Transcranial electric stimulation (tES) is a promising technique that has been shown to improve working memory (WM) performance and enhance the effect of cognitive training. However, experimental set up and electrode placement are not always determined based on neurofunctional knowledge about WM, leading to inconsistent results. Additional research on the effects of tES grounded on neurofunctional evidence is therefore necessary. Sixty young, healthy, volunteers, assigned to six different groups, participated in 5 days of stimulation or sham treatment. Twenty-five of these subjects also participated in MRI acquisition. We performed three experiments: In the first one, we evaluated tES using either direct current stimulation (tDCS) with bilateral stimulation of the frontal or parietal lobe; in the second one, we used the same tDCS protocol with a different electrode placement (i.e., supraorbital cathode); in the third one, we used alternating currents (tACS) of 35 Hz, applied bilaterally to either the frontal or parietal lobes. The behavioral outcome measure was the WM capacity (i.e., number of remembered spatial position) during the 5 days of training. In a subsample of subjects we evaluated the neural effects of tDCS by measuring resting state connectivity with functional MRI, before and after the 5 days of tDCS and visuo-spatial WM training. We found a significant impairment of WM training-related gains associated with parietal tACS and frontal tDCS. Five days of tDCS stimulation was also associated with significant change in resting state connectivity revealed by multivariate pattern analysis. None of the stimulation paradigms resulted in improved WM performance or enhanced WM training gains. These results show that tES can have negative effects on cognitive plasticity and affect resting-state functional connectivity.
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http://dx.doi.org/10.3389/fnhum.2017.00364 | DOI Listing |
BMC Psychiatry
January 2025
College of Artificial Intelligence, Southwest University, Chongqing, China.
Background: Although childhood maltreatment (CM) is widely recognized as a transdiagnostic risk factor for various internalizing and externalizing psychological disorders, the neural basis underlying this association remain unclear. The potential reasons for the inconsistent findings may be attributed to the involvement of both common and specific neural pathways that mediate the influence of childhood maltreatment on the emergence of psychopathological conditions.
Methods: This study aimed to delineate both the common and distinct neural pathways linking childhood maltreatment to depression and aggression.
Nat Commun
January 2025
Department of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, TX, USA.
SAMHD1 is a dNTPase that impedes replication of HIV-1 in myeloid cells and resting T lymphocytes. Here we elucidate the substrate activation mechanism of SAMHD1, which involves dNTP binding at allosteric sites and transient tetramerization. Our findings reveal that tetramerization alone is insufficient to promote dNTP hydrolysis; instead, the activation mechanism requires an inactive tetrameric intermediate with partially occupied allosteric sites.
View Article and Find Full Text PDFNat Commun
January 2025
Université Paris Cité, Institut Cochin, CNRS, INSERM, Paris, France.
Interferon (IFN)-α is the earliest cytokine signature observed in individuals at risk for type 1 diabetes (T1D), but the effect of IFN-α on the antigen repertoire of HLA Class I (HLA-I) in pancreatic β-cells is unknown. Here we characterize the HLA-I antigen presentation in resting and IFN-α-exposed β-cells and find that IFN-α increases HLA-I expression and expands peptide repertoire to those derived from alternative mRNA splicing, protein cis-splicing and post-translational modifications. While the resting β-cell immunopeptidome is dominated by HLA-A-restricted peptides, IFN-α largely favors HLA-B and only marginally upregulates HLA-A, translating into increased HLA-B-restricted peptide presentation and activation of HLA-B-restricted CD8 T cells.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
January 2025
School of Psychological Sciences, Sagol School of Neuroscience, Tel-Aviv University.
Background: Although combat-deployed soldiers are at a high risk for developing trauma-related psychopathology, most will remain resilient for the duration and aftermath of their deployment tour. The neural basis of this type of resilience is largely unknown, and few longitudinal studies exist on neural adaptation to combat in resilient individuals for whom a pre-exposure measurement was collected. Here, we delineate changes in the architecture of functional brain networks from pre- to post-combat in psychopathology-free, resilient participants.
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