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Unlabelled: Electroencephalography-based (EEG) microstate analysis is a promising and widely studied method in which spontaneous cerebral activity is segmented into sub second level quasi-stable states and analyzed. Currently it is being widely explored due to increasing evidence of the association of microstates with cognitive functioning and large-scale brain networks identified by functional magnetic resonance imaging (fMRI). In our study using the four archetypal microstates (A, B, C and D), we investigated the changes in resting state EEG microstate dynamics in persons with temporal lobe epilepsy (TLE) and idiopathic generalized epilepsy (IGE) compared to healthy controls (HC). Machine learning was applied to study its feasibility in differentiating between different groups using microstate statistics. We found significant differences in all parameters related to Microstate D (fronto-parietal network) in TLE patients and Microstate B (visual processing) in IGE patients compared to HCs. Occurrence, duration and time coverage of Microstate B was highest in IGE when compared to the other groups. We also found significant deviations in transition probabilities for both epilepsy groups, particularly into Microstate C (salience network) in IGE. Classification accuracy into clinical groups was found to exceed 70% using microstate parameters which improved on incorporating neuropsychological test differences. To the best of our knowledge, the current study is the first to compare and validate the use of microstate features to discriminate between two disparate epilepsy syndromes (TLE, IGE) and HCs using machine learning suggesting that resting state EEG microstates can be used for endophenotyping and to study resting state dysfunction in epilepsy.
Supplementary Information: The online version contains supplementary material available at 10.1007/s11571-024-10095-z.
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http://dx.doi.org/10.1007/s11571-024-10095-z | DOI Listing |
Mol Psychiatry
September 2025
Center for Depression, Anxiety and Stress Research, McLean Hospital, Belmont, MA, USA.
Dysregulated dopaminergic signaling has been implicated in the pathophysiology of major depressive disorder (MDD) and childhood sexual abuse (CSA), but inconsistencies abound. In a multimodal PET-functional MRI study, harnessing the highly selective tracer [C]altropane, we investigated dopamine transporter availability (DAT) and resting-state functional connectivity (rsFC) within reward-related regions among 112 unmedicated individuals (MDD: n = 37, MDD/CSA: n = 18; CSA no MDD: n = 14; controls: n = 43). Striatal DAT and seed-based rsFC were assessed in the dorsal and ventral striatum and the ventral tegmental area.
View Article and Find Full Text PDFGeroscience
September 2025
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA.
Cognitive decline is common in multiple sclerosis (MS), although neural mechanisms are not fully understood. The objective was to investigate the impact of mild cognitive impairment (MCI) on the relationship between resting state functional connectivity (RSFC) and cognitive function in older adults with multiple sclerosis (OAMS) and age matched healthy controls. Participants underwent magnetic resonance imaging (MRI) scans and cognitive assessments.
View Article and Find Full Text PDFNat Commun
September 2025
Institute of Neurosciences and Medicine, Brain & Behaviour (INM-7), Research Centre Juelich; Wilhelm-Johnen-Straße 1, Juelich, Germany.
Autism is a neurodevelopmental condition associated with altered resting-state brain function. An increased excitation-inhibition ratio is discussed as a pathomechanism but in-vivo evidence of disturbed neurotransmission underlying functional alterations remains scarce. We compare local resting-state brain activity and neurotransmitter co-localizations between autism (N = 405, N = 395) and neurotypical controls (N = 473, N = 474) in two independent cohorts and correlate them with excitation-inhibition changes induced by glutamatergic (ketamine) and GABAergic (midazolam) medication.
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September 2025
Department of Neuroscience, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
The purpose of this study was to investigate how Sphingosine-1-phosphate (S1P) signaling regulates glial phenotype, neuroprotection, and reprogramming of Müller glia (MG) into neurogenic MG-derived progenitor cells (MGPCs) in the adult male and female mouse retina. We found that S1P-related genes were dynamically regulated following retinal damage. (S1P receptor 1) and (sphingosine kinase 1) are expressed at low levels by resting MG and are rapidly upregulated following acute damage.
View Article and Find Full Text PDFOpen Biol
September 2025
National Brain Research Centre, Manesar, Haryana, India.
E3 ubiquitin ligases regulate the cellular proteome proteasome-dependent protein degradation; however, there exist limited studies outlining their non-canonical functions. RNA-binding ubiquitin ligases (RBULs) represent a subset of E3 ligases that harbour RNA-binding domains, making them uniquely positioned to function as both RNA-binding proteins and E3 ligases. Our initial microarray screen for E3 ligases from mouse cortical neural progenitor cells identified MEX3B, a known RNA-binding ubiquitin ligase, to be differentially expressed.
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