Pub Date : 2024-02-01DOI: 10.1136/gpsych-2023-101317
Yuan Li, Peiying Li, Mengyuan Yuan, Yonghan Li, Xueying Zhang, Juan Chen, Gengfu Wang, Puyu Su
Background In early adolescence, youth are highly prone to suicidal behaviours. Identifying modifiable risk factors during this critical phase is a priority to inform effective suicide prevention strategies. Aims To explore the risk and protective factors of suicidal behaviours (ie, suicidal ideation, plans and attempts) in early adolescence in China using a social-ecological perspective. Methods Using data from the cross-sectional project ‘Healthy and Risky Behaviours Among Middle School Students in Anhui Province, China’, stratified random cluster sampling was used to select 5724 middle school students who had completed self-report questionnaires in November 2020. Network analysis was employed to examine the correlates of suicidal ideation, plans and attempts at four levels, namely individual (sex, academic performance, serious physical illness/disability, history of self-harm, depression, impulsivity, sleep problems, resilience), family (family economic status, relationship with mother, relationship with father, family violence, childhood abuse, parental mental illness), school (relationship with teachers, relationship with classmates, school-bullying victimisation and perpetration) and social (social support, satisfaction with society). Results In total, 37.9%, 19.0% and 5.5% of the students reported suicidal ideation, plans and attempts in the past 6 months, respectively. The estimated network revealed that suicidal ideation, plans and attempts were collectively associated with a history of self-harm, sleep problems, childhood abuse, school bullying and victimisation. Centrality analysis indicated that the most influential nodes in the network were history of self-harm and childhood abuse. Notably, the network also showed unique correlates of suicidal ideation (sex, weight=0.60; impulsivity, weight=0.24; family violence, weight=0.17; relationship with teachers, weight=−0.03; school-bullying perpetration, weight=0.22), suicidal plans (social support, weight=−0.15) and suicidal attempts (relationship with mother, weight=−0.10; parental mental illness, weight=0.61). Conclusions This study identified the correlates of suicidal ideation, plans and attempts, and provided practical implications for suicide prevention for young adolescents in China. Firstly, this study highlighted the importance of joint interventions across multiple departments. Secondly, the common risk factors of suicidal ideation, plans and attempts were elucidated. Thirdly, this study proposed target interventions to address the unique influencing factors of suicidal ideation, plans and attempts. Data are available upon reasonable request.
{"title":"Social-ecological perspective on the suicidal behaviour factors of early adolescents in China: a network analysis","authors":"Yuan Li, Peiying Li, Mengyuan Yuan, Yonghan Li, Xueying Zhang, Juan Chen, Gengfu Wang, Puyu Su","doi":"10.1136/gpsych-2023-101317","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101317","url":null,"abstract":"Background In early adolescence, youth are highly prone to suicidal behaviours. Identifying modifiable risk factors during this critical phase is a priority to inform effective suicide prevention strategies. Aims To explore the risk and protective factors of suicidal behaviours (ie, suicidal ideation, plans and attempts) in early adolescence in China using a social-ecological perspective. Methods Using data from the cross-sectional project ‘Healthy and Risky Behaviours Among Middle School Students in Anhui Province, China’, stratified random cluster sampling was used to select 5724 middle school students who had completed self-report questionnaires in November 2020. Network analysis was employed to examine the correlates of suicidal ideation, plans and attempts at four levels, namely individual (sex, academic performance, serious physical illness/disability, history of self-harm, depression, impulsivity, sleep problems, resilience), family (family economic status, relationship with mother, relationship with father, family violence, childhood abuse, parental mental illness), school (relationship with teachers, relationship with classmates, school-bullying victimisation and perpetration) and social (social support, satisfaction with society). Results In total, 37.9%, 19.0% and 5.5% of the students reported suicidal ideation, plans and attempts in the past 6 months, respectively. The estimated network revealed that suicidal ideation, plans and attempts were collectively associated with a history of self-harm, sleep problems, childhood abuse, school bullying and victimisation. Centrality analysis indicated that the most influential nodes in the network were history of self-harm and childhood abuse. Notably, the network also showed unique correlates of suicidal ideation (sex, weight=0.60; impulsivity, weight=0.24; family violence, weight=0.17; relationship with teachers, weight=−0.03; school-bullying perpetration, weight=0.22), suicidal plans (social support, weight=−0.15) and suicidal attempts (relationship with mother, weight=−0.10; parental mental illness, weight=0.61). Conclusions This study identified the correlates of suicidal ideation, plans and attempts, and provided practical implications for suicide prevention for young adolescents in China. Firstly, this study highlighted the importance of joint interventions across multiple departments. Secondly, the common risk factors of suicidal ideation, plans and attempts were elucidated. Thirdly, this study proposed target interventions to address the unique influencing factors of suicidal ideation, plans and attempts. Data are available upon reasonable request.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"22 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139665873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-01DOI: 10.1136/gpsych-2023-101310
Lin Huang, Qinjie Li, Yao Lu, Fengfeng Pan, Liang Cui, Ying Wang, Ya Miao, Tianlu Chen, Yatian Li, Jingnan Wu, Xiaochun Chen, Jianping Jia, Qihao Guo
Alzheimer’s disease (AD) is a common cause of dementia, characterised by cerebral amyloid-β deposition, pathological tau and neurodegeneration. The prodromal stage of AD (pAD) refers to patients with mild cognitive impairment (MCI) and evidence of AD’s pathology. At this stage, disease-modifying interventions should be used to prevent the progression to dementia. Given the inherent heterogeneity of MCI, more specific biomarkers are needed to elucidate the underlying AD’s pathology. Although the uses of cerebrospinal fluid and positron emission tomography are widely accepted methods for detecting AD’s pathology, their clinical applications are limited by their high costs and invasiveness, particularly in low-income areas in China. Therefore, to improve the early detection of Alzheimer's disease (AD) pathology through cost-effective screening methods, a panel of 45 neurologists, psychiatrists and gerontologists was invited to establish a formal consensus on the screening of pAD in China. The supportive evidence and grades of recommendations are based on a systematic literature review and focus group discussion. National meetings were held to allow participants to review, vote and provide their expert opinions to reach a consensus. A majority (two-thirds) decision was used for questions for which consensus could not be reached. Recommended screening methods are presented in this publication, including neuropsychological assessment, peripheral biomarkers and brain imaging. In addition, a general workflow for screening pAD in China is established, which will help clinicians identify individuals at high risk and determine therapeutic targets.
