View clinical trials related to Anhedonia.
Filter by:Study of individualized accurate targeting rTMS intervention on motivational anhedonia of treatment resistant depression and brain network mechanism
Anhedonia and abnormalities in reward behavior are core features of overweight/obesity (OW), a highly prevalent condition within MDD populations, and is independently associated with reward disturbances. The investigators therefore aim to investigate the brain substrates subserving reward and motivation in adults with overweight/obesity. The primary aim of this pilot study is to determine whether associations exist between obesity and decreased performance on the respective motivation/reward paradigms.
The overarching aim of the study is to determine the role of insulin signaling on the neurobiological substrates subserving anhedonia within individuals with mood disorders (i.e., Bipolar Disorder (BD) and Major Depressive Disorder (MDD)). Specific aims include: 1. Molecular: Assessment of components of the insulin cascade, as well as of anhedonia and reward-related processes, using a proteomics and gene expression approach; 2. Physiology: Measurement of peripheral sensitivity to insulin and metabolic correlates, including body mass index and dyslipidemia; 3. Neural Circuits: Evaluation of the insulin sensitivity of prefrontal (e.g. prefrontal cortex) and striatal (e.g. nucleus accumbens, ventral tegmental area) networks in the resting-state and during an effort-based decision making test, using acutely administered intranasal insulin and functional magnetic resonance imaging (fMRI); 4. Behavioral: Measurement of willingness to make effort for rewards, as well as of other components of reward response and anhedonia, using validated behavioral tasks and clinical scales (e.g. Snaith-Hamilton Pleasure Scale - SHPS). This initiative represents a proof-of-concept study that insulin is important to anhedonia, neurocognitive functioning, and behavioural deficits in MDD, representing a novel and safe therapeutic avenue.
The proposed research addresses a major mental health issue (anhedonia) with a novel computationally-inspired translational technique in both humans and mice. This approach greatly increases the likelihood that a positive animal model result will be successfully translated to humans. This research plan thus offers a novel way to address the NIMH's mission of defining mechanisms of complex behaviors.
Compelling evidence indicates inflammation plays a role in depression, but potential mechanisms linking inflammation to depression, such as dysregulated reward processing, are poorly understood. This study comprehensively evaluates effects of inflammation on reward across dimensions (e.g., anticipating versus receiving a reward) and types (e.g., money vs. smiling faces) in younger and older women. Characterizing how inflammation shapes the dynamic and multidimensional reward system, and how this may differ by age, may give insight into risk factors for depression and help identify critical points for intervention.
Anhedonia is a symptom dimension that characterizes many individuals suffering from depression, as well as some types of anxiety, psychosis, and substance use. For the most part, treatments are effective in decreasing negative affect but ineffective in improving anhedonia, with some antidepressant medications even worsening symptoms of anhedonia. Yet anhedonia is a significant marker of poor prognosis as well as suicidal ideation and actual suicide. The development of effective treatments for anhedonia is thus of paramount importance. Advances in neuroscience indicate specific targets that may underlie anhedonia that can be shifted through behavioral training. The investigators have developed such a program and found it to be effective in raising positive affect, especially for depressed or anxious individuals with anhedonia at baseline. To date, this program has been implemented by highly trained clinicians, which have supervised its implementation on a large scale. Moreover, the behavior program is dependent on readily available rewarding experiences, which anhedonia obviously challenges. Furthermore, mechanistic evaluation is impeded by intra¬- and inter-¬individual variability in exposure to rewarding stimuli. Virtual Reality (VR) offsets these barriers by repeated controlled immersion in experiences designed to enhance approach motivation, initial responsiveness to reward attainment, and reward learning. In this current study, the investigators aim to measure clinical outcomes using Virtual Reality-Reward Training (VR-RT).
The effects of the seaweed extract were evaluated on the animal model equivalent of depression compared with a control group treated with the carrier (spring water) and a reference group treated with Imipramine and showed significative effect. This clinical trial was intended to confirm in humans the potential efficacy identified in animals. The primary objective was to compare against a placebo the effect of Ulva L.L extract in healthy volunteers whose anhedonia was characterized by a component of depression.
Rumination is significantly frequent in major depressive disorder. However, not a lot of studies have investigated the effects of repetitive transcranial magnetic stimulation on rumination and its electrophysiological correlates. This study recruited 61 participants who were randomly assigned to sham, bilateral, or unilateral stimulation groups to investigate the potential differences between these stimulation protocols and changes in the behavioral and electrophysiological outcomes after treatment.
The purpose of this study is to establish the dose-response curve for therapeutic doses of d-amphetamine on tasks of motivation and reward learning in the same participants and to use d-amphetamine as a dopaminergic probe to test newer theories about the role of dopamine in reward-related decision-making.
The purpose of the study is to determine whether motivation/reward deficits observed in schizophrenia are attenuated and whether cognitive impairment associated with schizophrenia is improved by add-on TAK-041 administration to antipsychotics in participants with stable schizophrenia.