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Objective: Alexithymia refers to an ineffective regulation and expression of emotions. It constitutes a major risk factor for a range of medical and psychiatric problems, including chronic pain, somatisation, anxiety and depression. Alexithymia is a multi-faceted concept, described in terms of cognitive and affective aspects. From a neuropsychological perspective, alexithymia can be defined as a disturbance in affective information processing and social cognition. As the growing literature on brain structures involved in alexithymia is fragmented and sometimes even contradictory, the aim of this article was to review findings on neural substrates with regard to their convergence.
Methods: A narrative review was performed, including both early neuropsychological and more recent imaging studies, in order to achieve a better understanding of the aetiology of alexithymia.
Results: Corpus callosum, cingulate cortex and insula are clearly involved in alexithymia. The amygdala and the orbitofrontal part of the cortex appear to be implicated as mediators, because of their broader involvement in emotional processing and executive control.
Conclusion: Notwithstanding the diffuse neural representation, the alexithymia construct can be usefully applied in the clinical and empirical studies of social cognition, particularly when adopting a dimensional neuropsychological approach.
Objective: There is clear evidence of a genetic component in major depression, and several studies indicate that neuropeptide Y (NPY) could play an important role in the pathophysiology of the disease. A well-known polymorphism encoding the substitution of leucine to proline in the signal peptide sequence of NPY (Leu7Pro variation) was previously found to protect against depression. Our study aimed at replicating this association in a large Danish population with major depression.
Method: Leu7Pro was studied in a sample of depressed patients and ethnically matched controls, as well as psychiatric disease controls with schizophrenia. Possible functional consequences of Leu7Pro were explored in vitro.
Results: In contrast to previous studies, Pro7 appeared to be a risk allele for depression, being significantly more frequent in the depression sample (5.5%, n = 593; p = 0.009; odds ratio, OR: 1.46) as compared to ethnically matched controls (3.8%, n = 2912), while schizophrenia patients (4.1%, n = 503) did not differ. In vitro, the Pro7 substitution appeared to be associated with reduced levels of NPY without affecting its mRNA level.
Conclusion: The Leu7Pro variation may increase the risk of major depression, possibly by affecting the biosynthesis of NPY.
Background: Yoga therapy (YT) improves cognitive function in healthy individuals, but its impact on cognitive function among persons with schizophrenia (SZ) has not been investigated.
Objective: To evaluate the adjunctive YT for cognitive domains impaired in SZ.
Methods: Patients with SZ received YT or treatment as usual (TAU; n = 65, n = 23, respectively). Accuracy and speed for seven cognitive domains were assessed using a computerised neurocognitive battery (CNB), thus minimising observer bias. Separately, YT was evaluated among patients with bipolar I disorder (n = 40), major depressive disorder (n = 37) and cardiology outpatients (n = 68). All patients also received routine pharmacotherapy. Patients were not randomised to YT or TAU.
Results: In comparison with the SZ/TAU group, the SZ/YT group showed significantly greater improvement with regard to measures of attention following corrections for multiple comparisons; the changes were more prominent among the men. In the other diagnostic groups, differing patterns of improvements were noted with small-to-medium effect sizes.
Conclusions: Our initial analyses suggest nominally significant improvement in cognitive function in SZ with adjunctive therapies such as YT. The magnitude of the change varies by cognitive domain and may also vary by diagnostic group.
Objective: Vitamin A is a redox-active molecule and its inadvertent utilisation as a preventive therapy against ageing or neurodegeneration has become a harmful habit among humans at different ages. Mitochondrial dysfunction and redox impairment may be induced by vitamin A supplementation experimentally. Nonetheless, it is still not clear by which mechanisms vitamin A elicits such effects. Then, we performed this investigation to analyse whether mitochondria isolated from frontal cortex and hippocampus of vitamin A-treated rats are more sensitive to a challenge with amyloid-β (Aβ) peptides 1–40 or 1–42.