阿尔茨海默病（AD）是痴呆症的常见病因，以脑淀粉样蛋白-β沉积、病理性 tau 和神经变性为特征。老年痴呆症的前驱期（pAD）是指有轻度认知障碍（MCI）和老年痴呆症病理证据的患者。在这一阶段，应采取改变病情的干预措施，防止病情恶化为痴呆症。鉴于 MCI 本身的异质性，需要更多特异性生物标志物来阐明 AD 的潜在病理。虽然脑脊液和正电子发射断层扫描是目前广泛接受的检测AD病理的方法，但其高昂的费用和侵入性限制了它们在临床上的应用，尤其是在中国的低收入地区。因此，为了通过经济有效的筛查方法提高阿尔茨海默病（AD）病理的早期发现率，我们邀请了 45 位神经科、精神科和老年病学专家组成专家组，就中国的 pAD 筛查达成正式共识。支持性证据和建议等级是基于系统的文献回顾和焦点小组讨论。通过召开全国性会议，让与会者审查、投票并提供专家意见，以达成共识。对于无法达成共识的问题，则采用多数（三分之二）决定。本出版物介绍了推荐的筛查方法，包括神经心理评估、外周生物标志物和脑成像。此外，还建立了中国 pAD 筛查的一般工作流程，这将有助于临床医生识别高危人群并确定治疗目标。
{"title":"Consensus on rapid screening for prodromal Alzheimer’s disease in China","authors":"Lin Huang, Qinjie Li, Yao Lu, Fengfeng Pan, Liang Cui, Ying Wang, Ya Miao, Tianlu Chen, Yatian Li, Jingnan Wu, Xiaochun Chen, Jianping Jia, Qihao Guo","doi":"10.1136/gpsych-2023-101310","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101310","url":null,"abstract":"Alzheimer’s disease (AD) is a common cause of dementia, characterised by cerebral amyloid-β deposition, pathological tau and neurodegeneration. The prodromal stage of AD (pAD) refers to patients with mild cognitive impairment (MCI) and evidence of AD’s pathology. At this stage, disease-modifying interventions should be used to prevent the progression to dementia. Given the inherent heterogeneity of MCI, more specific biomarkers are needed to elucidate the underlying AD’s pathology. Although the uses of cerebrospinal fluid and positron emission tomography are widely accepted methods for detecting AD’s pathology, their clinical applications are limited by their high costs and invasiveness, particularly in low-income areas in China. Therefore, to improve the early detection of Alzheimer's disease (AD) pathology through cost-effective screening methods, a panel of 45 neurologists, psychiatrists and gerontologists was invited to establish a formal consensus on the screening of pAD in China. The supportive evidence and grades of recommendations are based on a systematic literature review and focus group discussion. National meetings were held to allow participants to review, vote and provide their expert opinions to reach a consensus. A majority (two-thirds) decision was used for questions for which consensus could not be reached. Recommended screening methods are presented in this publication, including neuropsychological assessment, peripheral biomarkers and brain imaging. In addition, a general workflow for screening pAD in China is established, which will help clinicians identify individuals at high risk and determine therapeutic targets.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"6 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139665895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-01DOI: 10.1136/gpsych-2023-101369
Jiahao Zhu, Houpu Liu, Rui Gao, Lilu Ding, Jing Wang, Ye Yang, Dan Zhou, Yingjun Li
Background Educational inequalities in suicide have become increasingly prominent over the past decade. Elucidating modifiable risk factors that serve as intermediaries in the impact of low educational attainment on suicide has the potential to reduce health disparities. Aims To examine the risk factors that mediate the relationship between educational attainment and suicide attempts and quantify their contributions to the mediation effect. Methods We conducted a two-sample Mendelian randomisation (MR) analysis to estimate the causal effect of educational attainment on suicide attempts, utilising genome-wide association study summary statistics from the Integrative Psychiatric Research (iPSYCH; 6024 cases and 44 240 controls) and FinnGen (8978 cases and 368 299 controls). We systematically evaluated 42 putative mediators within the causal pathway connecting reduced educational attainment to suicide attempts and employed two-step and multivariable MR to quantify the proportion of the mediated effect. Results In the combined analysis of iPSYCH and FinnGen, each standard deviation (SD) decrease in genetically predicted educational attainment (equating to 3.4 years of education) was associated with a 105% higher risk of suicide attempts (odds ratio (OR): 2.05; 95% confidence interval (CI): 1.81 to 2.31). Of the 42 risk factors analysed, the two-step MR identified five factors that mediated the association between educational attainment and suicide attempts. The respective proportions of mediation were 47% (95% CI: 29% to 66%) for smoking behaviour, 36% (95% CI: 0% to 84%) for chronic pain, 49% (95% CI: 36% to 61%) for depression, 35% (95% CI: 12% to 59%) for anxiety and 26% (95% CI: 18% to 34%) for insomnia. Multivariable MR implicated these five mediators collectively, accounting for 68% (95% CI: 40% to 96%) of the total effect. Conclusions This study identified smoking, chronic pain and mental disorders as primary intervention targets for attenuating suicide risk attributable to lower educational levels in the European population. Data are available in a public, open access repository. Summary statistics for suicide attempts are publicly available in the Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH) at , reference [12] and in the FinnGen study at , reference [13].
