Accurate diagnosis of bipolar disorder (BPD) is difficult in clinical practice, with an average delay between symptom onset and diagnosis of about 7 years. A depressive episode often precedes the first manic episode, making it difficult to distinguish BPD from unipolar major depressive disorder (MDD).

We use genome-wide association analyses (GWAS) to identify differential genetic factors and to develop predictors based on polygenic risk scores (PRS) that may aid early differential diagnosis.

Based on individual genotypes from case–control cohorts of BPD and MDD shared through the Psychiatric Genomics Consortium, we compile case–case–control cohorts, applying a careful quality control procedure. In a resulting cohort of 51 149 individuals (15 532 BPD patients, 12 920 MDD patients and 22 697 controls), we perform a variety of GWAS and PRS analyses.

Although our GWAS is not well powered to identify genome-wide significant loci, we find significant chip heritability and demonstrate the ability of the resulting PRS to distinguish BPD from MDD, including BPD cases with depressive onset (BPD-D). We replicate our PRS findings in an independent Danish cohort (iPSYCH 2015, N = 25 966). We observe strong genetic correlation between our case–case GWAS and that of case–control BPD.

We find that MDD and BPD, including BPD-D are genetically distinct. Our findings support that controls, MDD and BPD patients primarily lie on a continuum of genetic risk. Future studies with larger and richer samples will likely yield a better understanding of these findings and enable the development of better genetic predictors distinguishing BPD and, importantly, BPD-D from MDD.

In response to the COVID-19 pandemic, we rapidly implemented a plasma coordination center, within two months, to support transfusion for two outpatient randomized controlled trials. The center design was based on an investigational drug services model and a Food and Drug Administration-compliant database to manage blood product inventory and trial safety.

A core investigational team adapted a cloud-based platform to randomize patient assignments and track inventory distribution of control plasma and high-titer COVID-19 convalescent plasma of different blood groups from 29 donor collection centers directly to blood banks serving 26 transfusion sites.

We performed 1,351 transfusions in 16 months. The transparency of the digital inventory at each site was critical to facilitate qualification, randomization, and overnight shipments of blood group-compatible plasma for transfusions into trial participants. While inventory challenges were heightened with COVID-19 convalescent plasma, the cloud-based system, and the flexible approach of the plasma coordination center staff across the blood bank network enabled decentralized procurement and distribution of investigational products to maintain inventory thresholds and overcome local supply chain restraints at the sites.

The rapid creation of a plasma coordination center for outpatient transfusions is infrequent in the academic setting. Distributing more than 3,100 plasma units to blood banks charged with managing investigational inventory across the U.S. in a decentralized manner posed operational and regulatory challenges while providing opportunities for the plasma coordination center to contribute to research of global importance. This program can serve as a template in subsequent public health emergencies.

Cross-sectional studies have identified health risks associated with epigenetic aging. However, it is unclear whether these risks make epigenetic clocks ‘tick faster’ (i.e. accelerate biological aging). The current study examines concurrent and lagged within-person changes of a variety of health risks associated with epigenetic aging.

Individuals from the Great Smoky Mountains Study were followed from age 9 to 35 years. DNA methylation profiles were assessed from blood, at multiple timepoints (i.e. waves) for each individual. Health risks were psychiatric, lifestyle, and adversity factors. Concurrent (N = 539 individuals; 1029 assessments) and lagged (N = 380 individuals; 760 assessments) analyses were used to determine the link between health risks and epigenetic aging.

Concurrent models showed that BMI (r = 0.15, PFDR < 0.01) was significantly correlated to epigenetic aging at the subject-level but not wave-level. Lagged models demonstrated that depressive symptoms (b = 1.67 months per symptom, PFDR = 0.02) in adolescence accelerated epigenetic aging in adulthood, also when models were fully adjusted for BMI, smoking, and cannabis and alcohol use.

