doi":"10.1016/j.bionps.2024.100103","DOIUrl":"10.1016/j.bionps.2024.100103","url":null,"abstract":"<div><p>Prenatal emotional distress is common in pregnant women. Altered emotional distress can occur from the very beginning to the end of pregnancy. Heart rate variability (HRV) has recently become considered to be a potentially reliable psychophysiological stress biomarker in adults. In the current study, we evaluated ultra-short-term HRV (1-minute measurement) as a psychophysiological biomarker by examining the association between HRV parameters and self-reported prenatal emotional distress among pregnant women (<em>N</em> = 230) across three trimesters of pregnancy.</p></div><div><h3>Results</h3><p>Prenatal emotional distress was associated with a lower root mean square of successive differences between normal heartbeats (RMSSD), NN50, and SDNN Index among pregnant women who are in the second trimester. For women in the first and third trimester of pregnancy, prenatal emotional distress was not significantly correlated with any HRV indicators.</p></div><div><h3>Limitations</h3><p>The cross-sectional nature of our results limits the directional expression and assessment of the relationships, and longitudinal studies that target the recruitment of more pregnant women with subtypes of emotional distress issues are also needed.</p></div><div><h3>Conclusions</h3><p>Time-domain parameters of low HRV (associated with reduced parasympathetic activity) can potentially serve as an efficient psychophysiological biomarker for prenatal emotional distress in the second trimester of pregnancy. However, the time-domain HRV indicators in pregnant women in the first and third trimesters may be affected by other physiological and psychological fluctuations, thus decreasing the HRV biomarker’s efficiency in predicting their prenatal emotional distress.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"11 ","pages":"Article 100103"},"PeriodicalIF":0.0,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000212/pdfft?md5=e9c0abe06f20dd4d7947b7af16759112&pid=1-s2.0-S2666144624000212-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141850955","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 : 2024-07-07DOI: 10.1016/j.bionps.2024.100102
Jonatan M. Panula , Athanasios Gotsopoulos , Jussi Alho , Jaana Suvisaari , Maija Lindgren , Tuula Kieseppä , Tuukka T. Raij
As many as one third of the patients diagnosed with schizophrenia do not respond to first-line antipsychotic medication. This group may benefit from the atypical antipsychotic medication clozapine, but initiation of treatment is often delayed, which may worsen prognosis. Predicting which patients do not respond to traditional antipsychotic medication at the onset of symptoms would provide fast-tracked treatment for this group of patients. We collected data from patient records of 38 first-episode psychosis patients, of whom seven did not respond to traditional antipsychotic medications. We used clinical data including medical records, voxel-based morphometry MRI data and inter-subject correlation fMRI data, obtained during movie viewing, to predict future treatment resistance. Using a neural network model, we correctly predicted future treatment resistance in six of the seven treatment resistance patients and 25 of 31 patients who did not require clozapine treatment. Prediction improved significantly when using imaging data in tandem with clinical data. The accuracy of the neural network model was significantly higher than the accuracy of a support vector machine algorithm. These results support the notion that treatment resistant schizophrenia could represent a separate entity of psychotic disorders, characterized by morphological and functional changes in the brain which could represent biomarkers detectable at early onset of symptoms.
