Pubertal development variations have consequences for adolescent internalizing problems, which likely continue into adulthood. Key questions concern the extent of these links between pubertal timing and adult symptoms, as well as the underlying mechanisms.

Longitudinal data were available for 475 female and 404 male participants. Pubertal timing was indicated by age at mid-puberty for both groups and age at menarche for female participants (both assessed continuously). Adult self-reported outcomes of recent and lifetime depression and anxiety were predicted from pubertal timing, also controlling for adolescent (then childhood) internalizing problems. Emerging adulthood self-esteem, body dissatisfaction, education level, and age at sexual initiation were examined as mediators of the pubertal timing-adult internalizing link. Multilevel models tested hypotheses.

Pubertal timing had persisting and sex-dependent psychological associations. Specifically, in female, but not male, adults, early puberty was associated with all adult internalizing outcomes, and for past year and lifetime depression symptoms, even after controlling for adolescent internalizing problems. Pubertal timing links with past-year depression symptoms were mediated by age at sexual initiation, while all other persisting pubertal timing links with adult symptoms were mediated by body dissatisfaction. Most findings concerning depression held when childhood internalizing problems were also a covariate.

Leveraging data spanning four developmental periods, findings highlight the associations between pubertal variations and adult internalizing symptoms by revealing underlying sex-dependent behavioral pathways. Only for female participants did pubertal timing affect depression and anxiety in established adulthood, with body dissatisfaction and age at sexual initiation as unique developmental mechanisms.

Social anhedonia, indicating reduced pleasure from social interaction, is heightened in autistic youth and associated with increased internalizing symptoms transdiagnostically. The stability of social anhedonia over time and its longitudinal impact on internalizing symptoms in autism have never been examined.

Participants were 276 autistic children (Mage = 8.60, SDage = 1.65; 211 male) with IQ ≥ 60 (MIQ = 96.74, SDIQ = 18.19). Autism severity was measured using the Autism Diagnostic Observation Schedule, Second Edition. Caregivers completed the Child and Adolescent Symptom Inventory, Fifth Edition (CASI-5) at baseline, 6 weeks, and 6 months. The CASI-5 includes a social anhedonia subscale derived from relevant items across domains. ICC (Intraclass Correlation Coefficient) analysis assessed stability, while cross-lagged panel models examined associations among social anhedonia, depression, and social anxiety across time.

At baseline, social anhedonia correlated with autism severity, as well as parent-reported social anxiety and depression. Social anhedonia showed relative stability (ICC = 0.763) over 6 months, with a significant decline between baseline and 6 weeks (β = −0.52, p < .001). Cross-lagged models revealed a bidirectional relationship between social anhedonia and depression over time, while social anxiety displayed concurrent, but not predictive, associations across time.

Social anhedonia demonstrated stability over 6 months, suggesting that it may be a relatively stable characteristic in autistic children. Concurrent relationships were observed between social anhedonia and depression, as well as social anxiety and attention-deficit/hyperactivity disorder. Only depression demonstrated a bidirectional longitudinal association with social anhedonia. This bidirectional relationship aligns with developmental models linking early negative social experiences to subsequent internalizing symptoms in autistic children, underscoring the clinical significance of social anhedonia assessment in this population.

The cumulative effects of long-term exposure to pandemic-related stressors and the severity of social restrictions may have been important determinants of mental distress in the time of COVID-19.

This study aimed to investigate mental health among a cohort of Chinese university students over a 28-month period, focusing on the effects of lockdown type.

Depression, anxiety, stress and fear of COVID-19 infection were measured ten times among 188 Chinese students (females 77.7%, meanage = 19.8, s.d.age = 0.97), every 3 months: from prior to the emergence of COVID-19 in November 2019 (T1) to March 2022 (T10).

Initially depression, anxiety and stress dipped from T1 to T2, followed by a sudden increase at T3 and a slow upward rise over the remainder of the study period (T3 to T10). When locked down at university, participants showed greater mental distress compared with both home lockdown (d = 0.35–0.48) and a no-lockdown comparison period (d = 0.28–0.40). Conversely, home lockdown was associated with less anxiety and stress (d = 0.19 and 0.21, respectively), but not with depression (d = 0.13) compared with a no-lockdown period.