{"title":"Understanding the educational inequalities in suicide attempts and their mediators: a Mendelian randomisation study","authors":"Jiahao Zhu, Houpu Liu, Rui Gao, Lilu Ding, Jing Wang, Ye Yang, Dan Zhou, Yingjun Li","doi":"10.1136/gpsych-2023-101369","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101369","url":null,"abstract":"Background Educational inequalities in suicide have become increasingly prominent over the past decade. Elucidating modifiable risk factors that serve as intermediaries in the impact of low educational attainment on suicide has the potential to reduce health disparities. Aims To examine the risk factors that mediate the relationship between educational attainment and suicide attempts and quantify their contributions to the mediation effect. Methods We conducted a two-sample Mendelian randomisation (MR) analysis to estimate the causal effect of educational attainment on suicide attempts, utilising genome-wide association study summary statistics from the Integrative Psychiatric Research (iPSYCH; 6024 cases and 44 240 controls) and FinnGen (8978 cases and 368 299 controls). We systematically evaluated 42 putative mediators within the causal pathway connecting reduced educational attainment to suicide attempts and employed two-step and multivariable MR to quantify the proportion of the mediated effect. Results In the combined analysis of iPSYCH and FinnGen, each standard deviation (SD) decrease in genetically predicted educational attainment (equating to 3.4 years of education) was associated with a 105% higher risk of suicide attempts (odds ratio (OR): 2.05; 95% confidence interval (CI): 1.81 to 2.31). Of the 42 risk factors analysed, the two-step MR identified five factors that mediated the association between educational attainment and suicide attempts. The respective proportions of mediation were 47% (95% CI: 29% to 66%) for smoking behaviour, 36% (95% CI: 0% to 84%) for chronic pain, 49% (95% CI: 36% to 61%) for depression, 35% (95% CI: 12% to 59%) for anxiety and 26% (95% CI: 18% to 34%) for insomnia. Multivariable MR implicated these five mediators collectively, accounting for 68% (95% CI: 40% to 96%) of the total effect. Conclusions This study identified smoking, chronic pain and mental disorders as primary intervention targets for attenuating suicide risk attributable to lower educational levels in the European population. Data are available in a public, open access repository. Summary statistics for suicide attempts are publicly available in the Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH) at <https://ipsych.dk/forskning/downloads>, reference [12] and in the FinnGen study at <https://finngen.gitbook.io/documentation/data-download>, reference [13].","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"476 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139927714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-12eCollection Date: 2024-01-01DOI: 10.1136/gpsych-2023-101311
Chengzhang Liu, Qiguo Meng, Yuanxiu Wei, Xinyue Su, Yuanyuan Zhang, Panpan He, Chun Zhou, Mengyi Liu, Ziliang Ye, Xianhui Qin
Background: The prospective association of dietary thiamine intake with the risk of cognitive decline among the general older adults remains uncertain.
Aims: To investigate the association between dietary thiamine intake and cognitive decline in cognitively healthy, older Chinese individuals.
Methods: The study included a total of 3106 participants capable of completing repeated cognitive function tests. Dietary nutrient intake information was collected through 3-day dietary recalls and using a 3-day food-weighed method to assess cooking oil and condiment consumption. Cognitive decline was defined as the 5-year decline rate in global or composite cognitive scores based on a subset of items from the Telephone Interview for Cognitive Status-modified.
Results: The median follow-up duration was 5.9 years. There was a J-shaped relationship between dietary thiamine intake and the 5-year decline rate in global and composite cognitive scores, with an inflection point of 0.68 mg/day (95% confidence interval (CI): 0.56 to 0.80) and a minimal risk at 0.60-1.00 mg/day of dietary thiamine intake. Before the inflection point, thiamine intake was not significantly associated with cognitive decline. Beyond the inflection point, each unit increase in thiamine intake (mg/day) was associated with a significant decrease of 4.24 (95% CI: 2.22 to 6.27) points in the global score and 0.49 (95% CI: 0.23 to 0.76) standard units in the composite score within 5 years. A stronger positive association between thiamine intake and cognitive decline was observed in those with hypertension, obesity and those who were non-smokers (all p<0.05).
Conclusions: This study revealed a J-shaped association between dietary thiamine intake and cognitive decline in cognitively healthy, older Chinese individuals, with an inflection point at 0.68 mg/day and a minimal risk at 0.60-1.00 mg/day of dietary thiamine intake.