Within-persons, changes in health risks were unaccompanied by concurrent changes in epigenetic aging, suggesting that it is unlikely for risks to immediately ‘accelerate’ epigenetic aging. However, time lagged analyses indicated that depressive symptoms in childhood/adolescence predicted epigenetic aging in adulthood. Together, findings suggest that age-related biological embedding of depressive symptoms is not instant but provides prognostic opportunities. Repeated measurements and longer follow-up times are needed to examine stable and dynamic contributions of childhood experiences to epigenetic aging across the lifespan.

Diagnostic criteria for major depressive disorder allow for heterogeneous symptom profiles but genetic analysis of major depressive symptoms has the potential to identify clinical and etiological subtypes. There are several challenges to integrating symptom data from genetically informative cohorts, such as sample size differences between clinical and community cohorts and various patterns of missing data.

We conducted genome-wide association studies of major depressive symptoms in three cohorts that were enriched for participants with a diagnosis of depression (Psychiatric Genomics Consortium, Australian Genetics of Depression Study, Generation Scotland) and three community cohorts who were not recruited on the basis of diagnosis (Avon Longitudinal Study of Parents and Children, Estonian Biobank, and UK Biobank). We fit a series of confirmatory factor models with factors that accounted for how symptom data was sampled and then compared alternative models with different symptom factors.

The best fitting model had a distinct factor for Appetite/Weight symptoms and an additional measurement factor that accounted for the skip-structure in community cohorts (use of Depression and Anhedonia as gating symptoms).

The results show the importance of assessing the directionality of symptoms (such as hypersomnia versus insomnia) and of accounting for study and measurement design when meta-analyzing genetic association data.

Auditory verbal hallucinations (AVHs) in schizophrenia have been suggested to arise from failure of corollary discharge mechanisms to correctly predict and suppress self-initiated inner speech. However, it is unclear whether such dysfunction is related to motor preparation of inner speech during which sensorimotor predictions are formed. The contingent negative variation (CNV) is a slow-going negative event-related potential that occurs prior to executing an action. A recent meta-analysis has revealed a large effect for CNV blunting in schizophrenia. Given that inner speech, similar to overt speech, has been shown to be preceded by a CNV, the present study tested the notion that AVHs are associated with inner speech-specific motor preparation deficits.

The present study aimed to provide a useful framework for directly testing the long-held idea that AVHs may be related to inner speech-specific CNV blunting in patients with schizophrenia. This may hold promise for a reliable biomarker of AVHs.

Hallucinating (n=52) and non-hallucinating (n=45) patients with schizophrenia, along with matched healthy controls (n=42), participated in a novel electroencephalographic (EEG) paradigm. In the Active condition, they were asked to imagine a single phoneme at a cue moment while, precisely at the same time, being presented with an auditory probe. In the Passive condition, they were asked to passively listen to the auditory probes. The amplitude of the CNV preceding the production of inner speech was examined.

Healthy controls showed a larger CNV amplitude (p = .002, d = .50) in the Active compared to the Passive condition, replicating previous results of a CNV preceding inner speech. However, both patient groups did not show a difference between the two conditions (p > .05). Importantly, a repeated measure ANOVA revealed a significant interaction effect (p = .007, ηp2 = .05). Follow-up contrasts showed that healthy controls exhibited a larger CNV amplitude in the Active condition than both the hallucinating (p = .013, d = .52) and non-hallucinating patients (p < .001, d = .88). No difference was found between the two patient groups (p = .320, d = .20).

The results indicated that motor preparation of inner speech in schizophrenia was disrupted. While the production of inner speech resulted in a larger CNV than passive listening in healthy controls, which was indicative of the involvement of motor planning, patients exhibited markedly blunted motor preparatory activity to inner speech. This may reflect dysfunction in the formation of corollary discharges. Interestingly, the deficits did not differ between hallucinating and non-hallucinating patients. Future work is needed to elucidate the specificity of inner speech-specific motor preparation deficits with AVHs. Overall, this study provides evidence in support of atypical inner speech monitoring in schizophrenia.

