Adolescent cannabis use has been consistently posited to contribute to the onset and progression of psychosis. However, alternative causal models may account for observed associations between cannabis use and psychosis risk, including shared vulnerability for both cannabis use and psychosis or efforts to self-medicate distress from psychosis spectrum symptomology.

Prolonged grief disorder (PGD) is included as a new diagnosis in international classification systems. Treatments following a cognitive behavioral model are most effective, but comparisons with active control treatments are scarce.

Brain translocator protein 18k Da (TSPO) binding, a putative marker of neuroinflammatory processes (eg, gliosis), is associated with stress and elevated in depressed and suicidal populations. However, it is unclear whether neuroinflammation moderates the impact of daily life stress on suicidal ideation and negative affect, thereby increasing risk for suicidal behavior.

Synaptic dysfunction is involved in schizophrenia pathophysiology. However, whether in vivo synaptic density is reduced in early stages of psychosis, including its high-risk states, remains unclear.

Interest in and use of hallucinogens has been increasing rapidly. While a frequently raised concern is that hallucinogens may be associated with an increased risk of psychosis, there are limited data on this association.

Preliminary studies suggest that glucagon-like peptide-1 receptor (GLP-1) agonists, used to treat type 2 diabetes and obesity, may decrease alcohol consumption.

Exposure to war is associated with poor mental health outcomes. Adverse and traumatic experiences can lead to long-lasting DNA methylation changes, potentially mediating the link between adversity and mental health. To date, limited studies have investigated the impact of war on DNA methylation in children or adolescents, hampering our understanding of the biological impact of war exposure.

The field of public mental health is evolving to tackle the profound impact of global challenges such as climate change, migration, and health crises. These issues accentuate health and social inequities, necessitating a focus on how to achieve interventions that are equitable and enhance mental health across all societal strata.

While adverse childhood experiences (ACEs) are known to impart significant risk for negative mental health and cognitive outcomes in youth, translation of ACE scores into clinical intervention is limited by poor specificity in predicting negative outcomes. This work expands on the ACE framework using a data-driven approach to identify 8 different forms of traumatic and adverse childhood experiences (TRACEs) and reveal their differential associations with psychiatric risk and cognition across development.

Depression is a leading contributor to mental health burdens globally and in India, the world's most populous country. National-level evidence on health coverage for adults with depression in India is lacking.

Cognitive functioning is associated with various factors, such as age, sex, education, and childhood adversity, and is impaired in people with psychosis. In addition to specific effects of the disorder, cognitive impairments may reflect a greater exposure to general risk factors for poor cognition.

Cognitive deficits are a substantial part of the symptoms of schizophrenia spectrum disorders (SSDs) and contribute heavily to the burden of disease. Antipsychotic drugs are not cognitive enhancers, but due to their different receptor-binding profiles, they could differ in their effects on cognition. No previous network meta-analysis compared antipsychotics to placebo, which is important to determine whether use of these drugs is associated with cognitive performance in SSDs at all.

In the neurotypical brain, regions develop in coordinated patterns, providing a fundamental scaffold for brain function and behavior. Whether altered patterns contribute to clinical profiles in neurodevelopmental conditions, including autism, remains unclear.

Older adults with major depressive disorder (MDD) or mild cognitive impairment (MCI) are at high risk for cognitive decline.

Male postpartum depression is prevalent across populations; however, there is limited evidence on strategies to address it, particularly in low-income settings.

Leveraging real-world clinical biobanks to investigate the associations between genetic and environmental risk factors for mental illness may help direct clinical screening efforts and evaluate the portability of polygenic scores across environmental contexts.