Journal of psychiatry and brain science最新文献

Digital health interventions are exploding in today's medical practice and have tremendous potential to support the treatment of substance use disorders (SUD). Developers and healthcare providers alike must be cognizant of the potential for digital interventions to exacerbate existing inequities in SUD treatment, particularly as they relate to Social Determinants of Health (SDoH). To explore this evolving area of study, this manuscript will review the existing concepts of the digital divide and digital inequities, and the role SDoH play as drivers of digital inequities. We will then explore how the data used and modeling strategies can create bias in digital health tools for SUD. Finally, we will discuss potential solutions and future directions to bridge these gaps including smartphone ownership, Wi-Fi access, digital literacy, and mitigation of historical, algorithmic, and measurement bias. Thoughtful design of digital interventions is quintessential to reduce the risk of bias, decrease the digital divide, and create equitable health outcomes for individuals with SUD.

The aging population of the world is increasing at an unprecedented rate which is expected to lead to a corresponding unparalleled increase in age related diseases. Of particular concern are the large number of older adults expected to develop Alzheimer's disease (AD), which will require extraordinary local, national and worldwide healthcare resources. In this context, innovative interventions are needed urgently to delay AD onset and thereby give our healthcare systems time to prepare and provide meaningful care to our aging populations. This focused review discusses the crucial role of frontal gamma oscillations as a therapeutic target to delay or ameliorate cognitive decline in AD. Frontal gamma oscillations, including from prefrontal cortical areas, serve as a biomarker for working memory and other cognitive functions, and their impairment is observed before clinical symptoms manifest. This review evaluates evidence from animal models and human subjects to highlight the correlation between gamma wave abnormalities and cognitive deterioration. Furthermore, the review summarizes 11 clinical studies using neuromodulation techniques designed to stimulate gamma oscillations in mild cognitive impairment (MCI) and AD patients, including transcranial electrical stimulation, transcranial magnetic stimulation, and rhythmic sensory stimulation. These interventions have shown promise in mitigating early-stage cognitive decline, as evidenced by improved performance on memory tests, increased gamma oscillatory responses, and some have even shown reduced brain atrophy. These early studies suggest that treatments that strengthen frontal gamma oscillatory responses through neuromodulation are a promising approach to delay cognitive decline, that may serve as an adjunct to other therapies or as a standalone treatment in some populations.

Perinatal mood and anxiety disorders (PMAD), which include depression and/or anxiety in the year before and/or after delivery, are common complications of pregnancy, affecting up to one in four perinatal individuals, with costs of over $15 billion per year in the US. In this paper, we provide an overview of the disparities in utilization and delivery outcomes for individuals with perinatal mood and anxiety disorders in the US. In addition, we discuss the current US screening and treatment guidelines as well as the high societal costs of illness of PMAD for both perinatal individuals and children. Finally, we outline opportunities for quality improvement of PMAD care in the US, including leveraging increased engagement with healthcare system during prenatal care, working toward a more cohesive national strategy to address PMAD, leaning into evidence-based policymaking through collaboration with a panel of experts, and generating state-level profiles focused on PMAD.

It is important to consider reciprocal associations between maternal and offspring mental health problems during early childhood. Existing interventions often focus narrowly on either adult or child mental health, missing the opportunity for holistic care. We describe the rationale and development of a pilot randomized clinical trial that explores their integration, combining an evidence-based parenting intervention with depression treatment to improve both maternal and child outcomes. Our approach is part of a growing field of two-generation interventions that offer a promising approach to enhance mental health support for caregivers and their young children.

Background: Non-suicidal self-injury (NSSI) is a highly prevalent clinical concern in adolescents and is associated with impaired functioning and suicide risk. The BRIDGES (BRain Imaging Development of Girls' Emotion and Self) study was designed to collect longitudinal clinical and neurobiological data to advance our understanding of NSSI in adolescents. The purpose of this paper is to describe the clinical data collected as part of this study, including psychiatric diagnoses, depression symptoms, episodes of non-suicidal self-injury, suicidal thoughts and behaviors, childhood trauma, and personality domains.