{"title":"Multimodal prediction of the need of clozapine in treatment resistant schizophrenia; a pilot study in first-episode psychosis","authors":"Jonatan M. Panula , Athanasios Gotsopoulos , Jussi Alho , Jaana Suvisaari , Maija Lindgren , Tuula Kieseppä , Tuukka T. Raij","doi":"10.1016/j.bionps.2024.100102","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100102","url":null,"abstract":"<div><p>As many as one third of the patients diagnosed with schizophrenia do not respond to first-line antipsychotic medication. This group may benefit from the atypical antipsychotic medication clozapine, but initiation of treatment is often delayed, which may worsen prognosis. Predicting which patients do not respond to traditional antipsychotic medication at the onset of symptoms would provide fast-tracked treatment for this group of patients. We collected data from patient records of 38 first-episode psychosis patients, of whom seven did not respond to traditional antipsychotic medications. We used clinical data including medical records, voxel-based morphometry MRI data and inter-subject correlation fMRI data, obtained during movie viewing, to predict future treatment resistance. Using a neural network model, we correctly predicted future treatment resistance in six of the seven treatment resistance patients and 25 of 31 patients who did not require clozapine treatment. Prediction improved significantly when using imaging data in tandem with clinical data. The accuracy of the neural network model was significantly higher than the accuracy of a support vector machine algorithm. These results support the notion that treatment resistant schizophrenia could represent a separate entity of psychotic disorders, characterized by morphological and functional changes in the brain which could represent biomarkers detectable at early onset of symptoms.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"11 ","pages":"Article 100102"},"PeriodicalIF":0.0,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000200/pdfft?md5=1537d8d8bee9b33c989ae141572cc29c&pid=1-s2.0-S2666144624000200-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141605922","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 : 2024-06-18DOI: 10.1016/j.bionps.2024.100098
Walter Paganin , Sabrina Signorini
Background
Stress and trauma significantly contribute to various psychiatric disorders, including schizophrenia. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, particularly abnormal cortisol secretion, is implicated in schizophrenia's pathophysiology. Salivary cortisol, a convenient measure, provides insights into HPA axis activity. This systematic review and meta-analysis assess salivary cortisol levels in individuals with schizophrenia compared to healthy controls, evaluating its potential as a biomarker for schizophrenia.
Aim
To assess the differences in salivary cortisol levels at baseline and in response to stress between patients with schizophrenia and healthy controls, determining the reliability of salivary cortisol as a biomarker for schizophrenia.
Methods
A systematic review and meta-analysis were conducted following PRISMA guidelines. We searched MEDLINE/PubMed, Cochrane Central, and EMBASE for human studies on schizophrenia and controls published from January 1, 2013, to July 1, 2023, reporting baseline or post-stress salivary cortisol levels. Exclusions were non-human studies, non-specific schizophrenia diagnoses, or missing cortisol data. Two reviewers independently extracted data and appraised quality, resolving discrepancies by consensus. Due to significant heterogeneity (I² = 94 % for baseline, 75 % for stress response), a random effects model was used.
Results
Nineteen studies were initially selected, with twelve excluded due to non-specific schizophrenia diagnoses and missing cortisol data. The final meta-analysis included seven studies with 507 schizophrenia patients and 175 healthy controls. Key findings include:
Baseline cortisol levels
No significant difference in baseline salivary cortisol levels between schizophrenia patients and healthy controls (pooled estimate: −0.02, 95 % CI: −0.47–0.42).
Cortisol response to stress
No significant difference in post-stress cortisol levels between the two groups (pooled estimate: 0.03, 95 % CI: −1.84–1.79).
Study variability
High variability across studies due to differences in design, patient characteristics, and cortisol measurement techniques. Despite some evidence of altered cortisol dynamics in schizophrenia, high variability in methodologies and confounding factors like medication use and psychosocial stressors complicate definitive conclusions.
Conclusion
The review underscores the potential of cortisol as a biomarker for stress response; however, its use in diagnosing schizophrenia remains inconclusive. Individual variability and methodological differences limit the diagnostic accuracy of salivary cortisol. Future research with larger sample sizes, uniform methodologies, and comprehensive control for confounding variables is essential to elucidate the role of salivary corti