Methods: Adult Wistar rats received vitamin A at 1000–9000 IU/kg/day orally for 28 days. Then, mitochondria were isolated and the challenge with Aβ peptides 1–40 or 1–42 (at 0.2 or 0.1 μM, respectively) for 10 min was carried out before mitochondrial electron transfer chain enzyme activity, superoxide anion radical (O2−•) production and 3-nitrotyrosine content quantification.
Results: Mitochondria obtained from vitamin A-treated rats are more sensitive to Aβ peptides 1–40 or 1–42 than mitochondria isolated from the control group, as decreased mitochondrial complex enzyme activity and increased O2−• production and 3-nitrotyrosine content were observed in incubated mitochondria isolated from vitamin A-treated rats.
Conclusion: These data suggest that oral intake of vitamin A at clinical doses increases the susceptibility of mitochondria to a neurotoxic agent even at low concentrations.
Objective: A case–control study was performed in Belgrade in order to investigate the association between Parkinson's disease (PD) and smoking, coffee and alcohol consumption.
Methods: During the period 2001–2005, 110 new PD cases and 220 hospital controls were interviewed. Cases and controls were matched by sex, age and place of residence (urban/rural). For the analysis of data conditional univariate and multivariate logistic regression methods were used.
Results: With PD were associated, independently from each other, current smoking [odds ratio (OR) = 0.44; 95% confidence interval (CI) = 0.23–0.82], alcohol consumption (OR = 4.78; 95% CI = 2.67–8.55) and coffee consumption (OR = 2.54; 95% CI = 1.36–4.75). In ever smokers the risk for PD significantly decreased with the increasing number of cigarettes smoked and with increasing duration of smoking. The risk for PD significantly increased with the increasing quantity of alcohol consumption. PD risk was significantly higher in subjects whose average daily consumption of coffee was 1 and 2–3 cups, and it was lower (but not significantly) in those whose daily coffee consumption was 4+ cups. Cases and controls did not differ in duration of alcohol and coffee consumption. The results of multivariate analyses did not substantially change after adjustment on family history positive on PD.
Conclusion: The findings of this study support the hypotheses of inverse association of smoking with PD, but an inverse association with coffee was not confirmed. PD was found to be positively associated with coffee and alcohol consumption.
Objectives: Based on the hypothesis that energy impairment may be involved in the pathophysiology of depression, we evaluated the activities of citrate synthase, malate dehydrogenase, succinate dehydrogenase (SDH), mitochondrial respiratory chain complexes I, II, II-III, IV and creatine kinase (CK) in the brain of rats submitted to chronic administration of bupropion.
Methods: Animals received daily administration of bupropion dissolved in saline (10 mg/kg, intraperitoneal) at 1.0 ml/kg body weight. The rats received injections once a day for 14 days; control rats received an equivalent volume of saline. Twelve hours after the last administration, the rats were killed by decapitation and brain was rapidly removed and kept on an ice plate. The activities of the enzymes were measured in different brain areas.
Results: We observed that the activities of citrate synthase and malate dehydrogenase, mithocondrial respiratory chain complexes I, II-III and IV and CK were not altered after chronic administration of bupropion. However, SDH activity was increased in the prefrontal cortex and cerebellum. In the hippocampus, cerebellum and striatum the activity of complex II was increased after chronic administration of bupropion.
Conclusions: Our results demonstrated that bupropion increased some enzymes of brain energy metabolism. These findings are in accordance with other studies which showed that some antidepressants may improve energy metabolism. The present results reinforce the hypothesis that antidepressants modulate brain energy metabolism.
Introduction: Palilalia is an acquired speech disorder characterised by involuntary and spontaneous repetition of words or phrases two or more times in a row. It can occur in a variety of disorders including postencephalic parkinsonism, pseudobulbar palsy, schizophrenia, Gilles de la Tourette syndrome and others.
Clinical Case: We describe a case of a 28-year-old man with refractory schizophrenia that developed palilalia with 300 mg of clozapine. In the patient evaluation we found unspecific alterations in the electroencephalogram, with normal blood tests and cerebral magnetic resonance imaging. Palilalia disappeared with lowering doses of clozapine.
Discussion: The appearance of palilalia induced by clozapine is a rare pharmacologic side-effect which physicians should be familiarised with when evaluating this symptom presentation.