{"title":"J-shaped association between dietary thiamine intake and the risk of cognitive decline in cognitively healthy, older Chinese individuals.","authors":"Chengzhang Liu, Qiguo Meng, Yuanxiu Wei, Xinyue Su, Yuanyuan Zhang, Panpan He, Chun Zhou, Mengyi Liu, Ziliang Ye, Xianhui Qin","doi":"10.1136/gpsych-2023-101311","DOIUrl":"10.1136/gpsych-2023-101311","url":null,"abstract":"<p><strong>Background: </strong>The prospective association of dietary thiamine intake with the risk of cognitive decline among the general older adults remains uncertain.</p><p><strong>Aims: </strong>To investigate the association between dietary thiamine intake and cognitive decline in cognitively healthy, older Chinese individuals.</p><p><strong>Methods: </strong>The study included a total of 3106 participants capable of completing repeated cognitive function tests. Dietary nutrient intake information was collected through 3-day dietary recalls and using a 3-day food-weighed method to assess cooking oil and condiment consumption. Cognitive decline was defined as the 5-year decline rate in global or composite cognitive scores based on a subset of items from the Telephone Interview for Cognitive Status-modified.</p><p><strong>Results: </strong>The median follow-up duration was 5.9 years. There was a J-shaped relationship between dietary thiamine intake and the 5-year decline rate in global and composite cognitive scores, with an inflection point of 0.68 mg/day (95% confidence interval (CI): 0.56 to 0.80) and a minimal risk at 0.60-1.00 mg/day of dietary thiamine intake. Before the inflection point, thiamine intake was not significantly associated with cognitive decline. Beyond the inflection point, each unit increase in thiamine intake (mg/day) was associated with a significant decrease of 4.24 (95% CI: 2.22 to 6.27) points in the global score and 0.49 (95% CI: 0.23 to 0.76) standard units in the composite score within 5 years. A stronger positive association between thiamine intake and cognitive decline was observed in those with hypertension, obesity and those who were non-smokers (all p<0.05).</p><p><strong>Conclusions: </strong>This study revealed a J-shaped association between dietary thiamine intake and cognitive decline in cognitively healthy, older Chinese individuals, with an inflection point at 0.68 mg/day and a minimal risk at 0.60-1.00 mg/day of dietary thiamine intake.</p>","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"37 1","pages":"e101311"},"PeriodicalIF":11.9,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139563834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1136/gpsych-2023-101106
Xingqi Wu, Yibing Yan, Panpan Hu, Lu Wang, Yue Wu, Pan Wu, Zhi Geng, Guixian Xiao, Shanshan Zhou, Gongjun Ji, Bensheng Qiu, Ling Wei, Yanghua Tian, Hesheng Liu, Kai Wang
Background Previous studies have demonstrated that excitatory repetitive transcranial magnetic stimulation (rTMS) can improve the cognitive function of patients with Alzheimer’s disease (AD). Intermittent theta burst stimulation (iTBS) is a novel excitatory rTMS protocol for brain activity stimulation with the ability to induce long-term potentiation-like plasticity and represents a promising treatment for AD. However, the long-term effects of iTBS on cognitive decline and brain structure in patients with AD are unknown. Aims We aimed to explore whether repeating accelerated iTBS every three months could slow down the cognitive decline in patients with AD. Methods In this randomised, assessor-blinded, controlled trial, iTBS was administered to the left dorsolateral prefrontal cortex (DLPFC) of 42 patients with AD for 14 days every 13 weeks. Measurements included the Montreal Cognitive Assessment (MoCA), a comprehensive neuropsychological battery, and the grey matter volume (GMV) of the hippocampus. Patients were evaluated at baseline and after follow-up. The longitudinal pipeline of the Computational Anatomy Toolbox for SPM was used to detect significant treatment-related changes over time. Results The iTBS group maintained MoCA scores relative to the control group (t=3.26, p=0.013) and reduced hippocampal atrophy, which was significantly correlated with global degeneration scale changes. The baseline Mini-Mental State Examination (MMSE) score, apolipoprotein E genotype and Clinical Dementia Rating were indicative of MoCA scores at follow-up. Moreover, the GMV of the left (t=0.08, p=0.996) and right (t=0.19, p=0.977) hippocampus were maintained in the active group but significantly declined in the control group (left: t=4.13, p<0.001; right: t=5.31, p < 0.001). GMV change in the left (r=0.35, p=0.023) and right (r=0.36, p=0.021) hippocampus across the intervention positively correlated with MoCA changes; left hippocampal GMV change was negatively correlated with global degeneration scale (r=−0.32, p=0.041) changes. Conclusions DLPFC-iTBS may be a feasible and easy-to-implement non-pharmacological intervention to slow down the progressive decline of overall cognition and quality of life in patients with AD, providing a new AD treatment option. Trial registration number [NCT04754152][1]. Data are available on reasonable request. The data supporting the findings of this trial are accessible on request from the corresponding authors. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT04754152&atom=%2Fgpsych%2F37%2F1%2Fe101106.atom
{"title":"Effects of a periodic intermittent theta burst stimulation in Alzheimer’s disease","authors":"Xingqi Wu, Yibing Yan, Panpan Hu, Lu Wang, Yue Wu, Pan Wu, Zhi Geng, Guixian Xiao, Shanshan Zhou, Gongjun Ji, Bensheng Qiu, Ling Wei, Yanghua Tian, Hesheng Liu, Kai Wang","doi":"10.1136/gpsych-2023-101106","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101106","url":null,"abstract":"Background Previous studies have demonstrated that excitatory repetitive transcranial magnetic stimulation (rTMS) can improve the cognitive function of patients with Alzheimer’s disease (AD). Intermittent theta burst stimulation (iTBS) is a novel excitatory rTMS protocol for brain activity stimulation with the ability to induce long-term potentiation-like plasticity and represents a promising treatment for AD. However, the long-term effects of iTBS on cognitive decline and brain structure in patients with AD are unknown. Aims We aimed to explore whether repeating accelerated iTBS every three months could slow down the cognitive decline in patients with AD. Methods In this randomised, assessor-blinded, controlled trial, iTBS was administered to the left dorsolateral prefrontal cortex (DLPFC) of 42 patients with AD for 14 days every 13 weeks. Measurements included the Montreal Cognitive Assessment (MoCA), a comprehensive neuropsychological battery, and the grey matter volume (GMV) of the hippocampus. Patients were evaluated at baseline and after follow-up. The longitudinal pipeline of the Computational Anatomy Toolbox for SPM was used to detect significant treatment-related changes over time. Results The iTBS group maintained MoCA scores relative to the control group (t=3.26, p=0.013) and