{"title":"Salivary cortisol in Schizophrenia: a selective review and meta-analysis of controlled studies of the past decade","authors":"Walter Paganin , Sabrina Signorini","doi":"10.1016/j.bionps.2024.100098","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100098","url":null,"abstract":"<div><h3>Background</h3><p>Stress and trauma significantly contribute to various psychiatric disorders, including schizophrenia. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, particularly abnormal cortisol secretion, is implicated in schizophrenia's pathophysiology. Salivary cortisol, a convenient measure, provides insights into HPA axis activity. This systematic review and meta-analysis assess salivary cortisol levels in individuals with schizophrenia compared to healthy controls, evaluating its potential as a biomarker for schizophrenia.</p></div><div><h3>Aim</h3><p>To assess the differences in salivary cortisol levels at baseline and in response to stress between patients with schizophrenia and healthy controls, determining the reliability of salivary cortisol as a biomarker for schizophrenia.</p></div><div><h3>Methods</h3><p>A systematic review and meta-analysis were conducted following PRISMA guidelines. We searched MEDLINE/PubMed, Cochrane Central, and EMBASE for human studies on schizophrenia and controls published from January 1, 2013, to July 1, 2023, reporting baseline or post-stress salivary cortisol levels. Exclusions were non-human studies, non-specific schizophrenia diagnoses, or missing cortisol data. Two reviewers independently extracted data and appraised quality, resolving discrepancies by consensus. Due to significant heterogeneity (I² = 94 % for baseline, 75 % for stress response), a random effects model was used.</p></div><div><h3>Results</h3><p>Nineteen studies were initially selected, with twelve excluded due to non-specific schizophrenia diagnoses and missing cortisol data. The final meta-analysis included seven studies with 507 schizophrenia patients and 175 healthy controls. Key findings include:</p></div><div><h3>Baseline cortisol levels</h3><p>No significant difference in baseline salivary cortisol levels between schizophrenia patients and healthy controls (pooled estimate: −0.02, 95 % CI: −0.47–0.42).</p></div><div><h3>Cortisol response to stress</h3><p>No significant difference in post-stress cortisol levels between the two groups (pooled estimate: 0.03, 95 % CI: −1.84–1.79).</p></div><div><h3>Study variability</h3><p>High variability across studies due to differences in design, patient characteristics, and cortisol measurement techniques. Despite some evidence of altered cortisol dynamics in schizophrenia, high variability in methodologies and confounding factors like medication use and psychosocial stressors complicate definitive conclusions.</p></div><div><h3>Conclusion</h3><p>The review underscores the potential of cortisol as a biomarker for stress response; however, its use in diagnosing schizophrenia remains inconclusive. Individual variability and methodological differences limit the diagnostic accuracy of salivary cortisol. Future research with larger sample sizes, uniform methodologies, and comprehensive control for confounding variables is essential to elucidate the role of salivary corti","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"11 ","pages":"Article 100098"},"PeriodicalIF":0.0,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000169/pdfft?md5=f058592a4a65c1f2622d205f6da551b1&pid=1-s2.0-S2666144624000169-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141434990","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 : 2024-06-01DOI: 10.1016/j.bionps.2024.100083
Rita Khoury, George Grossberg
{"title":"Biomarkers of neurocognitive disorders: A ray of hope on the horizon?","authors":"Rita Khoury, George Grossberg","doi":"10.1016/j.bionps.2024.100083","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100083","url":null,"abstract":"","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"10 ","pages":"Article 100083"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000017/pdfft?md5=3cf44bb55ff2b20223fe6b874e9a7eb2&pid=1-s2.0-S2666144624000017-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141328521","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 : 2024-06-01DOI: 10.1016/j.bionps.2024.100097
Eleftheria Kodosaki , Colm Healy , Jonah F. Byrne , Melanie Föcking , Mary Cannon , Diana O. Perkins , David Cotter , Meike Heurich
The complement system is an important part of the innate immune system and plays a key role in inflammatory processes. Concentrations of complement activation fragments in plasma are markers of systemic activation and have been found to be altered in a wide range of diseases. Some plasma activation marker levels can be influenced by sample processing and storage time. We quantified seven complement activation markers (C4a, C4d, C3a, iC3b, Bb, C5a, and sC5b-9 (TCC)) in EDTA-plasma as part of a multi-centre clinical study analysing complement activation in individuals with clinical high-risk (CHR) for psychosis compared with healthy controls. Samples had been collected, processed, and subsequently stored at -80°C over a period of 9.5–13.6 years, according to a standard operating protocol (SOP). Complement activation markers were quantified using commercially available and standardised enzyme-linked immunosorbent assays (ELISA). In a post hoc analysis of variables affecting the analyses we investigated the impact of EDTA-to-freezer processing time (<1–7.35 hours) and freezer storage time (9.5–13.6 years). EDTA-to-freezer processing time moderately correlated positively with C4a, C3a, iC3b and sC5b-9 levels. Storage time at -80°C was not significantly correlated with any complement activation marker. This study provides valuable insight into the impact of sample processing and long-term sample storage in complement activation marker studies. The results suggest that storage time in -80°C is not a confounding factor affecting non-specific complement activation in EDTA-plasma. Sample-processing time does moderately affect the levels of some complement activation markers. This should be considered as a co-variate when analysing complement activation marker levels. Further, the impact may vary for healthy or clinical samples where immune activation is part of the pathology. These findings are important when planning large-scale clinical studies that include quantification of complement components and its activation fragments as biomarkers. It supports the collection of EDTA-plasma and fast sample processing to be included into a study standard operating procedure.
