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anhedonia/inflamație

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Patients with chronic neuropathic pain (CNP) have a higher incidence to develop depression. However, its pathogenesis has not yet been fully elucidated. Here we aimed to investigate the role of inflammatory cytokines in CNP-related anhedonia, which is a core symptom of depression, and

Systemic N-terminal fragments of adrenocorticotropin reduce inflammation- and stress-induced anhedonia in rats.

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Emerging evidence implicates impaired self-regulation of the hypothalamic-pituitary-adrenal (HPA) axis and inflammation as important and closely related components of the pathophysiology of major depression. Antidepressants show anti-inflammatory effects and are suggested to enhance glucocorticoid

Anhedonia in cocaine use disorder is associated with inflammatory gene expression.

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Treatments for Cocaine Use Disorder (CUD) are variably effective, and there are no FDA-approved medications. One approach to developing new treatments for CUD may be to investigate and target poor prognostic signs. One such sign is anhedonia (i.e. a loss of pleasure or interest in non-drug rewards),

Anhedonia in irritable bowel syndrome and in inflammatory bowel diseases and its relationship with abdominal pain.

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Anhedonia is the lowered ability to experience pleasure from rewarding or enjoyable activities and is considered a symptom of depression. Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are frequently accompanied by psychiatric disorders such as depression. However,

Inflammation-induced anhedonia: endotoxin reduces ventral striatum responses to reward.

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BACKGROUND Although inflammatory activity is known to play a role in depression, no work has examined whether experimentally induced systemic inflammation alters neural activity that is associated with anhedonia, a key diagnostic symptom of depression. To investigate this, we examined the effect of

The effect of the antipsychotic drug quetiapine and its metabolite norquetiapine on acute inflammation, memory and anhedonia.

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The atypical antipsychotic drug, quetiapine, has recently been suggested to not only show efficacy in schizophrenia, bipolar, major depressive and general anxiety disorders, but to also have a possible anti-inflammatory effect, which could be important in the treatment of the inflammatory aspects of

Anhedonia as a clinical correlate of inflammation in adolescents across psychiatric conditions.

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OBJECTIVE Peripheral inflammation has been associated with multiple psychiatric disorders, particularly with depression. However, findings remain inconsistent and unreproducible, most likely due to the disorder's heterogeneity in phenotypic presentation. Therefore, in the present study, in an effort

Mapping inflammation onto mood: Inflammatory mediators of anhedonia.

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Evidence supports inflammatory involvement in mood and cognitive symptoms across psychiatric, neurological and medical disorders; however, inflammation is not a sensitive or specific characteristic of these diagnoses. The National Institute of Mental Health Research Domain Criteria (RDoC) ask for a

Inflammation, reward circuitry and symptoms of anhedonia and PTSD in trauma-exposed women.

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Trauma exposure is associated with increased inflammatory biomarkers (e.g. C-reactive protein [CRP] and cytokines), and inflammation has been shown to impact corticostriatal reward circuitry and increase anhedonia-related symptoms. We examined resting-state functional MRI in a high-trauma inner-city

Anti-cytokine agents for anhedonia: targeting inflammation and the immune system to treat dimensional disturbances in depression.

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The etiology of mood disorders is mechanistically heterogeneous, underscoring the need for a dimensional approach to identify and develop targeted treatments in psychiatry. Accumulating evidence implicates inflammation as an important contributor to the pathophysiology of depression and presents the
Combined increases in peripheral inflammation and brain glutamate may identify a subtype of depression with distinct neuroimaging signatures. Two contrasting subgroups of depressed subjects-with and without combined elevations in plasma C-reactive protein (CRP) and basal ganglia glutamate (high and

High-Fat Diet Induced Anxiety and Anhedonia: Impact on Brain Homeostasis and Inflammation.

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Depression and type 2 diabetes (T2D) are highly comorbid disorders that carry a large public health burden. However, there is a clear lack of knowledge of the neural pathological pathways underlying these illnesses. The present study aims to elucidate the molecular mechanisms by which a diet rich in
Major depression is a complex disease that originates from the interaction between a genetic background of susceptibility and environmental factors such as stress. At molecular level, it is characterized by dysfunctions of multiple systems including neurotransmitters, hormones, signalling pathways,

Reduced anti-inflammatory gut microbiota are associated with depression and anhedonia.

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Characterise gut microbiota distributions of participants with co-occurring depression and anxiety, in those with only depression or with anxiety, and determine if gut bacteria differentially correlates with distinct clinical presentations.Participants (10

Inflammation: opportunities for treatment stratification among individuals diagnosed with mood disorders.

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Mood disorders continue to be a significant burden to those affected, resulting in significant illness-associated disability and premature mortality. In addition to mood disturbance, individuals also suffer from other transdiagnostic impairments (eg, anhedonia and cognitive impairment). Although
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