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It has been suggested that an imbalance in mineral levels is involved in the pathophysiology of migraine. However, only a few studies have investigated the circulating levels of mineral in patients with migraine during the pain-free period (i.e. interictal). This study aimed to investigate whether the interictal plasma levels of minerals of women with migraine differ from those of women without migraine (controls). This is a cross-sectional study involving 67 women, of which 38 were diagnosed with migraine and 29 were controls. The groups were similar in age and body mass index. Plasma levels of magnesium (Mg), copper (Cu), calcium (Ca), zinc (Zn), iron (Fe), and selenium (Se) were measured. Dietary intake was assessed using a 24-hour food recall, and migraine impact was evaluated using the Headache Impact Test, version 6 (HIT-6). The association between migraine disability, and plasma levels and dietary intake of minerals was assessed through correlation and logistic regression analyses. Women with migraine had significantly lower plasma levels of Mg, Ca, Cu, and Zn than controls. In parallel, dietary intake of Mg, Cu, and Fe was significantly lower in patients with migraine. Migraine impact was not associated with plasma levels or dietary intake of minerals. The results suggest that patients with migraine have lower plasma levels of minerals, and dietary intervention to ensure adequate mineral intake should be considered as a therapeutic strategy for migraine. [ABSTRACT FROM AUTHOR]

The association between diet and migraine has been reported in the literature, but only a few studies have evaluated whether the diet consumed by patients with migraine differs from individuals without migraine. Herein, we aimed to investigate whether the quality and the Dietary Inflammatory Index (DII) of diet consumed by migraine patients differ from that consumed by healthy controls. We also evaluated whether the severity of migraine and headache frequency were associated with these parameters. Patients of both sexes, aged between 18 and 65, with episodic migraine and healthy controls were enrolled in this cross-sectional study. Disability and impact caused by migraine and depressive symptoms were evaluated. Dietary intake was assessed using a 24-hour dietary recall and a three-day non-consecutive food record. The quality of the diet was calculated using the Healthy Eating Index (HEI)−2015 adapted to the Brazilian population, and DII was calculated based on the method developed by Shivappa et al. (2014). Ninety patients with migraine and 62 individuals without migraine were included in this study. The groups did not differ regarding age, sex, marital status, years of schooling, anthropometric characteristics, and depressive symptoms. Patients with migraine had lower HEI total score than controls, indicating that these patients have a lower quality of the diet. Patients with migraine also had higher DII than controls. Nevertheless, HEI and DII scores did not correlate with migraine frequency and severity. This study corroborates the view that the characteristics of the diet might be involved in migraine pathophysiology. [ABSTRACT FROM AUTHOR]

The objective of this manuscript is to provide a comprehensive and critical overview of the current evidence on the association between Diabetes mellitus (DM) and mood disorders [i.e., Major depressive disorder (MDD) and bipolar disorder (BD)], and therapeutic opportunities. We searched in MEDLINE (via Ovid) for placebo-controlled clinical trials published in the last 20 years that assessed drug repurposing approaches for the treatment of DM or mood disorders. We found seven studies that aimed to verify the effects of antidepressants in patients diagnosed with DM, and eight studies that tested the effect of antidiabetic drugs in patients diagnosed with MDD or BD. Most studies published in the last two decades did not report a positive effect of antidepressants on glycemic control in patients with DM. On the other hand, antidiabetic drugs seem to have a positive effect on the treatment of MDD and BD. While effect of antidepressants on glycemic control in patients with DM is still controversial, the use of antidiabetic drugs may be a promising strategy for patients with MDD or BD. Prospective studies are still needed. Mood disorders in patients with DM affect glycemic control, potentially increasing mortality risk. The effect of antidepressants on glycemic control in patients with DM is still controversial. The coexistence of complicated DM and a mood disorders would require a careful, individualised, and comprehensive evaluation. Insulin resistance may increase the risk of depressive symptoms and is associated with worse outcomes in BD. The use antidiabetic drugs may be a promising strategy for patients with MDD or BD. However, prospective trials are needed to prove a potential antidepressant activity of antidiabetic drugs. [ABSTRACT FROM AUTHOR]