{"title":"Sample processing time but not storage time affects complement activation markers C4a, C4d, C3a, iC3b, Bb, C5a, and sC5b-9 levels in EDTA-plasma of individuals at clinical high-risk for psychosis","authors":"Eleftheria Kodosaki , Colm Healy , Jonah F. Byrne , Melanie Föcking , Mary Cannon , Diana O. Perkins , David Cotter , Meike Heurich","doi":"10.1016/j.bionps.2024.100097","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100097","url":null,"abstract":"<div><p>The complement system is an important part of the innate immune system and plays a key role in inflammatory processes. Concentrations of complement activation fragments in plasma are markers of systemic activation and have been found to be altered in a wide range of diseases. Some plasma activation marker levels can be influenced by sample processing and storage time. We quantified seven complement activation markers (C4a, C4d, C3a, iC3b, Bb, C5a, and sC5b-9 (TCC)) in EDTA-plasma as part of a multi-centre clinical study analysing complement activation in individuals with clinical high-risk (CHR) for psychosis compared with healthy controls. Samples had been collected, processed, and subsequently stored at -80°C over a period of 9.5–13.6 years, according to a standard operating protocol (SOP). Complement activation markers were quantified using commercially available and standardised enzyme-linked immunosorbent assays (ELISA). In a post hoc analysis of variables affecting the analyses we investigated the impact of EDTA-to-freezer processing time (<1–7.35 hours) and freezer storage time (9.5–13.6 years). EDTA-to-freezer processing time moderately correlated positively with C4a, C3a, iC3b and sC5b-9 levels. Storage time at -80°C was not significantly correlated with any complement activation marker. This study provides valuable insight into the impact of sample processing and long-term sample storage in complement activation marker studies. The results suggest that storage time in -80°C is not a confounding factor affecting non-specific complement activation in EDTA-plasma. Sample-processing time does moderately affect the levels of some complement activation markers. This should be considered as a co-variate when analysing complement activation marker levels. Further, the impact may vary for healthy or clinical samples where immune activation is part of the pathology. These findings are important when planning large-scale clinical studies that include quantification of complement components and its activation fragments as biomarkers. It supports the collection of EDTA-plasma and fast sample processing to be included into a study standard operating procedure.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"10 ","pages":"Article 100097"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000157/pdfft?md5=0a0106368bff106f05ce6aa033dba7d2&pid=1-s2.0-S2666144624000157-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141249850","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 : 2024-06-01DOI: 10.1016/j.bionps.2024.100100
Paulo Lizano , Steven M. Silverstein
{"title":"Guest editors' introduction: The retina as a biomarker in neuropsychiatric disorders","authors":"Paulo Lizano , Steven M. Silverstein","doi":"10.1016/j.bionps.2024.100100","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100100","url":null,"abstract":"","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"10 ","pages":"Article 100100"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000182/pdfft?md5=ad381bf3c94b33f85982379a674cda72&pid=1-s2.0-S2666144624000182-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141328477","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 : 2024-06-01DOI: 10.1016/j.bionps.2024.100099
Geng Li, Wenshu Ma Chen, Yuanyuan Ma, Yan Mi, Wei Liu
Background
Progress has been achieved in many fields in understanding the biological mechanisms of depression, including genome-wide association analysis, neurotransmitter system function, brain regions and neural networks, inflammatory response, neuroplasticity, neuroimaging, and neuro electrophysiology. These progresses provide a reliable basis for developing the medical and physical therapies for depression. However, the current treatments developed from biological mechanisms can only address less than 60 % of depressive symptoms and have limited efficacy in improving social functioning and reducing recurrence. Studies have explored the non-biological mechanisms of depression in mental fields. These progresses are helpful to develop more interventions that could alleviate depressive symptoms, improve functional impairments, and reduce recurrence, thereby promoting a more comprehensive recovery in depressed patients. However, there is not a systematic and deep review to highlight the non-biological mechanisms of depression.
Methods
This study summarizes the recent progress in the non-biological fields of depression by searching publications on human studies in PubMed, PMC, and Google Schooler with exclusion of animal studies.
Results
This study reviews the intergenerational transmission characteristics, the relationship between depression and emotional trauma, cognitive deficit, relationship impairment, self-function, sense of the meaning of life, motivation deficit, and psycho-rationality of depression.