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The Korean Basketball League(KBL) holds an annual draft to allow teams to select new players, mostly graduates from the elite college basketball teams even though some are from high school teams. In sports games, many factors might influence the success of an athlete. In addition to possessing excellent physical and technical factors, success in a sports game is also influenced by remarkable psychological factors. Several studies reported that elite sports players can control their anxiety during competition, which may lead to better performance. In particular, the temperament and characteristics of players have been regarded as crucial determinants of the player’s performance and goal. In this regard, numerous studies suggest that personality is considered to be an important predictor of long-term success in professional sports

Based on previous reports and studies, we hypothesized that physical status, temperament and characteristics, and neurocognitive functions of basketball players could predict the result of KBL draft selection. Especially, temperament and characteristics were associated with the result of KBL selection. The basketball performances including average scores and average rebound were associated with emotional perception and mental rotation.

We recruited the number of 44 college elite basketball players(KBL selection, n=17; Non-KBL selection, n=27), and the number of 35 age-matched healthy comparison subjects who major in sports education in college. All participants were assessed with the Temperament and Character Inventory(TCI), Sports Anxiety Scales(SAS), Beck Depression Inventory(BDI), Perceived Stress Scale (PSS-10), Trail Making Test(TMT), and Computerized Neuro-cognitive Test(CNT) for Emotional Perception and Mental Rotation.

Current results showed that physical status, temperament and characteristics, and Neurocognitive functions of college basketball players could predict the KBL draft selection. Among temperament and characteristics, novelty seeking and reward dependence were associated with KBL draft selection. The basketball performances including average scores and average rebound were associated with emotional perception and mental rotation.

In order to be a good basketball player for a long time, it was confirmed that temperamental factors and Neurocognitive factors were very closely related. Furthermore, it is also judged that these results can be used as basic data to predict potential professional basketball players.

None Declared

Older age is associated with an increase in altruistic behaviors such as charitable giving. However, few studies have investigated the cognitive correlates of financial altruism in older adults. This study investigated the cognitive correlates of financial altruism measured using an altruistic choice paradigm in a community-based sample of older adults.

In the present study, a sample of older adults (N = 67; M age = 69.21, SD = 11.23; M education years = 15.97, SD = 2.51; 58.2% female; 71.6% Non-Hispanic White) completed a comprehensive neuropsychological assessment and an altruistic choice paradigm in which they made decisions about allocating money between themselves and an anonymous person.

In multiple linear regression analyses that controlled for age, education, and sex, financial altruism was negatively associated with performance on cognitive measures typically sensitive to early Alzheimer’s Disease. These included CVLT-II Short Delay Free Recall (Beta=-0.26, p=0.03); CVLT-II Long Delay Cued Recall (Beta=-0.32, p=0.04), Craft Story 21 Delayed Recall (Beta=-0.32, p=0.01), and Animal Fluency (Beta=-0.27, p=0.02). Findings held when responses were grouped according to how much was given (Gave Equally, Gave More, Gave Less) for word list memory and story memory measures.

Findings of this study point to a negative relationship between financial altruism and cognitive functioning in older adults on measures known to be sensitive to Alzheimer’s Disease (AD). Findings also point to a potential link between financial exploitation risk and AD in older age.

In recent years, rates of alcohol consumption and alcohol use disorder have steadily increased among adults age 60 and older. Large studies have demonstrated that moderate-to-heavy alcohol consumption (>7 drinks per week) is a risk factor for developing various types of dementias. The effects of alcohol-related problems on cognition are less clear, and are particularly understudied in older adults. Similarly, while there is an established link between worse cognition and financial exploitation vulnerability in older adults, no studies have examined relationships between alcohol-related problems and financial exploitation in this population. The current study therefore explores whether alcohol-related problems are associated with neuropsychological performance and financial exploitation vulnerability in a sample of older adults.