reduced hippocampal atrophy, which was significantly correlated with global degeneration scale changes. The baseline Mini-Mental State Examination (MMSE) score, apolipoprotein E genotype and Clinical Dementia Rating were indicative of MoCA scores at follow-up. Moreover, the GMV of the left (t=0.08, p=0.996) and right (t=0.19, p=0.977) hippocampus were maintained in the active group but significantly declined in the control group (left: t=4.13, p<0.001; right: t=5.31, p < 0.001). GMV change in the left (r=0.35, p=0.023) and right (r=0.36, p=0.021) hippocampus across the intervention positively correlated with MoCA changes; left hippocampal GMV change was negatively correlated with global degeneration scale (r=−0.32, p=0.041) changes. Conclusions DLPFC-iTBS may be a feasible and easy-to-implement non-pharmacological intervention to slow down the progressive decline of overall cognition and quality of life in patients with AD, providing a new AD treatment option. Trial registration number [NCT04754152][1]. Data are available on reasonable request. The data supporting the findings of this trial are accessible on request from the corresponding authors. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT04754152&atom=%2Fgpsych%2F37%2F1%2Fe101106.atom","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"21 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139415109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1136/gpsych-2023-101398
Yankun Wu, Yun-Ai Su, Linlin Zhu, Jitao Li, Tianmei Si
Bipolar disorder is characterised by recurrent and alternating episodes of mania/hypomania and depression. Current breakthroughs in functional MRI techniques have uncovered the functional neuroanatomy of bipolar disorder. However, the pathophysiology underlying mood instability, mood switching and the development of extreme mood states is less well understood. This review presents a comprehensive overview of current evidence from functional MRI studies from the perspective of mood states. We first summarise the disrupted brain activation patterns and functional connectivity that have been reported in bipolar disorder, irrespective of the mood state. We next focus on research that solely included patients in a single mood state for a better understanding of the pathophysiology of bipolar disorder and research comparing patients with different mood states to dissect mood state-related effects. Finally, we briefly summarise current theoretical models and conclude this review by proposing potential avenues for future research. A comprehensive understanding of the pathophysiology with consideration of mood states could not only deepen our understanding of how acute mood episodes develop at a neurophysiological level but could also facilitate the identification of biological targets for personalised treatment and the development of new interventions for bipolar disorder.
{"title":"Advances in functional MRI research in bipolar disorder: from the perspective of mood states","authors":"Yankun Wu, Yun-Ai Su, Linlin Zhu, Jitao Li, Tianmei Si","doi":"10.1136/gpsych-2023-101398","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101398","url":null,"abstract":"Bipolar disorder is characterised by recurrent and alternating episodes of mania/hypomania and depression. Current breakthroughs in functional MRI techniques have uncovered the functional neuroanatomy of bipolar disorder. However, the pathophysiology underlying mood instability, mood switching and the development of extreme mood states is less well understood. This review presents a comprehensive overview of current evidence from functional MRI studies from the perspective of mood states. We first summarise the disrupted brain activation patterns and functional connectivity that have been reported in bipolar disorder, irrespective of the mood state. We next focus on research that solely included patients in a single mood state for a better understanding of the pathophysiology of bipolar disorder and research comparing patients with different mood states to dissect mood state-related effects. Finally, we briefly summarise current theoretical models and conclude this review by proposing potential avenues for future research. A comprehensive understanding of the pathophysiology with consideration of mood states could not only deepen our understanding of how acute mood episodes develop at a neurophysiological level but could also facilitate the identification of biological targets for personalised treatment and the development of new interventions for bipolar disorder.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"167 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139583763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background Depression, anxiety and schizophrenia among older persons have become global public health challenges. However, the burden of these disorders in ageing and aged countries has not been analysed. Aims To investigate the burden of depression, anxiety and schizophrenia among older adults in ageing and aged countries. Methods Using data from the Global Burden of Disease Study 2019, we calculated the estimated annual percentage change (EAPC) in the age-standardised incidence rates (ASIR) and age-standardised disability-adjusted life years (DALYs) rates (ASDR) for depression, anxiety and schizophrenia of older people in ageing countries (China, India, Indonesia) and aged countries (Japan, Italy, Portugal) between 1990 and 2019. Trends in incidence and DALYs were analysed by gender and age. Results In 2019, the highest incidence of depression, anxiety and schizophrenia in the older population in aged countries was in Japan (927 271.3 (752 552.3–1 125 796.5), 51 498.2 (37 625.7–70 487.3) and 126.0 (61.0–223.2), respectively), while the highest incidence in ageing countries was in China (5 797 556.9 (4 599 403.4–7 133 006.5), 330 256.1 (246 448.9–445 987.4) and 1067.7 (556.2–1775.9), respectively). DALYs for these disorders were similar, with the highest in Japan and China. From 1990 to 2019, the ASIR for depressive disorders decreased in aged countries but increased in ageing countries; the ASIR for anxiety disorders and schizophrenia declined in both ageing and aged countries. The ASDR for depressive disorders was consistent with the ASIR but not for anxiety disorders and schizophrenia. The ASIR for depressive disorders was higher in older women, while the opposite was observed in anxiety disorders and schizophrenia. Notably, the conditions of burden of depressive disorders, anxiety disorders and schizophrenia in the 65–70-year-old age group were the most burdensome. Conclusions The incidence and DALYs of these three mental disorders increased while exhibiting differences between ageing and aged countries. Raising awareness about formulating health policies for preventing and treating mental disorders in the older population is necessary to reduce the future burden posed by the ageing challenge. All data relevant to the study are included in the article or uploaded as supplementary information.