Conclusions
This study was clarified the non-biological mechanisms and characteristics of depression and provided a theoretical basis for the development of non-drug interventions.
背景在了解抑郁症的生物学机制方面，许多领域都取得了进展，包括全基因组关联分析、神经递质系统功能、脑区和神经网络、炎症反应、神经可塑性、神经影像学和神经电生理学。这些进展为开发抑郁症的医学和物理疗法提供了可靠的依据。然而，目前从生物学机制开发的治疗方法只能解决不到 60% 的抑郁症状，在改善社会功能和减少复发方面的疗效有限。研究已经在精神领域探索了抑郁症的非生物机制。这些进展有助于开发更多的干预措施，以缓解抑郁症状、改善功能障碍和减少复发，从而促进抑郁症患者更全面地康复。方法本研究通过检索 PubMed、PMC 和 Google Schooler 中有关人类研究的出版物，排除动物研究，总结了抑郁症非生物机制领域的最新进展。结果本研究综述了抑郁症的代际传递特征、抑郁症与情感创伤的关系、认知缺陷、人际关系障碍、自我功能、生命意义感、动机缺陷和心理理性。结论本研究阐明了抑郁症的非生物机制和特征，为开发非药物干预措施提供了理论依据。
{"title":"Research progress on non-biological mechanisms of depression","authors":"Geng Li, Wenshu Ma Chen, Yuanyuan Ma, Yan Mi, Wei Liu","doi":"10.1016/j.bionps.2024.100099","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100099","url":null,"abstract":"<div><h3>Background</h3><p>Progress has been achieved in many fields in understanding the biological mechanisms of depression, including genome-wide association analysis, neurotransmitter system function, brain regions and neural networks, inflammatory response, neuroplasticity, neuroimaging, and neuro electrophysiology. These progresses provide a reliable basis for developing the medical and physical therapies for depression. However, the current treatments developed from biological mechanisms can only address less than 60 % of depressive symptoms and have limited efficacy in improving social functioning and reducing recurrence. Studies have explored the non-biological mechanisms of depression in mental fields. These progresses are helpful to develop more interventions that could alleviate depressive symptoms, improve functional impairments, and reduce recurrence, thereby promoting a more comprehensive recovery in depressed patients. However, there is not a systematic and deep review to highlight the non-biological mechanisms of depression.</p></div><div><h3>Methods</h3><p>This study summarizes the recent progress in the non-biological fields of depression by searching publications on human studies in PubMed, PMC, and Google Schooler with exclusion of animal studies.</p></div><div><h3>Results</h3><p>This study reviews the intergenerational transmission characteristics, the relationship between depression and emotional trauma, cognitive deficit, relationship impairment, self-function, sense of the meaning of life, motivation deficit, and psycho-rationality of depression.</p></div><div><h3>Conclusions</h3><p>This study was clarified the non-biological mechanisms and characteristics of depression and provided a theoretical basis for the development of non-drug interventions.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"10 ","pages":"Article 100099"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000170/pdfft?md5=224c8c69183f18f99b9c8dd0a27566b5&pid=1-s2.0-S2666144624000170-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141240480","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 : 2024-05-08DOI: 10.1016/j.bionps.2024.100096
S. Patel , O. Bredemeyer , DJ Williamson , RR Struyven , Y. Zhou , AK Denniston , A. Petzold , CA Antoniades , PA Keane , SK Wagner
Objective
Atypical Parkinsonian syndrome (APS) describes a heterogeneous group of disorders mimicking the clinical presentation of Parkinson disease (PD) but with disparate natural history and pathophysiology. While retinal markers of PD are increasingly described, APS has been afforded less attention possibly owing to its lower prevalence. Here, we investigate retinal morphological differences in individuals with APS in a large real world cohort.
Methods
We conducted a cross-sectional analysis of the AlzEye study, a retrospective cohort where ophthalmic data of individuals attending Moorfields Eye Hospital between January 2008 and March 31st 2018 (inclusive) has been linked with systemic disease data through national hospital admissions. Retinal features were extracted from macula-centered color fundus photography (CFP) and optical coherence tomography (OCT) and compared between individuals with APS and those unaffected. Individuals with idiopathic PD were excluded. Retinal neural and vascular features were measured using automated segmentation and analyzed with multivariable-adjusted regression models.