Participants were a community sample of cognitively unimpaired adults over the age of 50 (N = 55, Age M(SD) = 69.1(6.2), 74.5% female, Years of education M(SD) = 16.8(2.3)). Interested individuals were excluded if they reported current or past substance use disorders. Participants completed a laboratory visit that included a neuropsychological assessment. Measures included the NIH Cognition toolbox, CVLT-II, Digit Span, Trails A/B, Benson Complex Figure Recall, and Verbal Fluency: Phonemic and Semantic, from the Alzheimer’s Disease Centers’ Uniform Data Set (UDS) version 3. Participants completed the CAGE Alcohol Abuse Screening Tool and the Short Michigan Alcohol Screener Test - Geriatric Version (SMAST) to assess alcohol-related problems. Both measures are used as clinical screening tools to measure likelihood of a substance use disorder and produce a summary score (0-4 for CAGE, 010 for SMAST) tabulating symptoms of alcohol-related problems. Participants also completed the Perceived Financial Vulnerability Scale (PFVS) to assess financial exploitation vulnerability. As a significant number of participants reported no drinking and therefore no alcohol-related problems, negative binomial regressions were used to test associations between neuropsychological measures, financial exploitation vulnerability, and alcohol-related problems.

After covarying for age and sex, SMAST was negatively associated with NIH toolbox total cognition (B(SE) = -.14(.07), p<.05) and marginally negatively associated with fluid cognition (B(SE) = -.07(.04), p=.06). Neither SMAST nor CAGE scores were significantly associated with performance on any other neuropsychological test (ps = .13-.99). SMAST was positively associated with financial exploitation vulnerability (B(SE) = .31(.16), p = .05); this effect remained significant after covarying for NIH total composite score in a secondary analysis.

In a community sample of cognitively unimpaired, low-drinking adults over the age of 50, more alcohol-related problems were associated with worse NIH toolbox cognition scores. Similarly, more alcohol-related problems were associated with greater financial exploitation vulnerability, and this relationship was not driven by worse cognition. These results suggest that even low amounts of drinking and alcohol-related problems may be associated with cognition and financial exploitation vulnerability in cognitively unimpaired older adults. This study also corroborates the use of the SMAST over the CAGE in older adult populations that may be more sensitive to cognitive changes.

Prior work suggests financial exploitation vulnerability may be an early behavioral manifestation of Alzheimer’s disease (AD). Brain morphometric measures of the parahippocampal gyrus and entorhinal cortex have been shown to be sensitive to early AD progression. We hypothesized that perceived financial exploitation vulnerability may be associated with morphometric measures of the parahippocampal gyrus and entorhinal cortex in cognitively unimpaired older adults. We secondarily investigated the association of morphometric measures with neuropsychological measures.

The sample consisted of 39 cognitively unimpaired older adults (mean age = 68.74 ± 6.43, mean education = 16.87 ± 2.35, 77% female). Cognitive impairment was screened using the telephone version of the Montreal Cognitive Assessment (MoCA) and the cut-off was 21 for study participation. Perceived financial exploitation vulnerability was characterized using a 6-item self-report measure derived from the contextual items of the Lichtenberg Financial Rating Scale. Neuropsychological measures included the CVLT-II Long Delay Free Recall (verbal memory), Benson Complex Figure Recall (visual memory), and Verbal Fluency: Phonemic Test from the Alzheimer’s Disease Centers’ Uniform Data Set (UDS) version 3. Brain images were collected on a 7 Tesla Siemens Magnetom with the following parameters: TE=2.95ms, TR=2200ms, 240 sagittal slices, acquired voxel size (avs)=0.7mm x 0.7mm x 0.7mm. Structural brain images were processed using FreeSurfer version 7.2.0. Cortical thickness and volume measures were generated using the Killiany/Desikian parcellation atlas. Regions were averaged across hemispheres to obtain a single value for each region. Volume measures were adjusted for intracranial volume. Bivariate analyses were conducted to assess relationships between each outcome variable and potential confounders (age, sex, and education). Linear regression models were adjusted for any covariates significantly associated with the outcome variable (none for perceived financial exploitation vulnerability; sex and age for verbal memory; education for visual memory; sex for verbal fluency).

