Alterations in Neurotrophins in Alcohol-Addicted Patients during Alcohol Withdrawal.

BACKGROUND: Alcohol use disorder (AUD) is related to mental and somatic disorders that result in alcohol withdrawal syndrome (AWS), with 30% of AWS cases leading to life-threatening delirium tremens (DTs). Currently, studies do not support using any one biomarker in DTs. Neurotrophins affect neuromodulation, playing a role in the pathogenesis of AUD, AWS, and DTs. METHODS: This review aims to summarize experimental and clinical data related to neurotrophins and S100B in neuroplasticity, as well as neurodegeneration in the context of AUD, AWS, and DTs. This work used publications that were selected based on the protocol consistent with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. RESULTS: The BDNF level could be a good candidate biomarker for relapse susceptibility, as it is significantly reduced during consumption and gradually increases during abstinence. GDNF influences AUD through its integral role in the function of dopaminergic neurons and ablates the return to alcohol-drinking behavior. NGF protects neurons from ethanol-induced cytotoxic damage and affects recovery from cognitive deficits after brain damage. The NT-3 level is decreased after alcohol exposure and is involved in compensatory mechanisms for cognitive decline in AUD. NT-4 affects oxidative stress, which is associated with chronic alcohol consumption. S100B is used as a biomarker of brain damage, with elevated levels in serum in AUD, and can protect 5-HT neurons from the damage caused by alcohol. CONCLUSIONS: BDNF, GDNF, NT-3, NT-4, NGF, and S100B may be valuable markers for withdrawal syndrome. In particular, the most relevant is their association with the development of delirium complications. However, there are few data concerning some neurotrophins in AWS and DTs, suggesting the need for further research.

Changes in Adipokine, Resitin, and BDNF Concentrations in Treatment-Resistant Depression after Electroconvulsive Therapy.

OBJECTIVES: One of the current challenges in psychiatry is the search for answers on how to effectively manage drug-resistant depression. The occurrence of drug resistance in patients is an indication for the use of electroconvulsive therapy (ECT). This method is highly effective and usually results in relatively quick health improvement. Despite the knowledge of how ECT works, not all of the biological pathways activated during its use have been identified. Hence, based on the neuroinflammatory hypothesis of depression, we investigated the concentration of two opposite-acting adipokines (anti-inflammatory adiponectin and proinflammatory resistin) and BDNF in antidepressant-resistant patients undergoing ECT. METHODS: The study group comprised 52 patients hospitalized due to episodes of depression in the course of unipolar and bipolar affective disorder. The serum concentration of adipokines and BDNF was determined before and after the therapeutic intervention using an ELISA method. In the analyses, we also included comparisons considering the type of depression, sex, and achieving remission. RESULTS: Adiponectin, resistin, and BDNF concentrations change after ECT treatment. These changes are correlated with an improvement in the severity of depressive symptoms and are more or less pronounced depending on the type of depression. CONCLUSIONS: Although not all observed changes reach statistical significance, adipokines in particular remain exciting candidates for biomarkers in assessing the course of the disease and response to ECT treatment.

The use of intranasal oxytocin in the treatment of eating disorders.

Oxytocin (OXT) is a hypothalamic peptide that plays a number of roles in the body, being involved in labor and lactation, as well as cognitive-emotional processes and social behavior. In recent years, knowledge of the physiology of OXT has been repeatedly used to explore its potential role in the treatment of numerous diseases, identifying a significant role for OXT in appetite regulation, eating behavior, weight regulation, and food-related beliefs. In this review we provide an overview of publications on this topic, but due to the wealth of research, we have limited our focus to studies based on the use of intranasal OXT in psychiatric diseases, with a particular focus on the role of oxytocin in eating disorders and obesity. Accumulating evidence that OXT intranasal supplementation may provide some therapeutic benefit seems promising. In individuals with autistic spectrum disorders (ASD) and schizophrenia, OXT may affect core deficits, improving social cognition and reducing symptom severity in schizophrenia. Dysregulation of serum and CSF OXT levels, as well as polymorphisms of its genes, may affect emotion perception in patients with eating disorders and correlate with co-occurring depressive and anxiety disorders. Nevertheless, there are still many critical questions regarding the pharmacokinetics and pharmacodynamics of intranasal OXT that can only be answered in larger randomized controlled trials.

Dysfunction of the Purinergic System in Bipolar Disorder.

OBJECTIVE: To verify the purinergic hypothesis of bipolar disorder (BD), we assessed the concentration of various components of the purinergic system in manic and depressed bipolar patients. METHODS: Sixty-two patients (19 male and 43 female), aged 22-69 (49 ± 14) years, with BD were studied. Twenty-three patients (9 male and 14 female) were assessed during a manic episode and subsequent remission, and 39 patients (10 male and 29 female) were investigated in a depressive episode and the following remission. Twenty-two healthy subjects (8 male and 14 female), aged 19-70 (41 ± 14) years, served as the control group (CG). The severity of symptoms was evaluated using the Hamilton Depression Rating Scale (HDRS) and the Young Mania Rating Scale (YMRS). The concentrations of uric acid (UA) were estimated by the uricase-based method, whereas xanthine dehydrogenase (XDH), adenosine (Ado), and adenosine deaminase (ADA) by ELISA. RESULTS: The mean score in the acute episode was 32 ± 8 points in the YMRS for mania and 31 ± 8 in the HDRS for depression. UA levels were significantly higher in female bipolar patients compared to the females in the CG. The concentrations of XDH, Ado, and ADA were significantly lower in bipolar patients both during an acute episode and remission compared to CG. CONCLUSIONS: A significant dysfunction of the purinergic system in patients with BD was observed. In most instances, the disturbances were not different in the acute episode than in remission what qualifies them as trait dependent. The results may confirm the role of the purinergic system in the pathogenesis of BD.

Disturbances of purinergic system in affective disorders and schizophrenia. / Zaburzenia ukladu purynergicznego w chorobach afektywnych i schizofrenii.

Purinergic system plays a role in the regulation of many psychological processes, including mood and activity. It consists of P1 receptors, with adenosine as the agonist, and P2 receptors, activated by nucleotides (e.g., adenosine 5'-triphosphate - ATP). Propounded disturbances of uric acid in affective disorders were related to the introduction of lithium for the treatment of these disorders in the 19th and 20th century. At the beginning of the 21st century, new evidence was accumulated concerning a role of uric acid in the pathogenesis and treatment of bipolar disorder (BD). In patients with BD, higher prevalence of gout and increased concentration of uric acid have been found as well as the therapeutic activity of allopurinol, used as an adjunct to mood stabilizers, has been demonstrated in mania. In recent years, the research on the role of the purinergic system in the pathogenesis and treatment of affective disorders and schizophrenia focuses on the role of adenosine (P1) receptors and nucleotide (P2) receptors. Activation of adenosine receptors is related to an antidepressant activity. Alterations of P2 receptors are also significant for the pathogenesis of affective disorders. The role of purinergic system in schizophrenia is related to the effect of adenosine and nucleotide receptors on dopaminergic and glutamatergic neurotransmission. A lot of data indicate that schizophrenia is related to a deficit of adenosine system. Changes in the purinergic system are also significant for psychopathological symptoms of schizophrenia and for the action of antipsychotic drugs.