{"title":"The burden of depression, anxiety and schizophrenia among the older population in ageing and aged countries: an analysis of the Global Burden of Disease Study 2019","authors":"Ying Cheng, Yu Fang, Jinxin Zheng, Shiyang Guan, Meiti Wang, Wu Hong","doi":"10.1136/gpsych-2023-101078","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101078","url":null,"abstract":"Background Depression, anxiety and schizophrenia among older persons have become global public health challenges. However, the burden of these disorders in ageing and aged countries has not been analysed. Aims To investigate the burden of depression, anxiety and schizophrenia among older adults in ageing and aged countries. Methods Using data from the Global Burden of Disease Study 2019, we calculated the estimated annual percentage change (EAPC) in the age-standardised incidence rates (ASIR) and age-standardised disability-adjusted life years (DALYs) rates (ASDR) for depression, anxiety and schizophrenia of older people in ageing countries (China, India, Indonesia) and aged countries (Japan, Italy, Portugal) between 1990 and 2019. Trends in incidence and DALYs were analysed by gender and age. Results In 2019, the highest incidence of depression, anxiety and schizophrenia in the older population in aged countries was in Japan (927 271.3 (752 552.3–1 125 796.5), 51 498.2 (37 625.7–70 487.3) and 126.0 (61.0–223.2), respectively), while the highest incidence in ageing countries was in China (5 797 556.9 (4 599 403.4–7 133 006.5), 330 256.1 (246 448.9–445 987.4) and 1067.7 (556.2–1775.9), respectively). DALYs for these disorders were similar, with the highest in Japan and China. From 1990 to 2019, the ASIR for depressive disorders decreased in aged countries but increased in ageing countries; the ASIR for anxiety disorders and schizophrenia declined in both ageing and aged countries. The ASDR for depressive disorders was consistent with the ASIR but not for anxiety disorders and schizophrenia. The ASIR for depressive disorders was higher in older women, while the opposite was observed in anxiety disorders and schizophrenia. Notably, the conditions of burden of depressive disorders, anxiety disorders and schizophrenia in the 65–70-year-old age group were the most burdensome. Conclusions The incidence and DALYs of these three mental disorders increased while exhibiting differences between ageing and aged countries. Raising awareness about formulating health policies for preventing and treating mental disorders in the older population is necessary to reduce the future burden posed by the ageing challenge. All data relevant to the study are included in the article or uploaded as supplementary information.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"28 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139506359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1136/gpsych-2023-101291
Panpan Hu, Qiuchen Cao, Hu Feng, Yun Liu, Yan Chen, Jingfan Xu, Weixi Feng, Huaiqing Sun, Huachen Ding, Chun Wang, Junying Gao, Ming Xiao
Background Increasing evidence supports the role of microRNAs (miRNAs) in major depressive disorder (MDD), but the pathophysiological mechanism remains elusive. Aims To explore the mechanism of microRNA-451a (miR-451a) in the pathology and behaviours of depression. Methods Abnormal miRNAs such as miR-451a reported previously in the serum of patients with MDD were screened and then confirmed in a mouse model of depression induced by chronic restraint stress (CRS). Eight-week-old male C57BL/6 mice had miR-451a overexpression in the medial prefrontal cortex (mPFC) via adeno-associated virus serotype 9 vectors encoding a pri-mmu-miR-451a-GFP fusion protein followed by behavioural and pathological analyses. Finally, molecular biological experiments were conducted to investigate the potential mechanism of miR-451a against depression. Results The serum levels of miRNA-451a were significantly lower in patients with MDD, with a negative correlation with the Hamilton Depression Scale scores. Additionally, a negative association between serum miR-451a and behavioural despair or anhedonia was observed in CRS mice. Notably, miR-451a expression was significantly downregulated in the mPFC of CRS-susceptible mice. Overexpressing miR-451a in the mPFC reversed the loss of dendritic spines and the depression-like phenotype of CRS mice. Mechanistically, miR-451a could inhibit CRS-induced corticotropin-releasing factor receptor 1 expression via targeting transcription factor 2, subsequently protecting dendritic spine plasticity. Conclusions Together, these results highlighted miR-451a as a candidate biomarker and therapeutic target for MDD. Data are available upon reasonable request.
