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Trinka, E.

Publications and source records attributed to Trinka, E..

8 recordsLinked to original sources

Non-invasive tracking of ripple-like activity during human sleep using MEG

Hippocampal ripples are considered a key mechanism of sleep-dependent memory consolidation. In humans, however, their direct investigation has relied on invasive recordings from patients with epilepsy, because EEG provides limited access to fast activity from deep medial temporal structures. Here, we tested whether source-resolved magnetoencephalography can reveal physiologically meaningful ripple-like activity during NREM sleep in healthy humans. These events showed hallmarks expected of sleep ripples: they were most prominent in medial temporal regions and embedded within slow oscillation (SO)-spindle dynamics, occurring preferentially during SO up-states and spindle centers. To test mnemonic relevance, we combined sleep MEG with targeted memory reactivation, in which learning cues were replayed during sleep. TMR improved memory performance, and later remembered cues preferentially recruited medial temporal ripple-like events alongside cortical spindles. Ripple-like events also coincided with enhanced item-specific reactivation during successful TMR. Together, these findings establish MEG as a non-invasive window onto hippocampo-cortical memory dynamics during sleep.

neuroscience↗

A Brain Circuit for Status Epilepticus

Status epilepticus (SE) is a life-threatening persistent epileptic seizure that can arise from various brain structures, leaving its brain circuit unknown. In this study, we utilize brain imaging changes during SE to reveal the brain architecture and circuit of persistent seizures. Multimodal lesion mapping identified that brain imaging changes during SE localize to a specific predisposed brain architecture characterized by increased metabolic rate, high synaptic and mitochondrial density, glutamate (mGLUR5 and NMDA) and GABA receptors. Gene expression patterns within lesion locations revealed a transcriptomic profile enriched for epilepsy pathologies (including SE), neuronal and synaptic processes, and glutamate signaling. Lesion network mapping demonstrated these same lesions map to a common brain circuit, unifying a traditionally heterogeneous patient population. Findings were validated in an independent cohort and the identified SE circuit distinguished brain imaging changes during SE from other lesion etiologies with excellent accuracy (91%), significantly outperforming all other tested maps. With this SE circuit, we identify therapeutic targets for precision therapy that could modulate this circuit. This study demonstrates brain imaging changes in SE converge on a unified brain circuit that could help diagnostic workup of patients in critical care and guide clinical trials of precision therapy for persistent seizures.

neuroscience↗

Accelerated neural aging as a systems-level vulnerability for tinnitus

Tinnitus, the perception of sound without an external source, affects 10-15% of individuals, yet its neural mechanisms remain poorly understood. Building on evidence that chronological age predicts tinnitus risk beyond hearing loss, we tested the hypothesis that accelerated neural aging increases susceptibility to tinnitus by integrating cross-sectional resting-state MEG with longitudinal structural imaging data. In a large MEG dataset, spectral parametrization revealed that age-neural relationships were amplified in the tinnitus group compared to age-, sex- & hearing-matched controls. Complementing these findings, prospective analyses using data from the UK Biobank showed that among participants without tinnitus at baseline, stronger age-related declines in white-matter density predicted later tinnitus onset. Collectively, these converging functional and structural findings support accelerated brain aging as a key risk factor for tinnitus.

neuroscience↗

Sequential coupling of sleep oscillations enables concept-neuron reactivation and supports information flow across the human hippocampal-cortical circuit

Effective memory consolidation during sleep is thought to rely on the transfer of reactivated memory traces from the hippocampus to the cortex. However, the mechanisms supporting this essential dialogue across brain areas remain poorly understood. Here, we recorded single-neuron activity (n = 1097) in the medial temporal lobe (MTL) of 10 epilepsy patients across 21 nights of sleep. Before sleep, patients engaged in a memory task with stimuli eliciting concept-neuron responses. During non-rapid eye movement (NREM) sleep, neuronal firing locked to sharp wave-ripples (SWR) revealed a directed flow of information from the hippocampus to cortical targets. Notably, within SWR-driven activity, experience-dependent concept neurons exhibited elevated co-activation both within and across MTL regions, indicating selective reactivation of behaviorally relevant information. Cross-regional co-activation of concept cells was markedly enhanced when hippocampal SWRs coincided with cortical slow oscillation-spindle complexes, suggesting an active role of the cortex in shaping interregional communication. These findings provide evidence that SWRs in humans selectively reactivate experience-related neural ensembles across the hippocampal-cortical network, while synergistic interactions with cortical slow oscillation-spindle events might facilitate effective memory consolidation.

neuroscience↗

Network topology in brain tumor patients with and without structural epilepsy- a prospective MEG-study