Aims: Recent findings suggest that cognitive impairment can be associated with inflammation and immune changes in schizophrenia. We aimed to study possible associations between cytokine levels and cognitive performance in a sample of patients with schizophrenia. Methods: Cognition was assessed with the brief assessment of cognition in schizophrenia in 63 clinically stable outpatients with schizophrenia. Blood was collected and cytokines (IL-2, IL-4, IL-6, IL-10, IL-17A, TNF-α, IFN-γ) were measured by cytometric bead array method. Psychopathological scales were also applied. Results: IL-6 correlated negatively with general cognitive performance (rho = –0.395, p =.017) and positively with antipsychotic dose (rho = 0.412, p =.004). Multiple regression analysis showed that cognitive performance is associated with age and antipsychotic dose (p =.000 and p =.033). Conclusion: The association between IL-6 levels and cognitive performance is dependent on age and antipsychotic dose. [ABSTRACT FROM AUTHOR]

Objectives. Abnormalities in neurotrophic systems have been reported in Alzheimer's disease (AD), as shown by decreased serum brain-derived neurotrophic factor (BDNF) levels and association with BDNF genetic polymorphisms. In this study, we investigate whether these findings can be detected in patients with mild cognitive impairment (MCI), which is recognized as a high risk condition for AD. We also address the impact of these variables on the progression of cognitive deficits within the MCI-AD continuum. Methods. One hundred and sixty older adults with varying degrees of cognitive impairment (30 patients with AD, 71 with MCI, and 59 healthy controls) were longitudinally assessed for up to 60 months. Baseline serum BDNF levels were determined by sandwich ELISA, and the presence of polymorphisms of BDNF and apolipoprotein E (Val66Met and APOE*E4, respectively) was determined by allelic discrimination analysis on real time PCR. Modifications of cognitive state were ascertained for non-demented subjects. Results. Mean serum BDNF levels were reduced in patients with MCI and AD, as compared to controls (509.2±210.5; 581.9±379.4; and 777.5±467.8 pg/l respectively; P<0.001). Baseline serum BDNF levels were not associated with the progression of cognitive impairment upon follow-up in patients with MCI (progressive MCI, 750.8±463.0; stable MCI, 724.0±343.4; P=0.8), nor with the conversion to AD. Although Val66Met polymorphisms were not associated with the cross-sectional diagnoses of MCI or AD, the presence of Met-BDNF allele was associated with a higher risk of disease-progression in patients with MCI (OR=3.0 CI95% [1.2–7.8], P=0.02). We also found a significant interaction between the APOE*E4 and Met-BDNF allele increasing the risk of progression of cognitive impairment in MCI patients (OR=4.4 CI95% [1.6–12.1], P=0.004). Conclusion. Decreased neurotrophic support, as indicated by a reduced systemic availability of BDNF, may play role in the neurodegenerative processes that underlie the continuum from MCI to AD. The presence of Met-BDNF allele, particularly in association with APOE*E4, may predict a worse cognitive outcome in patients with MCI. [ABSTRACT FROM AUTHOR]

Objectives. The aim of the present study is to investigate serum BDNF levels in older depressed patients as compared to healthy elderly controls. Methods. Twenty-nine elderly subjects with major depression and 42 healthy older adults were enrolled to this study. All depressed patients were antidepressant-free for at least 1 month prior clinical and laboratorial assessments. Serum BDNF levels were determined by sandwich ELISA. Results. BDNF levels were lower in elderly depressed patients as compared to controls ( P=0.034). Patients with late-onset depression had the lowest BDNF level (median 478.5, interquartile range 373.5–740.9 pg/l) when compared to early-onset depression (median 620.7, interquartile range 366.1–971.9 pg/l) and healthy controls (median 711.3, interquartile range 534.7–1181.0 pg/l) ( P<0.03). Conclusions. Reduced serum BDNF level may be a state marker of late-life depression in non-medicated elderly patients. Our findings provide further evidences that reduced neurotrophic support may have an important role in the physiopathology of late-life depression. [ABSTRACT FROM AUTHOR]