Anxiety disorders are a leading source of human misery, morbidity, and premature mortality. Existing treatments are far from curative for many, underscoring the need to clarify the underlying neural mechanisms. Although many brain regions contribute, the amygdala has received the most intense scientific attention. Over the past several decades, this scrutiny has yielded a detailed understanding of amygdala function, but it has failed to produce new clinical assays, biomarkers, or cures. Rising to this urgent public health challenge demands an honest reckoning with the functional-neuroanatomical complexity of the amygdala and a shift from theories anchored on "the amygdala" to models centered on specific amygdala nuclei and cell types. This review begins by examining evidence from studies of rodents, monkeys, and humans for the "canonical model," the idea that the amygdala plays a central role in fear- and anxiety-related states, traits, and disorders. Next, the authors selectively highlight work indicating that the canonical model, while true, is overly simplistic and fails to adequately capture the actual state of the evidentiary record, the breadth of amygdala-associated functions and illnesses, or the complexity of the amygdala's functional architecture. The authors describe the implications of these facts for basic and clinical neuroimaging research. The review concludes with some general recommendations for grappling with the complexity of the amygdala and accelerating efforts to understand and more effectively treat amygdala-related psychopathology.

Homelessness is a serious and increasing public health concern. Childhood maltreatment and psychiatric problems have been associated with homelessness as risk factors; however, reliance on cross-sectional studies introduces ambiguity into interpreting previous findings. This study seeks to understand whether psychiatric symptoms in part explain the relationship between childhood maltreatment and homelessness.

Posttraumatic stress disorder (PTSD) is a highly prevalent psychiatric disorder that can become chronic and debilitating when left untreated. The most commonly recommended first-line treatments for PTSD among adults are individual trauma-focused psychotherapies. Other evidence-based treatments include specific antidepressant medications and non-trauma-focused psychotherapies. Despite the effectiveness of these available treatments, many patients' symptoms do not remit. This has led to the search for novel treatments for PTSD. In this review, the authors critically evaluate the data supporting several emerging pharmacological and other somatic interventions in the categories of medication-assisted psychotherapy, novel medication monotherapy strategies, and neuromodulation, selected because of the salience of their mechanisms of action to the pathophysiology of PTSD (e.g., MDMA-assisted psychotherapy, ketamine, cannabidiol, transcranial magnetic stimulation). The authors also evaluate the evidence for treatments that are the focus of increasing scientific or public interest (i.e., hyperbaric oxygen therapy, stellate ganglion block, neurofeedback). To date, the evidence supporting most novel pharmacological and somatic treatments for PTSD is preliminary and highly variable; however, the data for several specific treatments, such as transcranial magnetic stimulation, are encouraging.

Discrimination exposure has a detrimental impact on mental health, increasing the risk of depression, anxiety, and posttraumatic stress. The impact discrimination exposure has on mental health is likely mediated by neural processes associated with emotion expression and regulation. However, the specific neural processes that mediate the relationship between discrimination exposure and mental health remain to be determined. The present study investigated the relationship adolescent discrimination exposure has with stress-elicited brain activity and mental health symptoms in young adulthood.

Theories of amygdala function are central to our understanding of psychiatric and neurodevelopmental disorders. However, limited knowledge of the molecular and cellular composition of the amygdala impedes translational research aimed at developing new treatments and interventions. The aim of this study was to characterize and compare the composition of amygdala cells to help bridge the gap between preclinical models and human psychiatric and neurodevelopmental disorders.

The authors examined racial/ethnic and socioeconomic disparities in receiving treatment for alcohol use disorder (AUD).

Midbrain dopamine function plays a key role in translational models of substance use disorders. Whether midbrain dopamine function is associated with substance use frequency and severity or reward function in 20-24 year-olds remains a critical gap in knowledge. The authors collected neuromelanin-sensitive magnetic resonance imaging (NM-MRI), a validated index of lifetime dopamine function in the substantia nigra/ventral tegmentum area (SN-VTA) complex, to characterize altered dopamine function.

Substance use disorder (SUD) is common in psychiatric patients and has a negative impact on health and well-being. However, SUD often goes untreated, and there is a need for psychiatrists, of all specialties, to address this pervasive clinical problem. In this review, the authors' goal is to provide a resource that describes treatments for SUD, using neuroscience as a framework. They discuss the effect of pharmacotherapy on craving, intoxication, and withdrawal and its ability to interrupt the cycle of substance use in SUD. The neuroscience of stress is reviewed, including medications targeting neurotransmitter systems activated by alarm and fear. Neuroplasticity and promising treatments that use this mechanism, including ketamine, psilocybin, and transcranial magnetic stimulation (TMS), are discussed. The authors conclude by listing resources and practice guidelines for physicians interested in learning more about treatments for SUD.

Increasingly large samples in genome-wide association studies (GWASs) for alcohol use behaviors (AUBs) have led to an influx of implicated genes, yet the clinical and functional understanding of these associations remains low, in part because most GWASs do not account for the complex and varied manifestations of AUBs. This study applied a multidimensional framework to investigate the latent genetic structure underlying heterogeneous dimensions of AUBs.

This exploratory analysis sought to determine whether decreases in cannabis use are associated with improvements in cannabis-related problems and functional outcomes, and if so, what percentage decrease is associated with improvement.

Conceptual similarities between depressive and negative symptoms complicate biomarker and intervention development. This study employed a data-driven approach to delineate the neural circuitry underlying depressive and negative symptoms in schizophrenia spectrum disorders (SSDs).