Active clinical trials for "Bipolar Disorder"

Early identification in individuals with bipolar disorder who are at risk for AUDs could inform novel intervention strategies and improve life-long outcomes. The primary objective of this protocol is to use alcohol administration procedures and alcohol biosensor technology to investigate responses to alcohol, compared to placebo, and relationship with parental risk for alcohol use disorders and/or bipolar disorder in young adults. Baseline clinical, cognitive, and behavioral assessments will be completed in 100 young adults (21-26 years; 50% women, no history of AUDs>mild). Participants would be equally divided among those with parental history of bipolar disorder but not AUDs, parental history of bipolar disorder and AUDs, parental history of AUDs but not bipolar disorder, and typically developing age- and sex-matched controls with no parental history of mood disorders or AUDs (N=25 per group). Then, while wearing Secure Continuous Remote Alcohol Monitoring [SCRAM] sensors, participants will complete within-person, counter-balanced, beverage sessions (following standard beverage administration procedures) in a simulated bar laboratory. Changes in heart rate, body sway and subjective self-report measurements of intoxication will also be completed while under the influence of alcohol or placebo. Specifically, individual differences in transdermal alcohol concentration (the primary data output from SCRAM sensors), physiological changes (e.g. heart rate), and the experience of stimulating, sedative, and anxiolytic effects of alcohol (measured with self-report surveys) will be investigated and differences between parental risk subgroups and healthy comparison participants investigated. Differences in transdermal alcohol concentration collected while under the influence of alcohol will be the primary data outcome assessed. Changes in heart rate, body sway, and experience of stimulating, sedative, and anxiolytic effects (from self-report survey data) while under the influence of alcohol compared to placebo session will also be investigated. Additionally, associations between objective and subjective responses to alcohol and drinking patterns will be explored (secondary outcome). The primary endpoint of the study will be after completion of both alcohol and placebo beverage conditions.

Cognitive Behavioral Therapy (CBT) is treatment of choice for insomnia. Many patients in psychiatric care have sleep problems including insomnia, but are rarely given the choice to participate in CBT to improve their sleep. Patients with Bipolar disorder is a patient group with high levels of sleep difficulties. Sleep problems in this patient group can be both more general such as insomnia, but can also be related to the Bipolar disorder. Other research groups have studied the use of behaviorally sleep treatments in patients with Bipolar disorder, but more studies are needed. In a previous pilot study, the investigators of the current study developed a CBT protocol that would target sleep problems in this population. The basis was CBT for insomnia (CBT-i), but with more emphasis on achieving sleep promoting behaviors specific to Bipolar patients, for instance techniques that would also alleviate sleep phase problems, (e.g. the systematic use of light and darkness), and techniques to target more general sleep related problems (e.g. difficulties waking up in the morning), that are also common in patients with Bipolar disorder. This treatment was well tolerated and gave moderate effects on insomnia severity in the pilot study. In a naturalistic randomized controlled trial, the investigators now evaluate the effects of this psychological treatment on sleep and Bipolar symptoms in patients at the departments of Affective disorders, Northern Stockholm Psychiatry and Southwest Psychiatry, Stockholm, Sweden.

Severe mental illness (SMI) refers to the most burdensome psychiatric conditions. The need to pre-empt the onset of SMI is pressing because once SMI develops, quality of life is poor and available treatments have limited efficacy. Most risk factors for SMI are either unchangeable (e.g., genetics) or difficult to alter (e.g., low socio-economic status). In contrast, cannabis use is one specific risk factor that could be avoided. Certain individuals are more vulnerable to the harmful effects of cannabis. Genetic factors can help us identify these high-risk individuals. One in three individuals are carriers of a higher-risk genetic variant, and cannabis users with this genotype are at up to 7-fold increased risk of developing schizophrenia. In our study, genetic counselling will be provided to participants by a board-certified genetic counsellor. During the genetic counselling session, participants will have the option to receive their genotype. Participants will be counselled regarding their individualized risk of developing and of not developing SMI based on family history, whether or not they choose to use cannabis, and genotype (if the participants accept the genetic test results). The investigators hypothesize that this intervention will reduce exposure to cannabis compared to the youth who are not offered the intervention.

The overall aim of this program of research is to improve the continuity of care for patients with serious mental illness (SMI) by supporting a safer and more efficient bridge from hospital to outpatient care using a mobile device-delivered app called Transition-FOCUS (tFOCUS), which has previously been tested in community samples. The purpose of the proposed project is to establish the effectiveness of our empirically-supported, multi-component mHealth intervention.