{"title":"MicroRNA-451a is a candidate biomarker and therapeutic target for major depressive disorder","authors":"Panpan Hu, Qiuchen Cao, Hu Feng, Yun Liu, Yan Chen, Jingfan Xu, Weixi Feng, Huaiqing Sun, Huachen Ding, Chun Wang, Junying Gao, Ming Xiao","doi":"10.1136/gpsych-2023-101291","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101291","url":null,"abstract":"Background Increasing evidence supports the role of microRNAs (miRNAs) in major depressive disorder (MDD), but the pathophysiological mechanism remains elusive. Aims To explore the mechanism of microRNA-451a (miR-451a) in the pathology and behaviours of depression. Methods Abnormal miRNAs such as miR-451a reported previously in the serum of patients with MDD were screened and then confirmed in a mouse model of depression induced by chronic restraint stress (CRS). Eight-week-old male C57BL/6 mice had miR-451a overexpression in the medial prefrontal cortex (mPFC) via adeno-associated virus serotype 9 vectors encoding a pri-mmu-miR-451a-GFP fusion protein followed by behavioural and pathological analyses. Finally, molecular biological experiments were conducted to investigate the potential mechanism of miR-451a against depression. Results The serum levels of miRNA-451a were significantly lower in patients with MDD, with a negative correlation with the Hamilton Depression Scale scores. Additionally, a negative association between serum miR-451a and behavioural despair or anhedonia was observed in CRS mice. Notably, miR-451a expression was significantly downregulated in the mPFC of CRS-susceptible mice. Overexpressing miR-451a in the mPFC reversed the loss of dendritic spines and the depression-like phenotype of CRS mice. Mechanistically, miR-451a could inhibit CRS-induced corticotropin-releasing factor receptor 1 expression via targeting transcription factor 2, subsequently protecting dendritic spine plasticity. Conclusions Together, these results highlighted miR-451a as a candidate biomarker and therapeutic target for MDD. Data are available upon reasonable request.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"39 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139658015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01DOI: 10.1136/gpsych-2023-101201
Viktor H Ahlqvist, Christina Dardani, Paul Madley-Dowd, Harriet Forbes, Jessica Rast, Caichen Zhong, Renee M Gardner, Christina Dalman, Kristen Lyall, Craig Newschaffer, Torbjörn Tomson, Michael Lundberg, Daniel Berglind, Neil M Davies, Brian K Lee, Cecilia Magnusson, Dheeraj Rai
Background Psychiatric comorbidities are common in patients with epilepsy. Reasons for the co-occurrence of psychiatric conditions and epilepsy remain poorly understood. Aim We aimed to triangulate the relationship between epilepsy and psychiatric conditions to determine the extent and possible origins of these conditions. Methods Using nationwide Swedish health registries, we quantified the lifetime prevalence of psychiatric disorders in patients with epilepsy. We then used summary data from genome-wide association studies to investigate whether the identified observational associations could be attributed to a shared underlying genetic aetiology using cross-trait linkage disequilibrium score regression. Finally, we assessed the potential bidirectional relationships using two-sample Mendelian randomisation. Results In a cohort of 7 628 495 individuals, we found that almost half of the 94 435 individuals diagnosed with epilepsy were also diagnosed with a psychiatric condition in their lifetime (adjusted lifetime prevalence, 44.09%; 95% confidence interval (CI) 43.78% to 44.39%). We found evidence for a genetic correlation between epilepsy and some neurodevelopmental and psychiatric conditions. For example, we observed a genetic correlation between epilepsy and attention-deficit/hyperactivity disorder (rg=0.18, 95% CI 0.09 to 0.27, p<0.001)—a correlation that was more pronounced in focal epilepsy (rg=0.23, 95% CI 0.09 to 0.36, p<0.001). Findings from Mendelian randomisation using common genetic variants did not support bidirectional effects between epilepsy and neurodevelopmental or psychiatric conditions. Conclusions Psychiatric comorbidities are common in patients with epilepsy. Genetic correlations may partially explain some comorbidities; however, there is little evidence of a bidirectional relationship between the genetic liability of epilepsy and psychiatric conditions. These findings highlight the need to understand the role of environmental factors or rare genetic variations in the origins of psychiatric comorbidities in epilepsy. No data are available. All genetic data produced in this study are publicly available in their original publication and upon reasonable request from the authors. Swedish privacy laws prohibit the authors from making registry data publicly available. The data supporting these findings were used under licence and ethical approval for this study. Readers interested in obtaining microdata or replicating this study may seek similar approval and enquiries from Statistics Sweden. For further advice, see , or contact Statistics Sweden at mikrodata{at}scb.se.
{"title":"Psychiatric comorbidities in epilepsy: population co-occurrence, genetic correlations and causal effects","authors":"Viktor H Ahlqvist, Christina Dardani, Paul Madley-Dowd, Harriet Forbes, Jessica Rast, Caichen Zhong, Renee M Gardner, Christina Dalman, Kristen Lyall, Craig Newschaffer, Torbjörn Tomson, Michael Lundberg, Daniel Berglind, Neil M Davies, Brian K Lee, Cecilia Magnusson, Dheeraj Rai","doi":"10.1136/gpsych-2023-101201","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101201","url":null,"abstract":"Background Psychiatric comorbidities are common in patients with epilepsy. Reasons for the co-occurrence of psychiatric conditions and epilepsy remain poorly understood. Aim We aimed to triangulate the relationship between epilepsy and psychiatric conditions to determine the extent and possible origins of these conditions. Methods Using nationwide Swedish health registries, we quantified the lifetime prevalence of psychiatric disorders in patients with epilepsy. We then used summary data from genome-wide association studies to investigate whether the identified observational associations could be attributed to a shared underlying genetic aetiology using cross-trait linkage disequilibrium score regression. Finally, we assessed the potential bidirectional relationships using two-sample Mendelian randomisation. Results In a cohort of 7 628 495 individuals, we found that almost half of the 94 435 individuals diagnosed with epilepsy were also diagnosed with a psychiatric condition in their lifetime (adjusted lifetime prevalence, 44.09%; 95% confidence interval (CI) 43.78% to 44.39%). We found evidence for a genetic correlation between epilepsy and some neurodevelopmental and psychiatric conditions. For example, we observed a genetic correlation