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There is accumulating evidence of the neurological and neuropsychiatric features of infection with SARS-CoV-2. In this systematic review and meta-analysis, we aimed to describe the characteristics of the early literature and estimate point prevalences for neurological and neuropsychiatric manifestations.We searched MEDLINE, Embase, PsycINFO and CINAHL up to 18 July 2020 for randomised controlled trials, cohort studies, case-control studies, cross-sectional studies and case series. Studies reporting prevalences of neurological or neuropsychiatric symptoms were synthesised into meta-analyses to estimate pooled prevalence.13 292 records were screened by at least two authors to identify 215 included studies, of which there were 37 cohort studies, 15 case-control studies, 80 cross-sectional studies and 83 case series from 30 countries. 147 studies were included in the meta-analysis. The symptoms with the highest prevalence were anosmia (43.1% (95% CI 35.2% to 51.3%), n=15 975, 63 studies), weakness (40.0% (95% CI 27.9% to 53.5%), n=221, 3 studies), fatigue (37.8% (95% CI 31.6% to 44.4%), n=21 101, 67 studies), dysgeusia (37.2% (95% CI 29.8% to 45.3%), n=13 686, 52 studies), myalgia (25.1% (95% CI 19.8% to 31.3%), n=66 268, 76 studies), depression (23.0% (95% CI 11.8% to 40.2%), n=43 128, 10 studies), headache (20.7% (95% CI 16.1% to 26.1%), n=64 613, 84 studies), anxiety (15.9% (5.6% to 37.7%), n=42 566, 9 studies) and altered mental status (8.2% (95% CI 4.4% to 14.8%), n=49 326, 19 studies). Heterogeneity for most clinical manifestations was high.Neurological and neuropsychiatric symptoms of COVID-19 in the pandemic’s early phase are varied and common. The neurological and psychiatric academic communities should develop systems to facilitate high-quality methodologies, including more rapid examination of the longitudinal course of neuropsychiatric complications of newly emerging diseases and their relationship to neuroimaging and inflammatory biomarkers.

\"Dr. Hellerstein, a psychiatrist at Columbia University's College of Physicians and Surgeons, puts this new form of psychiatry to the test. Depression and anxiety disorders damage the brain, but as Dr. Hellerstein explains, the right treatment can change the patterns of brain activity, brain cell connections, and even the brain's anatomy. To illustrate, he relates the stories of people as they travel through various phases of New Neuropsychiatry treatment, from evaluation to therapy to remission, and illustrates how this approach can help you progress through each phase as well\"--Bk. jacket.

Aim: This study aims to identify and describe prevalence rates for ASD in the Scandinavian countries (Denmark, Norway, Sweden), as well as the Nordic countries (Finland, Iceland, the Faroe Islands, and Greenland). Methods: A systematic review was conducted following PRISMA (2009) guidelines and based on the two databases: APA PsycINFO and MEDLINE (PubMed). Results: A total of 13 studies were included in the analyses. It was not possible to identify ASD prevalence studies for Greenland. However, for the remaining countries descriptive increases in ASD prevalence figures were observed. Increases were evident both in relation to age and birth cohort. Studies varied regarding which age group and cohort prevalence figures were reported. The most reported age group was the 7-12-year-olds. In this group, recent prevalence figures for Denmark ranged from 0.26% to 1.47%, in Norway 0.6%, in Sweden 0.23-0.68%, in Finland 0.22-0.86%, and in Iceland 2.40-3.13%. Iceland stood out in terms of higher prevalence figures compared to the other Scandinavian and Nordic countries. Two studies from the Faroe Islands reported ASD prevalence rates between 0.50% and 0.94% for 7-24-year-olds. These studies were based on nationwide figures, but not from national or official registers. Discussion and conclusion: This study documented increasing prevalence of ASD in Scandinavian and Nordic countries. Several explanations of aspects that may contribute to the increases were discussed, eg, heightened awareness of ASD and earlier diagnosis. The importance of considering differences in data sources was discussed, with an emphasis on the importance of using national registries when available as this source is the most reliable and valid. The absence of prevalence figures for Greenland may be attributed to structural as well as cultural aspects, eg, two parallel systems assessing ASD, cultural taboos as well as lack of awareness of ASD. Suggestions or how to gain knowledge on ASD prevalence in Greenland is presented. Keywords: autism spectrum disorder, prevalence, Scandinavia, Nordic

From its first depictions in ancient medical literature to contemporary depictions in brain imaging, mania has been largely associated with its Greek roots, \"to rage.\" Prior to the nineteenth century, \"mania\" was used interchangeably with \"madness.\" Although its meanings shifted over time, the word remained layered with the type of madness first-century writers described: rage, fury, frenzy. Even now, the mental illness we know as bipolar disorder describes conditions of extreme irritability, inflated grandiosity, and excessive impulsivity.Spanning several centuries,Manic Mindstraces the multiple ways in which the word \"mania\" has been used by popular, medical, and academic writers. It reveals why the rhetorical history of the word is key to appreciating descriptions and meanings of the \"manic\" episode.\" Lisa M. Hermsen examines the way medical professionals analyzed the manic condition during the nineteenth and twentieth centuries and offers the first in-depth analysis of contemporary manic autobiographies: bipolar figures who have written from within the illness itself.