Results
Among a cohort of 91,170 patients, there were 51 patients with APS and 91,119 controls. Individuals with APS were older and more likely to have hypertension and diabetes mellitus. After adjusting for age, sex, hypertension and diabetes melitus, individuals with APS had a thinner ganglion cell-inner plexiform layer (-3.95 microns, 95% CI: −7.53, −0.37, p = 0.031) but no difference in other retinoneural or retinovascular indices. Optic nerve cup-to-disc ratio was similar between groups.
Conclusion
Our cross-sectional analysis of the AlzEye cohort reveals distinct retinal morphological characteristics in APS compared to healthy controls. The study notably identifies a thinner ganglion cell-inner plexiform layer in APS patients, without accompanying changes in the inner nuclear layer or significant alterations in retinovascular indices and optic nerve cup-disc ratio. These changes are distinct from those observed in PD, where thinning of the inner nuclear layer (INL) is a characteristic feature.
Significance
These findings demonstrate a retinal phenotype in APS, markedly different from both healthy controls and idiopathic Parkinson's disease, highlighting the potential of retinal imaging in differentiating neurodegenerative disorders. By establishing a distinct retinal phenotype for APS, our findings underscore the potential of retinal imaging as a valuable, non-invasive diagnostic tool. This advancement is particularly significant for enhancing diagnostic accuracy, facilitating early detection, and offering a window into the underlying disease mechanisms in APS, thereby aiding in the development of targeted therapeutic interventions and personalized patient care strategies.
{"title":"Retinal morphological differences in atypical Parkinsonism: A cross-sectional analysis of the AlzEye cohort","authors":"S. Patel , O. Bredemeyer , DJ Williamson , RR Struyven , Y. Zhou , AK Denniston , A. Petzold , CA Antoniades , PA Keane , SK Wagner","doi":"10.1016/j.bionps.2024.100096","DOIUrl":"https://doi.org/10.1016/j.bionps.2024.100096","url":null,"abstract":"<div><h3>Objective</h3><p>Atypical Parkinsonian syndrome (APS) describes a heterogeneous group of disorders mimicking the clinical presentation of Parkinson disease (PD) but with disparate natural history and pathophysiology. While retinal markers of PD are increasingly described, APS has been afforded less attention possibly owing to its lower prevalence. Here, we investigate retinal morphological differences in individuals with APS in a large real world cohort.</p></div><div><h3>Methods</h3><p>We conducted a cross-sectional analysis of the AlzEye study, a retrospective cohort where ophthalmic data of individuals attending Moorfields Eye Hospital between January 2008 and March 31st 2018 (inclusive) has been linked with systemic disease data through national hospital admissions. Retinal features were extracted from macula-centered color fundus photography (CFP) and optical coherence tomography (OCT) and compared between individuals with APS and those unaffected. Individuals with idiopathic PD were excluded. Retinal neural and vascular features were measured using automated segmentation and analyzed with multivariable-adjusted regression models.</p></div><div><h3>Results</h3><p>Among a cohort of 91,170 patients, there were 51 patients with APS and 91,119 controls. Individuals with APS were older and more likely to have hypertension and diabetes mellitus. After adjusting for age, sex, hypertension and diabetes melitus, individuals with APS had a thinner ganglion cell-inner plexiform layer (-3.95 microns, 95% CI: −7.53, −0.37, p = 0.031) but no difference in other retinoneural or retinovascular indices. Optic nerve cup-to-disc ratio was similar between groups.</p></div><div><h3>Conclusion</h3><p>Our cross-sectional analysis of the AlzEye cohort reveals distinct retinal morphological characteristics in APS compared to healthy controls. The study notably identifies a thinner ganglion cell-inner plexiform layer in APS patients, without accompanying changes in the inner nuclear layer or significant alterations in retinovascular indices and optic nerve cup-disc ratio. These changes are distinct from those observed in PD, where thinning of the inner nuclear layer (INL) is a characteristic feature.</p></div><div><h3>Significance</h3><p>These findings demonstrate a retinal phenotype in APS, markedly different from both healthy controls and idiopathic Parkinson's disease, highlighting the potential of retinal imaging in differentiating neurodegenerative disorders. By establishing a distinct retinal phenotype for APS, our findings underscore the potential of retinal imaging as a valuable, non-invasive diagnostic tool. This advancement is particularly significant for enhancing diagnostic accuracy, facilitating early detection, and offering a window into the underlying disease mechanisms in APS, thereby aiding in the development of targeted therapeutic interventions and personalized patient care strategies.</p></div>","PeriodicalId":52767,"journal":{"name":"Biomarkers in Neuropsychiatry","volume":"10 ","pages":"Article 100096"},"PeriodicalIF":0.0,"publicationDate":"2024-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666144624000145/pdfft?md5=5d65634bfd6dc5a164c3aaf2db675424&pid=1-s2.0-S2666144624000145-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140893887","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 : 2024-04-30DOI: 10.1016/j.bionps.2024.100095
Jasmin Ricard , Nicolas Berthelot , Énora Fortin-Fabbro , Marie-Claude Boisvert , Julia Garon-Bissonnette , Eric Arsenault , Alexandre Bureau , Michel Maziade
Background
Exposure to childhood trauma may cause several alterations in brain structure and connectivity in adult patients having a major psychiatric disorder. Recent reports have shown that adult patients and young healthy offspring of patients carry similar abnormal retinal response. Because the retina and the brain have the same embryonic origin, the retina gives access to living neuronal tissue that may capture the early neurobiological effect of trauma.