This study highlights the cumulative effects of exposure to COVID-19 stressors over time. It also suggests that the way in which a lockdown is carried out can impact the well-being of those involved. Some forms of lockdown appear to pose a greater threat to mental health than others.

Previous findings in psychosis have revealed mixed findings on glutamate (Glu) levels in the dorsal anterior cingulate cortex (dACC). Factors such as illness chronicity, methodology, and medication status have impeded a more nuanced evaluation of Glu in psychosis. The goal of this longitudinal neuroimaging study was to investigate the role of antipsychotics on Glu in the dACC in antipsychotic-naïve first-episode psychosis (FEP) patients.

We enrolled 117 healthy controls (HCs) and 113 antipsychotic-naïve FEP patients for this study. 3T proton magnetic resonance spectroscopy (1H-MRS; PRESS; TE = 80 ms) data from a voxel prescribed in the dACC were collected from all participants at baseline, 6, and 16 weeks following antipsychotic treatment. Glutamate levels were quantified using the QUEST algorithm and analyzed longitudinally using linear mixed-effects models.

We found that baseline dACC glutamate levels in FEP were not significantly different than those of HCs. Examining Glu levels in FEP revealed a decrease in Glu levels after 16 weeks of antipsychotic treatment; this effect was weaker in HC. Finally, baseline Glu levels were associated with decreases in positive symptomology.

We report a progressive decrease of Glu levels over a period of 16 weeks after initiation of treatment and a baseline Glu level association with a reduction in positive symptomology, suggestive of a potential mechanism of antipsychotic drug (APD) action. Overall, these findings suggest that APDs can influence Glu within a period of 16 weeks, which has been deemed as an optimal window for symptom alleviation using APDs.

Genetically informative twin studies have consistently found that individual differences in anxiety and depression symptoms are stable and primarily attributable to time-invariant genetic influences, with non-shared environmental influences accounting for transient effects.

We explored the etiology of psychological and somatic distress in 2279 Australian twins assessed up to six times between ages 12–35. We evaluated autoregressive, latent growth, dual-change, common, and independent pathway models to identify which, if any, best describes the observed longitudinal covariance and accounts for genetic and environmental influences over time.

An autoregression model best explained both psychological and somatic distress. Familial aggregation was entirely explained by additive genetic influences, which were largely stable from ages 12 to 35. However, small but significant age-dependent genetic influences were observed at ages 20–27 and 32–35 for psychological distress and at ages 16–19 and 24–27 for somatic distress. In contrast, environmental influences were predominantly transient and age-specific.

The longitudinal trajectory of psychological distress from ages 12 to 35 can thus be largely explained by forward transmission of a stable additive genetic influence, alongside smaller age-specific genetic innovations. This study addresses the limitation of previous research by exhaustively exploring alternative theoretical explanations for the observed patterns in distress symptoms over time, providing a more comprehensive understanding of the genetic and environmental factors influencing psychological and somatic distress across this age range.

Recent stressful life events (SLEs) are an established risk factor for a range of psychiatric disorders. Animal studies have shown evidence of gray matter (GM) reductions associated with stress, and previous work has found similar associations in humans. However longitudinal studies investigating the association between stress and changes in brain structure are limited.

The current study uses longitudinal data from the UK Biobank and comprises 4,543 participants with structural neuroimaging and recent SLE data (mean age = 61.5 years). We analyzed the association between recent SLEs and changes in brain structure, determined using the longitudinal FreeSurfer pipeline, focusing on total GM volume and five a priori brain regions: the hippocampus, amygdala, anterior cingulate cortex, orbitofrontal cortex, and insula. We also examined if depression and childhood adversity moderated the relationship between SLEs and brain structure.

Individuals who had experienced recent SLEs exhibited a slower rate of hippocampal decrease over time compared to individuals who did not report any SLEs. Individuals with depression exhibited smaller GM volumes when exposed to recent SLEs. There was no effect of childhood adversity on the relationship between SLEs and brain structure.

Our findings suggest recent SLEs are not directly associated with an accelerated decline in brain volumes in a population sample of older adults, but instead may alter brain structure via affective disorder psychopathology. Further work is needed to investigate the effects of stress in younger populations who may be more vulnerable to stress-induced changes, and may yet pinpoint brain regions linked to stress-related disorders.

