Neurodevelopmental disorders, including autism spectrum disorder, result from complex interactions between genetic susceptibility and early-life environmental exposures that shape brain development. Their increasing prevalence represents a major public health challenge, highlighting the need for effective preventive strategies. This brief narrative review synthesizes current evidence on the converging etiopathogenetic pathways—including genetic vulnerability, environmental risk factors, epigenetic regulation, neuroinflammation, and gut microbiome alterations—that operate during the first 1000 days of life and collectively influence neurodevelopmental trajectories. We also discuss early prevention opportunities targeting modifiable risk factors during this critical developmental window, when heightened neuroplasticity may maximize the effectiveness of preventive interventions. Viewing autism spectrum disorder and related neurodevelopmental disorders through the lens of shared biological mechanisms, provides a framework for precision prevention, facilitates earlier identification of at-risk individuals, and supports the development of multidisciplinary strategies aimed at improving lifelong neurodevelopmental health and reducing the long-term burden on affected individuals, families, and healthcare systems.
After gambling disorder (GD) was included as the first behavioral addiction in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5), many studies focused on epidemiology and the impact of different risk factors. In this context, online gambling seems to show especially high addictive potential and, additionally, lacks government control and restrictions. In this study, we aimed to evaluate the prevalence of GD, as well as various aspects of gambling behavior in a representative Austrian sample (N = 3658). An adapted version of a standardized questionnaire was applied, which covered all nine DSM-5 criteria for GD. Results indicate a lifetime prevalence for gambling of 34.9
Psychoses are among the most debilitating mental disorders, making early detection a major public health priority. In extension of the ultra-high-risk (UHR) approach, which was developed to identify an imminent risk of psychosis, the basic symptom (BS) approach aims for the earliest possible detection of the developing disorder; it is increasingly used worldwide. Basic symptoms are subtle, self-perceived disturbances affecting various domains, such as cognition, perception, affect, and drive, that precede and scaffold the development of attenuated and frank psychotic symptoms. This narrative review outlines historical foundations, phenomenology, and assessment instruments for BSs. It summarizes empirical findings on their predictive value for subsequent psychosis and their specificity for psychotic disorders across all age groups. Furthermore, developmental aspects and neurobiological findings are highlighted that support one of the core assumptions of the BS concept, namely, that BSs represent the most immediate phenomenological manifestation of the cerebral alterations underlying the development of psychosis. Finally, evidence for the broader clinical significance of BSs beyond psychosis prediction is discussed, indicating that BSs as a whole are useful for both multi- and differential-diagnostic purposes. Overall, the reviewed findings underline the value of BSs for advancing neurobiological research on the etiopathology of psychoses and for developing individualized prediction models and targeted early interventions.
Major depressive disorder (MDD) is a heterogeneous, debilitating disorder. A distinct subgroup within the MDD spectrum is identified to have treatment-resistant depression (TRD). There is an impetus to find alternative treatments for TRD to reduce disease burden and improve quality of life. Psychedelics have been used in the treatment of various psychiatric disorders since the 1950s, with potential benefits in TRD. Aiming to summarize the evidence of using psychedelics for TRD by exploring mechanisms and potential benefits, we conducted a literature search on different psychedelics with their mechanisms from clinical and preclinical evidence. Psychedelics have been examined in many preclinical studies for efficacy and mechanisms with fewer clinical studies on patients with TRD. Besides serotonergic agonism, glutamate surge and monoamine release, psychedelics promote neuroplasticity, corticolimbic function, and epigenetic changes. Psilocybin, ketamine, and esketamine are the most researched agents of psychedelics in the context of TRD. Psilocybin-assisted therapy has been shown to induce short-term improvement in symptoms that can persist for weeks and months, with some meta-analyses consolidating such findings. Ketamine, as an atypical psychedelic, in many clinical trials of intravenous, subcutaneous, and oral forms, had rapid and robust effects in reducing depressive symptoms and relapses without decreasing cognitive function. Similarly, esketamine induced early and clinically meaningful improvements in function and productivity. Ayahuasca also showed fast and sustained effects with higher remission rates and good safety. Psychedelics have significant potential in TRD with superior mechanisms over traditional antidepressants. Despite the encouraging findings of the existing studies, large, well-designed studies are needed to extend their use as part of standard recommendations.
