The heterogeneity of chronic post-COVID neuropsychiatric symptoms (PCNPS), especially after infection by the Omicron strain, has not been adequately explored.

To explore the clustering pattern of chronic PCNPS in a cohort of patients having their first COVID infection during the ‘Omicron wave’ and discover phenotypes of patients based on their symptoms’ patterns using a pre-registered protocol.

We assessed 1205 eligible subjects in Hong Kong using app-based questionnaires and cognitive tasks.

Partial network analysis of chronic PCNPS in this cohort produced two major symptom clusters (cognitive complaint–fatigue and anxiety–depression) and a minor headache–dizziness cluster, like our pre-Omicron cohort. Participants with high numbers of symptoms could be further grouped into two distinct phenotypes: a cognitive complaint–fatigue predominant phenotype and another with symptoms across multiple clusters. Multiple logistic regression showed that both phenotypes were predicted by the level of pre-infection deprivation (adjusted P-values of 0.025 and 0.0054, respectively). The severity of acute COVID (adjusted P = 0.023) and the number of pre-existing medical conditions predicted only the cognitive complaint–fatigue predominant phenotype (adjusted P = 0.003), and past suicidal ideas predicted only the symptoms across multiple clusters phenotype (adjusted P < 0.001). Pre-infection vaccination status did not predict either phenotype.

Our findings suggest that we should pursue a phenotype-driven approach with holistic biopsychosocial perspectives in disentangling the heterogeneity under the umbrella of chronic PCNPS. Management of patients complaining of chronic PCNPS should be stratified according to their phenotypes. Clinicians should recognise that depression and anxiety cannot explain all chronic post-COVID cognitive symptoms.

The negative impact of adverse childhood experiences (ACEs) on mental health has been well documented. While most of the evidence comes from samples of adolescents and young adults, few studies have investigated whether ACEs contribute to poorer mental health among older adults. In particular, depressive symptoms are common in old age, and they display heterogeneous patterns of development across individuals. Therefore, it is important to examine if ACEs are predictive of distinct trajectories of depressive symptoms among older adults.

Using longitudinal data from the English Longitudinal Study of Ageing (ELSA), we aimed to examine if ACEs could differentiate between distinct trajectories of depressive symptoms over eight years in community-dwelling older adults.

Participants from ELSA aged 60 or above who reported no psychiatric diagnoses and completed the items of ACEs at baseline (wave 3) were included in the current study. Nine items of ACEs were subject to a principal component analysis to identify the underlying subtypes. Data of depressive symptoms from waves 3 to 7 (2-year apart), assessed with the 8-item Centre for Epidemiological Studies Depression Scale, were extracted for modelling the distinct trajectories using latent class growth analysis. The trajectories were predicted by subtypes of ACEs using multinomial logistic regression, adjusting for childhood socioeconomic status, sex, age and ethnicity.

The final sample consisted of 4057 participants (54.4% female, mean age= 71.34 (SD= 8.14)). We identified five trajectories of depressive symptoms (Figure 1): ‘low stable’ (73.4%), ‘increasing then decreasing’ (9.9%), ‘high decreasing’ (7.1%), ‘high stable’ (5.7%) and ‘moderate increasing’ (4.0%). Four subtypes of ACEs (i.e., sexual abuse, separation from natural parents, family dysfunction and physical assault) were evident. Compared to the ‘low stable’ group, higher levels of family dysfunction were reported in the ‘increasing then decreasing’ (aOR = 1.35, 95% CI [1.10 - 1.66], p = .012), ‘high stable’ (aOR = 1.59, 95% CI [1.30 - 1.96], p < .001) and ‘moderate increasing’ (aOR = 1.55, 95% CI [1.18 - 2.04], p = .011) groups. The ‘high stable’ group also reported a higher level of separation from natural parents than the ‘low stable’ group (aOR = 1.34, 95% CI [1.04 - 1.72], p = .047). Sexual abuse and physical assault did not predict any group differences.

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Distinct trajectories of depressive symptoms among older adults were predicted by family dysfunction in childhood. Our findings suggested that the negative impact of ACEs on mental health may extend beyond adolescence and young adulthood into the old age.

None Declared

The risk of antipsychotic-associated cardiovascular and metabolic events may differ among countries, and limited real-world evidence has been available comparing the corresponding risks among children and young adults. We, therefore, evaluated the risks of cardiovascular and metabolic events in children and young adults receiving antipsychotics.

