Aim: Patients with epilepsy (PE) develop persistent mental disorders identified as significant personal and affective disorders, especially of depressive and anxiety spectrum, observed in the interictal period of the disease. To study the frequency of non-psychotic mental disorders in patients with epilepsy, to specify the clinical features of non-psychotic affective disorders and to analyze the association of different variants of affective disorders with symptoms of drug-resistance in epilepsy (DRE).
Material And Methods: One hundred and sixty patients with epilepsy, including 80 patients with DRE and 80 patients with controlled epilepsy (CE), were studied using a battery of psychometric scales.
Results And Conclusion: The variety of depressive and anxious psychiatric condition was detected in 59.4% of PE, in 86.3% of patients with DRE and in 32.5% with CE. A clinical and psychopathological analysis of non-psychotic mental disorders showed that the frequency of affective disorders as well as great «structural complexity» and the depth of depressive and anxiety disorders were significantly higher in the group of patients with DRE compared to patients with CE. Patients with affective symptoms had earlier onset and the longer course of disease.
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http://dx.doi.org/10.17116/jnevro20171172110-14 | DOI Listing |
Sci Rep
December 2024
Department of Psychiatry and Behavioral Sciences and Weill Center for Neurosciences, University of California, San Francisco, CA, 94107, USA.
Telomere attrition is a hallmark of biological aging, contributing to cellular replicative senescence. However, few studies have examined the determinants of telomere attrition in vivo in humans. Mitochondrial Health Index (MHI), a composite marker integrating mitochondrial energy-transformation capacity and content, may be one important mediator of telomere attrition, as it could impact telomerase activity, a direct regulator of telomere maintenance.
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December 2024
Department of Drug Prohibition and Public Security, Criminal Investigation Police University of China, Shenyang, 110035, China.
Methamphetamine use disorder has emerged as a significant public health concern globally. This study endeavors to elucidate the alterations in expression changes of miRNAs in the plasma of methamphetamine use disorder and elucidate the alterations in miRNA expression in the plasma of individuals with methamphetamine use disorder and investigate the relationship between these differentially expressed miRNAs and the disorder itself, cravings for methamphetamine, and associated mental disorders. Furthermore, the study seeks to clarify the expression of downstream target molecules of specific miRNAs in the plasma of methamphetamine use disorder, assess the diagnostic utility of these miRNAs and their target molecules, explore their potential as biomarkers, and identify potential targets for the diagnosis and treatment of methamphetamine use disorder.
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December 2024
Department of Neuroscience, Baylor College of Medicine, Houston, TX, 77030, USA.
The bipolar disorder (BD) risk gene ANK3 encodes the scaffolding protein AnkyrinG (AnkG). In neurons, AnkG regulates polarity and ion channel clustering at axon initial segments and nodes of Ranvier. Disruption of neuronal AnkG causes BD-like phenotypes in mice.
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December 2024
Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
The mechanism(s) underlying gut microbial metabolite (GMM) contribution towards alcohol-mediated cardiovascular disease (CVD) is unknown. Herein we observe elevation in circulating phenylacetylglutamine (PAGln), a known CVD-associated GMM, in individuals living with alcohol use disorder. In a male murine binge-on-chronic alcohol model, we confirm gut microbial reorganization, elevation in PAGln levels, and the presence of cardiovascular pathophysiology.
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December 2024
Department of Theory and Bio-Systems, Max Planck Institute of Colloids and Interfaces, 14476, Potsdam, Germany.
Neurodegeneration in Huntington's disease (HD) is accompanied by the aggregation of fragments of the mutant huntingtin protein, a biomarker of disease progression. A particular pathogenic role has been attributed to the aggregation-prone huntingtin exon 1 (HTTex1), generated by aberrant splicing or proteolysis, and containing the expanded polyglutamine (polyQ) segment. Unlike amyloid fibrils from Parkinson's and Alzheimer's diseases, the atomic-level structure of HTTex1 fibrils has remained unknown, limiting diagnostic and treatment efforts.
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