Smaller entorhinal cortex volume (β = -1275.14, SE = 582.79, p < 0.05) and lower parahippocampal gyrus thickness (β = -3.37, SE = 1.57, p < 0.05) were significantly associated with greater perceived financial exploitation vulnerability. Lower entorhinal cortex thickness was marginally associated with greater perceived financial exploitation vulnerability (β = -2.03, SE = 1.11, p = 0.08). Higher parahippocampal gyrus thickness was associated with better verbal fluency (β = 17.66, SE = 7.01, p < 0.05). Higher entorhinal cortex thickness was associated with better visual memory (β = 4.71, SE = 1.73, p < 0.05). No significant associations were observed between structural brain measures and verbal memory.

These results suggest smaller entorhinal cortex volume and lower parahippocampal gyrus thickness are associated with higher perceived financial exploitation vulnerability in cognitively normal older adults. Additionally, parahippocampal gyrus thickness appears to be associated with verbal fluency abilities while entorhinal cortex thickness appears to be associated with visual memory. Taken together, these findings lend support to the notion that financial exploitation vulnerability may serve as an early behavioral manifestation of preclinical AD. Longitudinal studies are needed to better understand the temporal nature of these relationships.

We investigate if covariation between parental and child attention-deficit hyperactivity disorder (ADHD) behaviors can be explained by environmental and/or genetic transmission.

We employed a large children-of-twins-and-siblings sample (N = 22 276 parents and 11 566 8-year-old children) of the Norwegian Mother, Father and Child Cohort Study. This enabled us to disentangle intergenerational influences via parental genes and parental behaviors (i.e. genetic and environmental transmission, respectively). Fathers reported on their own symptoms and mothers on their own and their child's symptoms.

Child ADHD behaviors correlated with their mother's (0.24) and father's (0.10) ADHD behaviors. These correlations were largely due to additive genetic transmission. Variation in children's ADHD behaviors was explained by genetic factors active in both generations (11%) and genetic factors specific to the children (46%), giving a total heritability of 57%. There were small effects of parental ADHD behaviors (2% environmental transmission) and gene–environment correlation (3%). The remaining variability in ADHD behaviors was due to individual-specific environmental factors.

The intergenerational resemblance of ADHD behaviors is primarily due to genetic transmission, with little evidence for parental ADHD behaviors causing children's ADHD behaviors. This contradicts theories proposing environmental explanations of intergenerational transmission of ADHD, such as parenting theories or psychological life-history theory.

Body dysmorphic disorder (BDD) is defined in DSM5 as a preoccupation with one or more perceived defects or flaws in physical appearance causing significant distress or impairment in social and occupational functioning. Despite many studies on mental health disorders related to BDD, the diagnosis is still frequently overlooked.

Previous studies have examined the general personality characteristics of BDD. The objective of this study is to find out how socially aversive personality traits are related.

Total of 86 mentally and physically healthy adults participated. BDD was assessed by BDDE-SR, and aversive personality was assessed by Short Dark Triad (SD3: Machiavellianism, narcissism, psychopathy), Assessment of Sadistic Personality (ASP), and paranoid (PAR), borderline (BOR), and antisocial (ANT) features of the clinical subscales of Personality Assessment Inventory(PAI). Correlations between the reported scores were investigated using Pearson’s and regression was performed on relevant scales.

Thirty seven males and 49 females (mean age 23.8 years) showed no statistically significant difference in total BDDE-SR was reported based on sex(p=0.18) or BMI(underweight, normal, overweight, p=0.236). BDDE-SR, SD3 and ASP were not statistically correlated, but all of the subscales of PAR(PAR-H, PAR-P, PAR-R), BOR(BOR-A, BOR-I, BOR-N, BOR-S) and ANT(ANT-A, ANT-E, ANT-S) were associated with BDDE-SR. Regression results demonstrated in Table 1 show that BOR-I and PAR-R predict BDDE-SR. Correlation of BOR-I and PAR-R with BDDE-SR factors was shown in Table 2.Table 1.Hierarchical multiple linear regression analysis for BOR-I, PAR-R in predicting BDD symptoms

This study shows that BDD symptoms are associated with borderline-identity problems and paranoia-resentment and suggests that we should consider the diagnosis of BDD for individuals with high BOR and PAR scores.

None Declared