It has been proposed that functional connectivity (FC) and network topology (NT) are altered in patients with glial brain tumors. So far there is no consensus on the pattern of these changes, furthermore data on FC in patients with brain metastases (BMs) as well as on the presence and absence of tumor-related epilepsy is lacking. We aimed to analyze preoperative NT of newly diagnosed, singular, supratentorial glial brain tumors (GBTs) and BMs with and without structural epilepsy. FC and NT derived from resting state magnetoencephalography (MEG) were compared between patients (PAs) and matched healthy controls (HCs), between GBTs and BMs as well as between patients with and without structural epilepsy. We investigated all patients, who met our inclusion criteria from February 2019 to March 2021. Clinical data was collected from patients electronic medical charts. We analyzed whole brain (wb) connectivity in six frequency bands, calculated three different network topological parameters (node degree (ND), shortest path length (L), clustering coefficient (CC)) and performed a stratification, where differences in the power were to be found. For data analysis we used Fieldtrip, Brain Connectivity Matlab toolboxes and in-house built scripts. We consecutively included 41 patients (21 men), mean age 60.1ys (range 23-82), who were operated on at our institution. Tumor histology included high-grade gliomas (n=18), low-grade gliomas (n=4), dysembryoplastic neuroepithelial tumor (DNET, n=1), BMs (n=14) and others (n=4). Statistical analysis revealed a significant decrease for wb ND in patients compared to healthy controls in every frequency range analyzed at the descriptive and corrected level (p1-30Hz=0.002, p{gamma}=0.002, p{beta}=0.002, p=0.002, p{theta}=0.024, p{delta}=0.002). Furthermore, at the descriptive level, we found a significant augmentation for wb CC (p1-30Hz=0.031, p{delta}=0.013) in PAs compared to HCs, which did not persist the false discovery rate (FDR) correction. There were no differences in the networks of glial brain tumors and metastases identified. However, we found a significant increase in wb CC in patients with structural epilepsy (p{theta}= 0.048), and significantly lower wb ND (p= 0.039) at the uncorrected level. Our data suggests that network topology is altered in brain tumor patients, which is in line with previous studies. Tumor histology per se might not influence the brains functional network, however, tumor-related epilepsy seems to do so. Longitudinal studies and in-depth analysis of possible factors and confounders might be helpful to further substantiate these findings.

neuroscience↗

Age-related changes in 'cortical' 1/f dynamics are explained by cardiac activity

The power of electrophysiologically measured cortical activity decays with an approximately 1/fX function. The slope of this decay (i.e. the spectral exponent, X) is modulated by various factors such as age, cognitive states or psychiatric/neurological disorders. Interestingly, a mostly parallel line of research has also uncovered similar effects for the spectral slope in the electrocardiogram (ECG). This raises the question whether these bodywide changes in spectral slopes are (in-)dependent. Focusing on well-established age-related changes in spectral slopes we analyzed a total of 1282 recordings of magnetoencephalography (MEG) resting state measurements with concurrent ECG in an age-diverse sample (18-88 years). Using a diverse array of analytical approaches, we demonstrate that the aperiodic signal recorded via surface electrodes/sensors originates from multiple physiological sources. Furthermore, our results suggest that common "artifact" rejection approaches (i.e. ICA) may not be sufficient to separate cardiac from neural activity. In particular, significant parts of age-related changes in aperiodic activity normally interpreted to be of neural origin can be explained by cardiac activity. Moreover, our results suggest that changes (flattening/steepening) of the spectral slope with age are dependent on the recording site and investigated frequency range. Our results highlight the complexity of aperiodic activity while raising concerns when interpreting aperiodic activity as "cortical" without considering physiological influences.

neuroscience↗

Allergy-induced systemic inflammation impairs tendon quality

Treatment of tendinopathies still present a major challenge, since the aetiology of the disease remains poorly understood. To determine whether the systemic inflammation accompanying predisposing factors including rheumatoid arthritis, diabetes or smoking contributes to the onset of tendinopathy, we studied the effect of a systemic inflammation induced by an allergic episode on tendon properties. To this end, we elicited an allergic response in mice by exposing them to a plant allergen and subsequently analysed both their flexor and Achilles tendons. Biomechanical testing and histological analysis revealed that tendons from allergic mice not only showed a significant reduction of both elastic modulus and tensile stress, but also alterations of the tendon matrix. Moreover, 3D tendon-like constructs treated with sera from allergic mice displayed a matrix-remodelling expression profile and the expression of macrophage-associated markers and matrix metalloproteinase 2 (MMP2) was increased in allergic Achilles tendons. Analysing data from an epidemiologic study comprising data from more than 10.000 persons, we found that persons suffering from an allergic condition appeared to have an increased propensity to develop a tendinopathy. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=137 SRC="FIGDIR/small/450910v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@1263836org.highwire.dtl.DTLVardef@349621org.highwire.dtl.DTLVardef@6c9142org.highwire.dtl.DTLVardef@1b49bdd_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

Actigraphy in brain-injured patients - A valid measurement for assessing circadian rhythms?

BackgroundActigraphy has received increasing attention in classifying rest-activity cycles. However, in patients with disorders of consciousness (DOC), actigraphy data may be considerably confounded by passive movements, such as nursing activities and therapies. Consequently, this study verified whether circadian rhythmicity is (still) visible in actigraphy data from patients with DOC after correcting for passive movements. MethodsWrist actigraphy was recorded over 7-8 consecutive days in patients with DOC (diagnosed with unresponsive wakefulness syndrome [UWS; n=19] and [exit] minimally conscious state [MCS/EMCS; n=11]). Presence and actions of clinical and research staff as well as visitors were indicated using a tablet in the patients room. Following removal and interpolation of passive movements, non-parametric rank-based tests were computed to identify differences between circadian parameters of uncorrected and corrected actigraphy data. ResultsUncorrected actigraphy data overestimated the interdaily stability and intradaily variability of patients activity and underestimated the deviation from a circadian 24h rhythm. Only 5/30 (17%) patients deviated more than 1h from 24h in the uncorrected data, whereas this was the case for 17/30 (57%) patients in the corrected data. When contrasting diagnoses based on the corrected dataset, stronger circadian rhythms and higher activity levels were observed in MCS/EMCS as compared to UWS patients. Day-to-night differences in activity were evident for both patient groups. ConclusionOur findings indicate that uncorrected actigraphy data overestimates the circadian rhythmicity of patients activity, as nursing activities, therapies, and visits by relatives follow a circadian pattern itself. Therefore, we suggest correcting actigraphy data from patients with reduced mobility.

neuroscience↗