Methods: The baseline sample included 164 adolescents aged 12-16 assigned female at birth (Mean age = 14.97, SD = 1.20) with NSSI histories ranging from none to severe. Participants and their parent/guardian were invited to provide data at three time points spaced approximately one year apart. Descriptive analyses were conducted to provide estimates of rates and trajectories of clinical data.

Results: Of the 164 study participants, 75.61% and 57.93% completed the second and third time points, respectively. Visual inspection of the data suggests an overall trend of decreasing severity of psychopathology over time, and adolescents with a history of NSSI appeared to have higher rates of psychopathology than those without.

Conclusions: This paper describes longitudinal clinical trajectories in adolescents with a range of NSSI histories and presents readers with an overview of the rich, publicly available dataset that we hope will inspire future research to advance the understanding of the neurodevelopmental trajectories associated with NSSI, depression, and suicide risk.

Background: Despite the effectiveness and growing availability of treatment for opioid use disorder (OUD) with buprenorphine, many people with OUD do not access treatment services. This article describes the rationale, methodological design, evolution, and progress of an ongoing clinical trial of treatment linkage strategies for people with untreated OUD.

Methods: The study, titled Opioid Use Disorder Treatment Linkage at Strategic Touchpoints using Buprenorphine (OUTLAST-B), uses "strategic touchpoints", initially sexual health clinics and subsequently broadened to other service venues and participant social networks, for recruitment and screening. Adults with untreated OUD (target N = 360) are randomized to one of the three arms: Usual Care (UC, enhanced with overdose education and naloxone distribution), Patient Navigation (PN), or Patient Navigation with an immediate short-term bridge prescription for buprenorphine (PN + BUP). In the PN and PN + BUP arms, the Patient Navigator works with participants for 2 months to facilitate treatment entry and early retention, resolve barriers (e.g., ID cards, transportation), and provide motivational support.

Results: The primary outcome is OUD treatment entry within 30 days of enrollment. Participants are assessed at baseline and followed at 3- and 6-months post-enrollment on measures of healthcare utilization, substance use, and general functioning. Challenges and recruitment adaptations pursuant to the COVID-19 pandemic are discussed.

Conclusions: This study could provide insights on how to reach people with untreated OUD and link them to care through non-traditional routes.

Trial registration: The study is registered at ClinicalTrials.gov (NCT04991974).

High titers of anti-NMDAR1 IgG autoantibodies were found in the brains of patients with anti-NMDAR1 encephalitis that exhibits psychosis, impaired memory, and many other psychiatric symptoms in addition to neurological symptoms. Low titers of blood circulating anti-NMDAR1 IgG autoantibodies are sufficient to robustly impair spatial working memory in mice with intact blood-brain barriers (BBB). On the other hand, anti-NMDAR1 autoantibodies were reported to protect against neuronal excitotoxicity caused by excessive glutamate in neurological diseases. Activation of extrasynaptic NMDARs is responsible for neuronal excitotoxicity, whereas activation of synaptic NMDARs within the synaptic cleft is pro-survival and essential for NMDAR-mediated neurotransmission. Unlike small IgG, IgM antibodies are large and pentameric (diameter of ~30 nm). It is plausible that IgM anti-NMDAR1 autoantibodies may be restricted to bind extrasynaptic NMDARs and thereby specifically inhibit neuronal excitotoxicity, but physically too large to enter the synaptic cleft (width: 20-30 nm) to suppress synaptic NMDAR-mediated neurotransmission in modulation of cognitive function and neuronal pro-survival signaling. Hence, blood circulating anti-NMDAR1 IgM autoantibodies are both neuroprotective and pro-cognitive, whereas blood circulating anti-NMDAR1 IgG and IgA autoantibodies are detrimental to cognitive function. Investigation of anti-NMDAR1 IgM autoantibodies may open up a new avenue for the development of long-lasting preventive and therapeutic IgM anti-NMDAR1 autoantibodies that protect from neuronal excitotoxicity in many neurological diseases and psychiatric disorders.