Biology subjects

Truong, H.

Publications and source records attributed to Truong, H..

4 recordsLinked to original sources

bioRxiv2026

Alpha-range neural oscillations are associated with multiple dynamic brain networks

We asked whether alpha range (8-12 Hz) EEG neural oscillations, a robust indicator of cortical excitability, are associated with dynamic BOLD brain networks. Two independent EEG-fMRI resting-state datasets (discovery: n = 94 and replication: n = 33) show that low- and high-alpha periods are associated with dynamic BOLD coactivation patterns (dCAPS) involving multiple dynamic networks rather than a single static network. Unique BOLD dCAPs consisting of visual cortex activation along with sensorimotor and attention networks in addition to the posterior thalamus, were mainly associated with periods of low-alpha power. However, overlapping BOLD dCAPs consisting of default, control, and attention networks were associated with periods of both low- and high-alpha power. The results suggest low-alpha dCAPS contain unique temporal-dependent configurations related to visual, sensorimotor, and attention networks while both low- and high-alpha dCAPs consist of overlapping temporal-dependent configurations involving CON, DMN, and attention networks involved in internal and external cognition. These findings reconcile discrepancies across static connectivity EEG-fMRI findings by showing that distinct transient BOLD configurations are associated with similar patterns of alpha EEG modulation in visual cortex, providing a dynamic framework for the gating function of alpha oscillations.

neuroscience↗

bioRxiv2026

Spectral and non-spectral EEG measures in the prediction of working memory task performance and psychopathology

Working memory (WM) supports the temporary maintenance of goal-relevant information and is disrupted across many neuropsychiatric disorders. We examined whether scalp electroencephalography (EEG) data features beyond spectral power, including waveform shape, broadband spectral structure, and signal complexity, provide complementary information for predicting cognitive and clinical outcomes. EEG was recorded from 200 adults spanning a broad range of neuropsychiatric symptom severity while they completed three WM task paradigms: Sternberg spatial WM (SWM), delayed face recognition (DFR), and dot pattern expectancy (DPX). Separate machine learning models were trained on EEG features from the encoding, delay, and probe phase of each task to predict participants task accuracy, reaction time (RT) variability, WM capacity, and psychopathology scores (Brief Psychiatric Rating Scale). A split-half analytic framework was used, with cross-validated model development in an exploratory dataset (N=100) and evaluation of statistically significant models in a held-out validation dataset (N=100). In the exploratory dataset, SWM task data best predicted WM capacity, DPX task data predicted RT variability, and DFR task data predicted psychopathology, suggesting that these three WM paradigms engage distinct neural processes relevant to different outcomes. No models reliably predicted task accuracy. Models incorporating features beyond spectral power generally outperformed power-only models, and task-derived features outperformed resting-state-derived features. However, only those models predicting WM capacity and RT variability generalized to the validation dataset; models predicting psychopathology did not. These findings demonstrate functional heterogeneity across WM paradigms, show that complementary EEG features enhance predictive modeling, and highlight the importance of rigorous validation for identifying robust brain-behavior relationships.

neuroscience↗

bioRxiv2024

Tumour-derived gliogenesis sustains dedifferentiation-dependent tumour growth in the Drosophila CNS

Fate-restricted cells can acquire stem cell-like properties through dedifferentiation, enabling them to gain the plasticity required for differentiation into multiple lineages. Tumour plasticity is prominently observed in brain cancers, where transient cell state changes are linked to resistance to conventional therapies. In this study, we demonstrate that a sub-population of dedifferentiated tumour neural stem cells (NSCs) in Drosophila, induced by the knockdown of prospero (pros), can generate its own glial niche. Temporal patterning, known to influence oncogenic competence and tumour malignancy, plays a key role in this process. Specifically, we show that de novo gliogenesis occurs in the more differentiated Syncrip+ (Syp+) NSC population. Modulating Syp levels alters the size of the glial niche, subsequently affecting tumour size. Furthermore, the tumour-associated glial niche expands through cell division and fails to cease proliferation on time due to dysregulated ecdysone signalling, contributing to niche expansion. Our findings reveal that tumours arising via dedifferentiation establish their own supportive glial microenvironment, which sustains tumour growth.

developmental biology↗

bioRxiv2021

Loss of CEP162 function at the primary cilium delays ciliogenesis and causes retinal ciliopathy in humans

Defects in primary or motile cilia result in a variety of human pathologies, and retinal degeneration is frequently associated with these so-called ciliopathies. We show that homozygosity for a truncating variant in CEP162, a centrosome and microtubule-associated protein required for transition zone (TZ) assembly during ciliogenesis and neuronal differentiation in the retina, causes late-onset retinitis pigmentosa in 2 unrelated families. The mutant CEP162-E646R*5 protein is expressed and properly localized to the mitotic spindle but missing from the basal body in primary and photoreceptor cilia. This impairs recruitment of TZ components to the basal body and corresponds to complete loss of CEP162 function at the ciliary compartment, reflected by delayed formation of dysmorphic cilia. In contrast, rescue of increased cell death in the developing mouse retina after shRNA knockdown of Cep162 by expression of CEP162-E646R*5 indicates that the mutant retains its role for retinal neurogenesis. Human retinal degeneration thus results from specific loss of ciliary CEP162 function. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=134 HEIGHT=200 SRC="FIGDIR/small/469779v3_ufig1.gif" ALT="Figure 1"> View larger version (53K): org.highwire.dtl.DTLVardef@593dccorg.highwire.dtl.DTLVardef@e84d7forg.highwire.dtl.DTLVardef@137ce56org.highwire.dtl.DTLVardef@cba1f7_HPS_FORMAT_FIGEXP M_FIG C_FIG

genetics↗