Abstract Introduction Changes in brain-derived neurotrophic factor (BDNF) have been linked to the neuroadaptative consequences of chronic alcohol use and associated with disease severity and prognosis. Few studies have evaluated the influence of drug withdrawal and clinical and sociodemographic data on BDNF levels in severe alcohol users. Objectives Our goals were (1) to evaluate variation in BDNF levels during alcohol withdrawal and, (2) to assess the influence of putative confounding factors on BDNF levels. Methods Our sample consists of 62 men with alcohol use disorder undergoing a detoxification process. Serum BDNF levels were measured using a commercial sandwich-ELISA kit, at two points: before and after the detoxification period. Results We found an increase in BDNF levels during alcohol withdrawal (25.4±9.6 at admission vs. 29.8±10.2 ng/ml at discharge; p < 0.001), even after controlling for potential confounders (positive family history, number of days between blood sample collections, and age) (Generalized Estimating Equation: coefficient = -4.37, 95% confidence interval [95%CI] -6.3; -2.4; p < 0.001). Moreover, individuals who had first-degree relative with alcohol dependence had smaller increases in BDNF levels than individuals with no family history (14.8 [95%CI -5.3; 35.6] vs. 35.3 [95%CI 15.4; 74.8]; p = 0.005). Conclusions In summary, variation in BDNF levels seems to be influenced by withdrawal in severe alcohol users. A positive family history of alcohol dependence could also be a factor that influences variation in this biomarker.

Abstract Introduction Gender dysphoria (GD) is characterized by a marked incongruence between experienced gender and one’s gender assigned at birth. Transsexual individuals present a higher prevalence of psychiatric disorders when compared to non-transsexual populations, and it has been proposed that minority stress, i.e., discrimination or prejudice, has a relevant impact on these outcomes. Transsexuals also show increased chances of having experienced maltreatment during childhood. Interleukin (IL)-1β, IL-6, IL-10 and tumor necrosis factor-alpha (TNF-α) are inflammatory cytokines that regulate our immune system. Imbalanced levels in such cytokines are linked to history of childhood maltreatment and psychiatric disorders. We compared differences in IL-1β, IL-6, IL-10 and TNF-α levels and exposure to traumatic events in childhood and adulthood in individuals with and without GD (DSM-5). Methods Cross-sectional controlled study comparing 34 transsexual women and 31 non-transsexual men. They underwent a thorough structured interview, assessing sociodemographic information, mood and anxiety symptoms, childhood maltreatment, explicit discrimination and suicidal ideation. Inflammatory cytokine levels (IL-1β, IL-6, IL-10 and TNF-α) were measured by multiplex immunoassay. Results Individuals with GD experienced more discrimination (p = 0.002) and childhood maltreatment (p = 0.046) than non-transsexual men. Higher suicidal ideation (p < 0.001) and previous suicide attempt (p = 0.001) rates were observed in transsexual women. However, no differences were observed in the levels of any cytokine. Conclusions These results suggest that transsexual women are more exposed to stressful events from childhood to adulthood than non-transsexual men and that GD per se does not play a role in inflammatory markers.

Objective: To evaluate whether an animal model of mania induced by lisdexamfetamine dimesylate (LDX) has an inflammatory profile and whether immune activation by lipopolysaccharides (LPS) has a cumulative effect on subsequent stimuli in this model. We also evaluated the action of lithium (Li) on inflammatory and neurotrophic factors. Methods: Adult male Wistar rats were subjected to an animal model of mania. After the open-field test, they were given LPS to induce systemic immune activation. Subsequently, the animals’ blood was collected, and their serum levels of brain-derived neurotrophic factor and inflammatory markers (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-1β, IL-10, and inducible nitric oxide synthase [iNOS]) were measured. Results: LDX induced hyperactivity in the animals, but no inflammatory marker levels increased except brain-derived neurotrophic factor (BDNF). Li had no effect on serum BDNF levels but prevented iNOS levels from increasing in animals subjected to immune activation. Conclusion: Although Li prevented an LPS-induced increase in serum iNOS levels, its potential anti-inflammatory effects in this animal model of mania were conflicting.

Objective: Unaffected relatives of bipolar disorder (BD) patients have been investigated for the identification of endophenotypes in an attempt to further elucidate the pathophysiology of the disease. Brain-derived neurotrophic factor (BDNF) is considered to be implicated in the pathophysiology of BD, but its role as an endophenotype has been poorly studied. We investigated abnormal serum BDNF levels in BD patients, in their unaffected relatives, and in healthy controls. Methods: BDNF levels were obtained from 25 DSM-IV bipolar I disorder patients, 23 unaffected relatives, and 27 healthy controls. All BD patients were in remission. The unaffected subjects were first-degree relatives of the proband who had no lifetime DSM-IV diagnosis of axis I disorder. BDNF serum levels were determined by sandwich ELISA using monoclonal BDNF-specific antibodies. Results: There were no statistical differences in BDNF levels among BD patients, relatives, and healthy controls. Conclusion: Serum BDNF levels may not indicate high genetic risk for BD, possibly acting as state markers rather than trait markers of the disease.