Major depressive disorder (MDD) affects more than 280 million people worldwide and is one of the leading contributors to disability, premature mortality, and overall disease burden. Nearly 60% of individuals who die by suicide have an MDD diagnosis, underscoring its profound impact on both individuals and society. MDD arises from a complex interplay of genetic vulnerability, life experiences, and molecular alterations. Among these, epigenetic mechanisms have received particular attention because they help explain how environmental stress—especially chronic stress—can produce enduring biological changes. MicroRNAs (miRNAs) represent a key class of epigenetic regulators. These small, noncoding RNAs influence the efficiency with which target genes are translated into protein, thereby exerting potent post-transcriptional control over gene expression. Approximately 70% of known miRNAs are expressed in the brain, where they shape neuronal development, synaptic plasticity, and stress responsivity. Dysregulation of miRNA expression can disrupt coordinated gene networks and has been repeatedly associated with impairments in neurogenesis, neurotransmission, neuroinflammation, and endocrine signaling—processes central to the pathophysiology of MDD and other stress-related psychiatric conditions. Within this broader landscape, miR-425 has emerged as a particularly relevant epigenetic regulator across several brain disorders. Alterations in miR-425 expression have been reported in individuals with stress-related conditions and in animal models of chronic stress exposure. Emerging evidence suggests that miR-425 modulates several mood-relevant pathways, including regulation of the hypothalamic–pituitary–adrenal (HPA) axis, neuronal cell death, inflammatory signaling, and antidepressant treatment response as well as key signaling networks such as MAPK and Wnt. Given its regulatory role and disease-associated expression changes, miR-425 has gained significant interest as both a biomarker and a potential therapeutic target. In this review, we examine its biogenesis, molecular targets, and translational importance, positioning miR-425 as a promising candidate for psychiatric intervention strategies. A substantial knowledge gap remains and needs further study. For example, the functions of miR-425 within specific cell types and neural circuits are less defined, and most available evidence derives from rodent studies. Also, the support for miR-425 as a biomarker needs large, standardized, multisite, longitudinal studies integrating neuroimaging, proteomics, and detailed clinical phenotyping. In addition, we are only beginning to understand how pharmacologic and lifestyle interventions influence miR-425 expression. Finally, key downstream targets of miR-425 and safe, cell–type–specific delivery approaches for miR-425–based therapeutics remain underdeveloped. Collectively, these gaps underscore the need for rigorous, multimodal, translational research to determine the potential of miR-425 as both a biomarker and a target for novel treatments. Major depressive disorder affects hundreds of millions of individuals worldwide and represents a leading cause of disability and suicide. Its development reflects a complex interplay among genetic vulnerability, environmental stressors, and dysregulated gene expression. One key mechanism underlying this dysregulation involves microRNAs (miRNAs), small noncoding RNAs that regulate gene expression in the brain. Many miRNAs are enriched in neural circuits governing mood, stress reactivity, and emotional regulation. Altered microRNA expression can disrupt neuronal communication, inflammatory signaling, and stress-response pathways. Emerging evidence identifies miR-425 as a critical regulator of these processes, highlighting its potential as a biomarker and therapeutic target in depression.

De novo and inherited rare genetic disorders (RGDs) are a major cause of human morbidity, frequently involving neuropsychiatric symptoms. Recent advances in genomic technologies and data sharing have revolutionized the identification and diagnosis of RGDs, presenting an opportunity to elucidate the mechanisms underlying neuropsychiatric disorders by investigating the pathophysiology of high-penetrance genetic risk factors. Here we seek out the best path forward for achieving these goals. We think future research will require consistent approaches across multiple RGDs and developmental stages, involving both the characterization of shared neuropsychiatric dimensions in humans and the identification of neurobiological commonalities in model systems. A coordinated and concerted effort across patients, families, researchers, clinicians and institutions, including rapid and broad sharing of data, is now needed to translate these discoveries into urgently needed therapies. Rare genetic diseases frequently involve a neuropsychiatric component for which a defined framework of investigation will expedite our understanding for these diseases as a whole.