Objective
Evaluate the association between exposure to childhood trauma and anomalies in cone (photopic) and rod (scotopic) responses assessed by electroretinography (ERG) in children and adolescents at familial risk (FHRs) of psychosis or mood disorders.
Methods
ERG recordings (n=194) undertaken on 134 offspring (Mage of 1st recording=15.7, 49% females) enrolled in our longitudinal study and born to a parent having DSM-IV schizophrenia, bipolar disorder or major depressive disorder were analyzed using repeated measures linear mixed models and applying multiple comparisons. The scotopic and photopic a- and b-wave latencies and amplitudes were recorded. Five types of childhood trauma were assessed prospectively and retrospectively in FHRs: physical abuse, sexual abuse, emotional abuse, neglect and witnessing domestic violence.
Results
None of the ERG scotopic or photopic parameters were associated with the global measure of exposure to trauma. However, when analyzing the specific effect of each type of trauma, data suggested that physical abuse in girls would be significantly associated with a prolonged scotopic a-wave latency (p=0.024, ES=0.28) and a trend of association was observed with a prolonged photopic b-wave latency (p=0.099, ES=0.27).
Conclusion
Our study did not suggest a substantial effect of childhood trauma on previously reported ERG anomalies in the cone and rod response in youth at familial risk of psychosis or mood disorder. Only one type of trauma i.e., physical violence toward the child, could have a specific effect on the cone and rod prolonged latencies in girls. Methodological limitations are discussed for consideration in interpreting the findings.
背景童年时期的创伤可能会导致成年重性精神病患者的大脑结构和连接性发生一些改变。最近的报告显示，成年患者和患者的年轻健康后代都有类似的视网膜异常反应。目的评估童年创伤暴露与视网膜电图（ERG）评估的精神错乱或情绪障碍家族风险（FHRs）儿童和青少年视锥（光视）和视杆（光视）反应异常之间的关联。我们采用重复测量线性混合模型和多重比较方法，分析了134名参加纵向研究、父母一方患有DSM-IV精神分裂症、双相情感障碍或重度抑郁障碍的后代（第一次记录年龄为15.7岁，49%为女性）的视网膜电图记录（n=194）。我们还记录了散光和光感 a 波和 b 波的潜伏期和振幅。在FHR中对五种类型的童年创伤进行了前瞻性和回顾性评估：身体虐待、性虐待、情感虐待、忽视和目睹家庭暴力。然而，在分析每种创伤的具体影响时，数据表明，女孩遭受身体虐待与光镜 a 波潜伏期延长有显著关联（p=0.024，ES=0.28），与光镜 b 波潜伏期延长有关联趋势（p=0.099，ES=0.27）。结论我们的研究并未表明童年创伤对之前报道的有家族性精神病或情绪障碍风险的青少年锥体和杆状反应的ERG异常有实质性影响。只有一种类型的创伤，即对儿童的身体暴力，会对女孩的锥体和杆状反应潜伏期延长产生特定影响。本文还讨论了研究方法的局限性，以便在解释研究结果时加以考虑。
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