Executive dysfunctions are frequently seen in patients with major depressive disorder (MDD) and normalise in many cases during effective antidepressant therapy. This study investigated whether a normalisation of executive dysfunctions during antidepressant treatment correlates with or can be predicted by clinical parameters or levels of brain-derived neurotrophic factor (BDNF). In 110 MDD patients with executive dysfunctions (percentile <16), executive functions and plasma BDNF levels were analysed at baseline, and days 14 and 56 of an antidepressant treatment. BDNF exon IV and P11 methylation status was studied at baseline. Eighty patients (73%) experienced a normalisation of executive dysfunctions, while 30 (27%) suffered from persistent dysfunctions until day 56. Patients with persistent dysfunctions had significantly higher HAMD scores at days 14 and 56, and lower plasma BDNF levels at each time point than patients with a normalisation of dysfunctions (= 10.18; = 0.002). This was seen for verbal fluency, but not processing speed. BDNF exon IV and p11 promoter methylation was not associated with test performance. Our results corroborate a concomitant amelioration of executive dysfunctions with successful antidepressant therapy and support a role of BDNF in the neural mechanisms underlying the normalisation of executive dysfunctions in MDD. NCT00974155; EudraCT: 2008-008280-96.
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http://dx.doi.org/10.1080/15622975.2018.1425478 | DOI Listing |
Pain Ther
January 2025
Robert Wood Johnson University Hospital/Rutgers Medical School, New Brunswick, NJ, USA.
Introduction: Many interventional strategies are commonly used to treat chronic low back pain (CLBP), though few are specifically intended to target the distinct underlying pathomechanisms causing low back pain. Restorative neurostimulation has been suggested as a specific treatment for mechanical CLBP resulting from multifidus dysfunction. In this randomized controlled trial, we report outcomes from a cohort of patients with CLBP associated with multifidus dysfunction treated with restorative neurostimulation compared to those randomized to a control group receiving optimal medical management (OMM) over 1 year.
View Article and Find Full Text PDFJ Neurol
January 2025
NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.
Cognitive impairment (CI) in multiple sclerosis (MS) is only partially explained by whole-brain volume measures, but independent component analysis (ICA) can extract regional patterns of damage in grey matter (GM) or white matter (WM) that have proven more closely associated with CI. Pathology in GM and WM occurs in parallel, and so patterns can span both. This study assessed whether joint-ICA of GM and WM features better explained cognitive function compared to single-tissue ICA.
View Article and Find Full Text PDFERJ Open Res
January 2025
Department of Otolaryngology-Head and Neck Surgery, University of California, Los Angeles, Los Angeles, CA, USA.
Background: Chronic rhinosinusitis (CRS) and olfactory dysfunction (OD) are prevalent disease complications in people with cystic fibrosis. These understudied comorbidities significantly impact quality of life. The impact of highly effective modulator therapy (HEMT) in young children with cystic fibrosis (YCwCF) on these disease complications is unknown.
View Article and Find Full Text PDFDement Neuropsychol
January 2025
Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Psiquiatria, Campinas SP, Brazil.
Unlabelled: Neuropsychiatric symptoms (NPS) such as depression, anxiety, and apathy are present in mild cognitive impairment (MCI) and are risk factors for cognitive decline. However, the relationship between NPS and specific cognitive domains is less clear.
Objective: This study aimed to assess whether there is a correlation between NPS and specific cognitive domains.
J Neuroinflammation
January 2025
Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA.
The thrombolytic protease tissue plasminogen activator (tPA) is expressed in the CNS, where it regulates diverse functions including neuronal plasticity, neuroinflammation, and blood-brain-barrier integrity. However, its role in different brain regions such as the substantia nigra (SN) is largely unexplored. In this study, we characterize tPA expression, activity, and localization in the SN using a combination of retrograde tracing and β-galactosidase tPA reporter mice.
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