Neuropsychiatric symptoms (NPS) are considered diagnostic and prognostic indicators of dementia and are attributable to neurodegenerative processes. Little is known about the prognostic value of early NPS on executive functioning (EF) decline in Alzheimer’s disease and related dementias (ADRD). We examined whether baseline NPS predicted the rate of executive function (EF) decline among older adults with ADRD.

Older adults (n = 1625) with cognitive impairment were selected from the National Alzheimer’s Coordinating Center database. EF was estimated with a latent factor indicated by scores on Number Span Backward, Letter Fluency, and Trail Making-Part B. A curve of factors (CUFF) latent growth curve model was estimated to examine rate of change over four years. Baseline NPS severity was entered as a predictor in the model to examine its influence on the rate of change in EF over time.

The CUFF models exhibited good fit. EF significantly declined over four waves (slope = −.16, p < .001). Initial visit NPS severity predicted decline in EF (slope = .013, p < .001), such that those with greater baseline NPS severity demonstrated a more rapid decline in EF performance over time. Presence of 2 NPS significantly predicted EF decline, and those with medium total NPS severity (NPS score of 2–4) at baseline exhibited a sharper decline in EF.

Findings underscore the importance of targeting NPS early across ADRD syndromes to minimize EF decline, offering novel insights into how early NPS treatment may alter cognitive trajectories. We provide an innovative, user-friendly web-based application that may be helpful for personalized treatment planning.

Prior studies suggest that childhood maltreatment is associated with altered hippocampal volume. However, longitudinal studies are currently scarce, making it difficult to determine how alterations in hippocampal volume evolve over time. The current study examined the relationship between childhood maltreatment and hippocampal volumetric development across childhood and adolescence in a community sample.

In this longitudinal study, a community sample of 795 participants underwent brain magnetic resonance imaging (MRI) in three waves spanning ages 6–21 years. Childhood maltreatment was assessed using parent-report and children´s self-report at baseline (6–12 years old). Mixed models were used to examine the relationship between childhood maltreatment and hippocampal volume across time.

The quadratic term of age was significantly associated with both right and left hippocampal volume development. High exposure to childhood maltreatment was associated with reduced offset of right hippocampal volume and persistent reduced volume throughout adolescence.

Critically, the relationship between childhood maltreatment and reduced right hippocampal volume remained significant after adjusting for the presence of any depressive disorder during late childhood and adolescence and hippocampal volume polygenic risk scores. Time-by-CM and Sex-by-CM interactions were not statistically significant.

The present study showed that childhood maltreatment is associated with persistent reduction of hippocampal volume in children and adolescents, even after adjusting for the presence of major depressive disorder and genetic determinants of hippocampal structure.

Research examining (MCI) criteria in diverse and/or health-disparate populations is limited. There is a critical need to investigate the predictive validity for incident dementia of widely used MCI definitions in diverse populations.

Eligible participants were non-Hispanic White or Black Bronx community residents, free of dementia at enrollment, with at least one annual follow-up visit after baseline. Participants completed annual neurological and neuropsychological evaluations to determine cognitive status. Dementia was defined based on DSM-IV criteria using case conferences. Cox proportional hazard models assessed predictive validity for incident dementia of four specific MCI definitions (Petersen, Jak/Bondi, number of impaired tests, Global Clinical Ratings) at baseline, controlling for age, sex, education, and race/ethnicity. Time-dependent sensitivity and specificity at 2–7 years for each definition, and Youden’s index were calculated as accuracy measures.

Participants (N = 1073) ranged in age from 70 to 100 (mean = 78.4 ± 5.3) years at baseline. The sample was 62.5% female, and educational achievement averaged 13.9 ± 3.5 years. Most participants identified as White (70.0%), though Black participants were well-represented (30.0%). In general, MCI definitions differed in sensitivity and specificity for incident dementia. However, there were no significant differences in Youden’s index for any definition, across all years of follow-up.

This work provides an important step toward improving the generalizability of the MCI diagnosis to underrepresented/health-disparate populations. While our findings suggest the studied MCI classifications are comparable, researchers and clinicians may choose to consider one method over another depending on the rationale for evaluation or question of interest.