We conducted a multinational self-controlled case series (SCCS) study and included patients aged 6–30 years old who had both exposure to antipsychotics and study outcomes from four nationwide databases of Taiwan (2004–2012), Korea (2010–2016), Hong Kong (2001–2014) and the UK (1997–2016) that covers a total of approximately 100 million individuals. We investigated three antipsychotics exposure windows (i.e., 90 days pre-exposure, 1–30 days, 30–90 days and 90 + days of exposure). The outcomes were cardiovascular events (stroke, ischaemic heart disease and acute myocardial infarction), or metabolic events (hypertension, type 2 diabetes mellitus and dyslipidaemia).

We included a total of 48 515 individuals in the SCCS analysis. We found an increased risk of metabolic events only in the risk window with more than 90-day exposure, with a pooled IRR of 1.29 (95% CI 1.20–1.38). The pooled IRR was 0.98 (0.90–1.06) for 1–30 days and 0.88 (0.76–1.02) for 31–90 days. We found no association in any exposure window for cardiovascular events. The pooled IRR was 1.86 (0.74–4.64) for 1–30 days, 1.35 (0.74–2.47) for 31–90 days and 1.29 (0.98–1.70) for 90 + days.

Long-term exposure to antipsychotics was associated with an increased risk of metabolic events but did not trigger cardiovascular events in children and young adults.

Alcohol use disorder (AUD) and schizophrenia (SCZ) frequently co-occur, and large-scale genome-wide association studies (GWAS) have identified significant genetic correlations between these disorders.

We used the largest published GWAS for AUD (total cases = 77 822) and SCZ (total cases = 46 827) to identify genetic variants that influence both disorders (with either the same or opposite direction of effect) and those that are disorder specific.

We identified 55 independent genome-wide significant single nucleotide polymorphisms with the same direction of effect on AUD and SCZ, 8 with robust effects in opposite directions, and 98 with disorder-specific effects. We also found evidence for 12 genes whose pleiotropic associations with AUD and SCZ are consistent with mediation via gene expression in the prefrontal cortex. The genetic covariance between AUD and SCZ was concentrated in genomic regions functional in brain tissues (p = 0.001).

Our findings provide further evidence that SCZ shares meaningful genetic overlap with AUD.

This study was designed to apply subcortical analysis of first episode drug naïve major depressive disorder with panic disorder patients.

All the participating subjects received scales rating for depression and panic disorder. 15 patients and 15 healthy controls were compared to explore the differences of subcortical structures, such as hippocampus, putamen and thalamus. A new semi-automatic toolbox for computing subcortical areas by a shape and surface model was utilized for the comparison. The volumes of subcortical structures were also compared by using nonparametric t test of SPSS software to support the findings from the FSL FIRST toolbox (FMRIB Software Library, FMRIB's Integrated Registration and Segmentation Tool).

The patient group had significantly lower volumes in the left hippocampus, thalamus and putamen. The volumetric differences were also significant in these areas (2 tailed p < 0.05; Mann-Whitney U test). The volumes of thalamus and putamen were also well correlated with clinical rating scales. The relationship between left hippocampal volumes and clinical rating scales was modest. The volumes of right hippocampus were not correlated with clinical rating scales.

The structural abnormalities of putamen and thalamus might represent a specific pathology for major depressive disorder co-morbid with panic disorder. The limited deficits of hippocampal volumes should represent an intermediate type between major depressive disorder and panic disorder. The co-morbidity might have a different subcortical pathology.

Menopausal syndrome has been reported to be a worldwide women's mental health problem. Aborigines in rural areas have poorer access to mental health services. Thus, it is important to evaluate such symptoms of female aborigines with different menopausal statuses and their association with depression.

The aim of the study is to evaluate the association between physiological menopausal symptoms and depression during different menopausal period among female Taiwanese aborigines.

A total of 672 Taiwanese aboriginal women, aged 40–60, were recruited in the interviewing study and classified as pre-, peri-, and postmenopausal according to menstrual bleeding patterns in the previous 12 months. Then, the postmenopausal symptoms, depression, self-perceived health, family support, and associated demographic variables were assessed by questionnaire based on the results of interviewing by research assistants.

The results revealed that perimenopausal statuses were associated with depression and women with a perimenopausal status had a higher prevalence of depression than those with a premenopausal status. A higher score on physiological postmenopausal symptoms was found to be significantly associated with depression. Furthermore, somatic symptoms were associated with depression for pre-, peri-, and postmenopausal statuses. Moreover, sexual dysfunction and vasomotor symptoms were associated with depression only in the premenopausal status and postmenopausal status, respectively.

Depression should be routinely evaluated for female Taiwanese aborigines consulting with physicians for menopause symptoms, especially for somatic symptoms. Furthermore, attention should be provided to premenopausal women with sexual dysfunction and postmenopausal women with vasomotor symptoms for depression.

Alcohol consumption is a part of the aboriginal culture. It was found that is a predominant health problem in aboriginal community. There was little research describing whether gender differences in harmful drinking and adverse drinking consequence among aborigines. Thus, it is important to evaluate such differences in order to provide evidence for developing interventions in problem drinking.

