Objective: In this study, we aimed to characterize the plasma metabolic profiles of brain atrophy and alcohol dependence (s) and to identify the underlying pathogenesis of brain atrophy related to alcohol dependence.
Methods: We acquired the plasma samples of alcohol-dependent patients and performed non-targeted metabolomic profiling analysis to identify alterations of key metabolites in the plasma of BA-ADPs. Machine learning algorithms and bioinformatic analysis were also used to identify predictive biomarkers and investigate their possible roles in brain atrophy related to alcohol dependence.
Results: A total of 26 plasma metabolites were significantly altered in the BA-ADPs group when compared with a group featuring alcohol-dependent patients without brain atrophy (NBA-ADPs). Nine of these differential metabolites were further identified as potential biomarkers for BA-ADPs. Receiver operating characteristic curves demonstrated that these potential biomarkers exhibited good sensitivity and specificity for distinguishing BA-ADPs from NBA-ADPs. Moreover, metabolic pathway analysis suggested that glycerophospholipid metabolism may be highly involved in the pathogenesis of alcohol-induced brain atrophy.
Conclusion: This plasma metabolomic study provides a valuable resource for enhancing our understanding of alcohol-induced brain atrophy and offers potential targets for therapeutic intervention.
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http://dx.doi.org/10.3389/fnmol.2022.999938 | DOI Listing |
Prog Neuropsychopharmacol Biol Psychiatry
December 2024
Department of Geriatric Psychiatry, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. Electronic address:
Backgrounds: Aberrant brain structures in schizophrenia have been widely explored. However, the causal effects of negative symptoms on brain structural alterations are still unclear. This study aims to explore the synchronous and progressive alterations in gray matter volume (GMV) associated with negative symptoms.
View Article and Find Full Text PDFMech Ageing Dev
December 2024
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, 79430, TX, USA; Nutritional Sciences Department, College Human Sciences, Texas Tech University, Lubbock, TX 79409; Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Speech, Language, and Hearing Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Electronic address:
Chronic sleep deprivation and lack of physical exercise may have detrimental effects on overall health, particularly in terms of brain health, with significant implications for cognitive function and well-being. This review explores the impact of chronic sleep deprivation and physical exercise on brain atrophy in mild cognitive impairment (MCI) and Alzheimer's disease (AD). Drawing insights from 40 selected studies, the review synthesizes evidence on these lifestyle factors' correlations with neurodegenerative changes.
View Article and Find Full Text PDFActa Neurochir (Wien)
December 2024
Medical Faculty of Heidelberg University, Heidelberg, Germany.
Introduction: Tumorous growths in the sellar region pose significant clinical challenges due to their proximity to critical visual structures such as the optic chiasm and optic nerves. Given their proximity to the optic system, these tumors are often diagnosed due to a progressive decrease in visual acuity. Thus, surgical intervention is crucial to prevent irreversible damage, as timely decompression can halt the progression of edema and subsequent optic atrophy.
View Article and Find Full Text PDFTransl Neurodegener
December 2024
Department of Neurosciences, Hengyang Medical School, University of South China, Hengyang, 421009, China.
Background: Neurological complications are a significant concern of Coronavirus Disease 2019 (COVID-19). However, the pathogenic mechanism of neurological symptoms associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is poorly understood.
Methods: We used Drosophila as a model to systematically analyze SARS-CoV-2 genes encoding structural and accessory proteins and identified the membrane protein (M) that disrupted mitochondrial functions in vivo.
Transl Neurodegener
December 2024
Department of Anatomy and Medical Imaging, University of Auckland, 85 Park Road, Grafton, , Auckland, 1142, New Zealand.
Background: Parkinson's disease (PD) and multiple system atrophy (MSA) are classified as α-synucleinopathies and are primarily differentiated by their clinical phenotypes. Delineating these diseases based on their specific α-synuclein (α-Syn) proteoform pathologies is crucial for accurate antemortem biomarker diagnosis. Newly identified α-Syn pathologies in PD raise questions about whether MSA exhibits a similar diversity.
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