Major Depression is often resistant to treatment, and all of the currently marketed anti-depressants can cause significant side effects and may precipitate mania. The aim of this proposal is to perform a proof-of-concept RCT testing Palmitoylethanolamide (PEA) as a treatment for unipolar or bipolar depression, randomizing 100 patients to 6-week treatment with PEA 1200 mg/d or matching placebo. There are several rationales for this study: (A) PEA acts at the peroxisome proliferator-activated receptor-alpha (PPAR-α), stimulating Allo biosynthesis. Allo is an endogenous, positive allosteric modulator of GABA-A receptors in glutamatergic neurons, including cortical and hippocampal pyramidal glutamatergic neurons and may be one of the endogenous regulators of depression and anxiety. (B) Sage Therapeutics has developed Allo which is FDA approved to treat post-partum depression, and is testing a molecular modification which can be administered orally for post-partum depression and unipolar depression, with mixed efficacy results. Pregnenolone, a precursor of neurosteroids, has also been reported to improve bipolar depression. Based on animal models, PEA increases Allo synthesis in areas of the brain thought to be involved in anxiety and depression. It may also favor the biosynthesis of sulfated forms of Allo and congeners that inhibit tonic rather than phasic NMDA-mediated excitatory neurotransmission. Showing that PEA-induced selective inhibition of tonic NMDA neurotransmission improves depression might enable development of steroid-based NMDA-inhibitor therapeutics. In addition, PEA-induced Allo upregulation potentiates GABA-A receptor-mediated inhibition. The NMDA and the GABAergic mechanisms may act in concert to improve behavioral outcomes. Since PEA increases Allo in the brain where it is endogenously formed, it might be more effective compared with exogenous administration, which is not site specific. There is evidence of a role of inflammation in depression; PEA has potent immunoregulatory and anti-inflammatory effects by directly activating PPAR-α, which has a protective role against neuroinflammation by inhibiting the signaling mediated by toll-like receptor 4.There is one published study which shows that PEA has an antidepressant effect in unipolar depression, 58 patients were randomized to receive 1200 mg/d of PEA or placebo added-on to citalopram, showing clinical improvements in patients receiving PEA.

The primary objective of this grant is to develop and evaluate an Artificial Intelligence-based clinical training tool--CBTpro--to support high-quality skills training in CBT for psychosis (CBTp). CBTpro will provide a rapid means of scaling and sustaining high-quality CBTp in routine care settings across the US.

The purpose of this study is to determine if taking a probiotic supplement versus a placebo will reduce relapse and improve the clinical course among participants who have been hospitalized for bipolar depression.

The purpose of this study is to test the hypothesis that the anti-depressant and anti-suicidal effects of the N-methyl-D-aspartate receptor (NMDAR) antagonist Ketamine is critically dependent on stimulation of Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid receptors (AMPAR).

This study examines the feasibility and acceptability of a virtual tumor board for cancer and mental illness for patients with serious mental illness and a new cancer diagnosis. The study also examines the impact on patient care, psychiatric symptoms, and clinician self-efficacy in managing this population.

Wide ranging cognitive deficits are major drivers of functional decline and poor outcomes in people with schizophrenia (SZ) and bipolar disorder (BD). Medications do not target pathophysiological mechanisms thought to underlie these deficits. In the search for interventions targeting underlying cognitive impairment in SZ and BD, we look comprehensively beyond just the brain and to the potential role of dysfunctional systemic metabolism. Disrupted insulin and glucose metabolism are seen in medication-naïve first-episode SZ, suggesting that SZ itself, and not just the medications used to treat it, is associated with risk of Type 2 diabetes, cardiovascular morbidity and mortality, and more generally, accelerated aging. Even young people with SZ have increased risk of metabolic disease and cognitive deficits. Sadly, their life span is shortened by 15-20 years. BD is associated with similar but less severe disruptions in glucose and insulin metabolism and life expectancy. Although the human brain is 2% of the body's volume, it consumes over 20% of its energy, and accordingly, the brain is particularly vulnerable to the dysregulation of glucose metabolism seen in SZ and BD. While glucose is considered to be the brain's default fuel, ketones provide 27% more free energy and are a major source of energy for the brain. Ketones prevent or improve various age-associated diseases, and a ketogenic diet (70% fat, 20% protein, 10% carbohydrates) has been posited as an anti-aging and dementia antidote. The premise of the work is based on recent evidence that ketogenic diets improve dynamic neural network instability, related to cognitive deficits, aging, and Type 2 diabetes (Mujica-Parodi et al., Proc Natl Acad Sci U S A. 2020;117(11):6170-7.). The rigor of the work rests on findings of (1) poor cerebral glucose homeostasis in SZ and BD, (2) neural network instability in SZ and BD, and (3) direct effects of ketosis on network instability. Unknown is whether ketogenic diets can improve network instability in people with SZ and BD.