The aim of the study is to examine the gender differences in the prevalence, correlates, and adverse drinking consequences among harmful alcohol users in Taiwanese aborigines.

A cross-sectional survey was conducted. 449 study participants, aged 18-60, were recruited into the study from community-dwelling aborigines in southern Taiwan. Alcohol Use Disorders Identification Test (AUDIT) was used to collect information regarding harmful alcohol drinking. Personal characteristics, related risk factors and adverse drinking consequences were assessed by questionnaire.

The result revealed that the prevalence of harmful drinking in male users was 71.6%, female users were 49.2%. The results showed that female harmful alcohol users were more likely to have poor mental health, 58% of them with suicidal ideation, 50% with depression, more inactive in religious practice, and unemployed. It was also found that more than half of the male harmful alcohol users have adverse drinking consequence, including accidental injury, quarreled with others, and unable to work.

Harmful drinking was a predominant health problem in aborigines. This finding suggested that depression and suicidal ideation should be routinely evaluated for female harmful alcohol users by the professional of primary care.

Studies suggest that alcohol consumption and alcohol use disorders have distinct genetic backgrounds.

We examined whether polygenic risk scores (PRS) for consumption and problem subscales of the Alcohol Use Disorders Identification Test (AUDIT-C, AUDIT-P) in the UK Biobank (UKB; N = 121 630) correlate with alcohol outcomes in four independent samples: an ascertained cohort, the Collaborative Study on the Genetics of Alcoholism (COGA; N = 6850), and population-based cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC; N = 5911), Generation Scotland (GS; N = 17 461), and an independent subset of UKB (N = 245 947). Regression models and survival analyses tested whether the PRS were associated with the alcohol-related outcomes.

In COGA, AUDIT-P PRS was associated with alcohol dependence, AUD symptom count, maximum drinks (R2 = 0.47–0.68%, p = 2.0 × 10−8–1.0 × 10−10), and increased likelihood of onset of alcohol dependence (hazard ratio = 1.15, p = 4.7 × 10−8); AUDIT-C PRS was not an independent predictor of any phenotype. In ALSPAC, the AUDIT-C PRS was associated with alcohol dependence (R2 = 0.96%, p = 4.8 × 10−6). In GS, AUDIT-C PRS was a better predictor of weekly alcohol use (R2 = 0.27%, p = 5.5 × 10−11), while AUDIT-P PRS was more associated with problem drinking (R2 = 0.40%, p = 9.0 × 10−7). Lastly, AUDIT-P PRS was associated with ICD-based alcohol-related disorders in the UKB subset (R2 = 0.18%, p < 2.0 × 10−16).

AUDIT-P PRS was associated with a range of alcohol-related phenotypes across population-based and ascertained cohorts, while AUDIT-C PRS showed less utility in the ascertained cohort. We show that AUDIT-P is genetically correlated with both use and misuse and demonstrate the influence of ascertainment schemes on PRS analyses.

• Understand the theoretical background, mechanism of action and clinical applications of fNIRS and compare it to other neuroimaging modalities

• Understand the use of fNIRS in academic and clinical psychiatry through current research findings

• Be able to evaluate the future potential of fNIRS and formulate new ideas for using fNIRS in academic and clinical psychiatry

Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder, yet the search for definite genetic etiologies remains elusive. Delineating ASD endophenotypes can boost the statistical power to identify the genetic etiologies and pathophysiology of ASD. We aimed to test for endophenotypes of neuroanatomy and associated intrinsic functional connectivity (iFC) via contrasting male youth with ASD, their unaffected brothers and typically developing (TD) males.

The 94 participants (aged 9–19 years) – 20 male youth with ASD, 20 unaffected brothers and 54 TD males – received clinical assessments, and undertook structural and resting-state functional magnetic resonance imaging scans. Voxel-based morphometry was performed to obtain regional gray and white matter volumes. A seed-based approach, with seeds defined by the regions demonstrating atypical neuroanatomy shared by youth with ASD and unaffected brothers, was implemented to derive iFC. General linear models were used to compare brain structures and iFC among the three groups. Assessment of familiality was investigated by permutation tests for variance of the within-family pair difference.

We found that atypical gray matter volume in the mid-cingulate cortex was shared between male youth with ASD and their unaffected brothers as compared with TD males. Moreover, reduced iFC between the mid-cingulate cortex and the right inferior frontal gyrus, and increased iFC between the mid-cingulate cortex and bilateral middle occipital gyrus were the shared features of male ASD youth and unaffected brothers.

Atypical neuroanatomy and iFC surrounding the mid-cingulate cortex may be a potential endophenotypic marker for ASD in males.