between epilepsy and attention-deficit/hyperactivity disorder (rg=0.18, 95% CI 0.09 to 0.27, p<0.001)—a correlation that was more pronounced in focal epilepsy (rg=0.23, 95% CI 0.09 to 0.36, p<0.001). Findings from Mendelian randomisation using common genetic variants did not support bidirectional effects between epilepsy and neurodevelopmental or psychiatric conditions. Conclusions Psychiatric comorbidities are common in patients with epilepsy. Genetic correlations may partially explain some comorbidities; however, there is little evidence of a bidirectional relationship between the genetic liability of epilepsy and psychiatric conditions. These findings highlight the need to understand the role of environmental factors or rare genetic variations in the origins of psychiatric comorbidities in epilepsy. No data are available. All genetic data produced in this study are publicly available in their original publication and upon reasonable request from the authors. Swedish privacy laws prohibit the authors from making registry data publicly available. The data supporting these findings were used under licence and ethical approval for this study. Readers interested in obtaining microdata or replicating this study may seek similar approval and enquiries from Statistics Sweden. For further advice, see <https://www.scb.se/en/services/guidance-for-researchers-and-universities/>, or contact Statistics Sweden at mikrodata{at}scb.se.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"10 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139648107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background Cardiovascular risk burden is associated with dementia risk and neurodegeneration-related brain structure, while the role of genetics and incident cardiovascular disease (CVD) remains unclear. Aims To examine the association of overall cardiovascular risk burden with the risk of major dementia subtypes and volumes of related brain regions in a large sample, and to explore the role of genetics and CVD onset. Methods A prospective study among 354 654 participants free of CVD and dementia (2006–2010, mean age 56.4 years) was conducted within the UK Biobank, with brain magnetic resonance imaging (MRI) measurement available for 15 104 participants since 2014. CVD risk burden was evaluated by the Framingham General Cardiovascular Risk Score (FGCRS). Dementia diagnosis was ascertained from inpatient and death register data. Results Over a median 12.0-year follow-up, 3998 all-cause dementia cases were identified. Higher FGCRS was associated with increased all-cause dementia risk after adjusting for demographic, major lifestyle, clinical factors and the polygenic risk score (PRS) of Alzheimer’s disease. Comparing the high versus low tertile of FGCRS, the odds ratios (ORs) and 95% confidence intervals (CIs) were 1.26 (1.12 to 1.41) for all-cause dementia, 1.67 (1.33 to 2.09) for Alzheimer’s disease and 1.53 (1.07 to 2.16) for vascular dementia (all ptrend<0.05). Incident stroke and coronary heart disease accounted for 14% (95% CI: 9% to 21%) of the association between FGCRS and all-cause dementia. Interactions were not detected for FGCRS and PRS on the risk of any dementia subtype. We observed an 83% (95% CI: 47% to 128%) higher all-cause dementia risk comparing the high–high versus low–low FGCRS–PRS category. For brain volumes, higher FGCRS was associated with greater log-transformed white matter hyperintensities, smaller cortical volume and smaller grey matter volume. Conclusions Our findings suggest that the positive association of cardiovascular risk burden with dementia risk also applies to major dementia subtypes. The association of cardiovascular risk burden with all-cause dementia is largely independent of CVD onset and genetic predisposition to dementia. Data may be obtained from a third party and are not publicly available. Data access to the UK Biobank is available upon application.
{"title":"Cardiovascular risk burden, dementia risk and brain structural imaging markers: a study from UK Biobank","authors":"Yaying Cao, Gaohong Zhu, Chengwu Feng, Jing Chen, Wei Gan, Yuan Ma, Yonghua Hu, Klodian Dhana, Trudy Voortman, Jie Shen, Ting Li, Yan Zheng, Changzheng Yuan, Geng Zong","doi":"10.1136/gpsych-2023-101209","DOIUrl":"https://doi.org/10.1136/gpsych-2023-101209","url":null,"abstract":"Background Cardiovascular risk burden is associated with dementia risk and neurodegeneration-related brain structure, while the role of genetics and incident cardiovascular disease (CVD) remains unclear. Aims To examine the association of overall cardiovascular risk burden with the risk of major dementia subtypes and volumes of related brain regions in a large sample, and to explore the role of genetics and CVD onset. Methods A prospective study among 354 654 participants free of CVD and dementia (2006–2010, mean age 56.4 years) was conducted within the UK Biobank, with brain magnetic resonance imaging (MRI) measurement available for 15 104 participants since 2014. CVD risk burden was evaluated by the Framingham General Cardiovascular Risk Score (FGCRS). Dementia diagnosis was ascertained from inpatient and death register data. Results Over a median 12.0-year follow-up, 3998 all-cause dementia cases were identified. Higher FGCRS was associated with increased all-cause dementia risk after adjusting for demographic, major lifestyle, clinical factors and the polygenic risk score (PRS) of Alzheimer’s disease. Comparing the high versus low tertile of FGCRS, the odds ratios (ORs) and 95% confidence intervals (CIs) were 1.26 (1.12 to 1.41) for all-cause dementia, 1.67 (1.33 to 2.09) for Alzheimer’s disease and 1.53 (1.07 to 2.16) for vascular dementia (all ptrend<0.05). Incident stroke and coronary heart disease accounted for 14% (95% CI: 9% to 21%) of the association between FGCRS and all-cause dementia. Interactions were not detected for FGCRS and PRS on the risk of any dementia subtype. We observed an 83% (95% CI: 47% to 128%) higher all-cause dementia risk comparing the high–high versus low–low FGCRS–PRS category. For brain volumes, higher FGCRS was associated with greater log-transformed white matter hyperintensities, smaller cortical volume and smaller grey matter volume. Conclusions Our findings suggest that the positive association of cardiovascular risk burden with dementia risk also applies to major dementia subtypes. The association of cardiovascular risk burden with all-cause dementia is largely independent of CVD onset and genetic predisposition to dementia. Data may be obtained from a third party and are not publicly available. Data access to the UK Biobank is available upon application.","PeriodicalId":12549,"journal":{"name":"General Psychiatry","volume":"154 1","pages":""},"PeriodicalIF":11.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139583133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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