Biology subjects

Pobric, G.

Publications and source records attributed to Pobric, G..

5 recordsLinked to original sources

bioRxiv2026

Altered Aperiodic EEG Activity in Adolescents with Neurofibromatosis Type 1

BackgroundThe balance between excitatory and inhibitory neuronal signalling (E/I balance), proposed as a key mechanism controlling neuronal activity, is disrupted in many neurodevelopmental conditions. One such condition is Neurofibromatosis Type 1, a monogenic neurodevelopmental disorder characterised by increased inhibitory tone. While previous research suggests that E/I balance may be altered in infancy, it is unknown whether E/I balance remains altered during adolescence in NF1. Here we investigated this question using the aperiodic exponent of the resting electroencephalogram (EEG) power spectrum, a proposed electrophysiological index of E/I balance. MethodThe aperiodic exponent of the EEG power spectrum ( 1/f) was estimated for 16 adolescents with NF1 diagnosis aged 11-16, and 16 age- and sex-matched neurotypical controls. General linear models (GLM) were fit to estimate effects of NF1 diagnosis, age and their interaction on aperiodic exponent. We also estimated the peak dominant frequency and power in oscillatory activity of the EEG signal and fitted the same structure of GLM models. Cognitive assessments across domains of memory, executive function and attention were also analysed with GLM to examine brain-cognition associations. ResultsThe NF1 group had higher aperiodic exponent compared to neurotypical controls, but the aperiodic exponent was not associated with cognitive performance. After accounting for aperiodic activity, the NF1 group also had lower dominant oscillatory frequency than the control group. There was no significant interaction between NF1 diagnosis and age on PAF. There were no group differences in peak alpha power. ConclusionsWe demonstrate for the first time that the alterations to aperiodic activity in NF1 are consistent with the proposed mechanism of increased inhibitory tone. These findings show the potential of this paradigm for future pharmacological and brain stimulation trials investigating treatment-related changes in cortical function.

neuroscience↗

bioRxiv2023

The multidimensional neurocognitive geometry in Alzheimer's disease and posterior cortical atrophy

Background and ObjectivesAlzheimers disease spans heterogeneous typical and atypical phenotypes. Posterior cortical atrophy is one striking example, characterised by prominent impairment in visual and other posterior functions in contrast to typical, amnestic Alzheimers disease. The primary study objective was to establish how the similarities and differences of cognition and brain volumes within Alzheimers disease and posterior cortical atrophy (and by extension other Alzheimers disease variants), can be conceptualised as systematic variations across a transdiagnostic, graded multidimensional space. MethodsThis was a cross-sectional, single-center, observational, cohort study performed at the National Hospital for Neurology & Neurosurgery, London, UK. Data were collected from a cohort of PCA and AD patients, matched for age, disease duration and MMSE scores. There were two sets of outcome measures: (1) scores on a neuropsychological battery containing 22 tests spanning visuoperceptual and visuospatial processing, episodic memory, language, executive functions, calculation, and visuospatial processing; and (2) measures extracted from high-resolution T1-weighted volumetric MRI scans. Principal component analysis was used to extract the transdiagnostic dimensions of phenotypical variation from the detailed neuropsychological data. Voxel-based morphometry was used to examine associations between the PCA-derived clinical phenotypes and the structural measures. ResultsWe enrolled 93 PCA participants (mean: age = 59.9 yrs, MMSE = 21.2; 59/93 female) and 58 AD participants (mean: age = 57.1 yrs, MMSE = 19.7; 22/58 female). The principal component analysis for posterior cortical atrophy (sample adequacy confirmed: Kaiser-Meyer-Olkin = 0.865) extracted three dimensions accounting for 61.0% of variance in patients performance, reflecting general cognitive impairment, visuoperceptual deficits and visuospatial impairments. Plotting Alzheimers disease cases into the posterior cortical atrophy-derived multidimensional space, and vice versa, revealed graded, overlapping variations between cases along these dimensions, with no evidence for categorical-like patient clustering. Likewise, the relationship between brain volumes and scores on the extracted dimensions was overlapping for posterior cortical atrophy and Alzheimers disease cases. DiscussionThese results provide evidence supporting a reconceptualization of clinical and radiological variation in these heterogenous Alzheimers disease phenotypes as being along shared phenotypic continua spanning posterior cortical atrophy and Alzheimers disease, arising from systematic graded variations within a transdiagnostic, multidimensional neurocognitive geometry.

neuroscience↗

bioRxiv2022

Transcranial electrical stimulation modulates emotional experience and metabolites in the prefrontal cortex in a donation task

In this study we investigated whether transcranial Direct Current Stimulation (tDCS) applied to two prefrontal cortex regions, the ventromedial prefrontal cortex (vmPFC, anode) and right dorsolateral prefrontal cortex (DLPFC, cathode) can be used to induce changes in self-reported emotions and modulate metabolite concentrations under both electrodes. We employed in vivo quantitative MR Spectroscopy (MRS) in healthy adult participants and quantified the changes in GABA and Glx complex (Glutamate and Glutamine) before and after five sessions of tDCS stimulation. tDCS was delivered at 2mA intensity for 20 minutes for the active group and 1 minute for the sham group. tDCS was applied over five days while participants were engaged in a charitable donation task, known to engage the reward network. We observed increased levels of GABA in vmPFC, but not in DLPFC. Glx levels were decreased in both vmPFC and DLPFC. We found that self-reported happiness increased significantly over time only in the active group. There was a decrease in self-reported guiltiness in both active and sham groups. Altogether, the results indicate that self-reported emotions can be modulated by prefrontal stimulation. This may be because the changes in GABA and Glx concentrations following repeated stimulation induce remote changes in the reward network through interactions with other metabolites, previously thought to be unreachable with noninvasive stimulation techniques.

neuroscience↗

bioRxiv2021

Emotion increases the similarity between neural representations of pictures, but not their perceived similarity.

Stimuli that evoke the same feelings can nevertheless look different and have different semantic meanings. Although we know much about the neural representation of emotion, the neural underpinnings that govern judgements of emotional similarity are unknown. One possibility is that the same brain regions will represent similarity between emotional and neutral stimuli, perhaps with different strengths. Alternatively, emotional similarity could be coded in separate regions, possibly those known to express emotional valence and arousal preferentially. In behaviour, the extent to which people consider similarity along the emotional dimension when they evaluate the overall similarity between stimuli has never been investigated. While the emotional features of stimuli may dominate explicit ratings of similarity, it is also possible that people neglect the emotional dimension as irrelevant. We contrasted these hypotheses with two measures of similarity and two different databases of complex negative and neutral pictures, the second of which afforded exquisite control over semantic and visual attributes. Emotion increased neural similarity in a set of regions that represented both emotional and neutral stimuli, including the inferior temporal cortex, the fusiform face area, and the precuneus. Emotion also increased neural similarity in early visual cortex, anterior insula and dorsal anterior cingulate cortex, despite no increase in BOLD-signal amplitudes in these regions. Despite the stronger neural similarity between emotional stimuli, participants rated pictures taken from two distinct emotional categories as equally similar. These results contribute to our understanding of how emotion is represented within a general conceptual workspace.

neuroscience↗

bioRxiv2019

Graded, multi dimensional intragroup and intergroup variations in primary progressive aphasia and post stroke aphasia.

Language impairments caused by stroke (post-stroke aphasia) and neurodegeneration (primary progressive aphasia) have overlapping symptomatology, nomenclature and are classically divided into categorical subtypes. Surprisingly, primary progressive aphasia (PPA) and post-stroke aphasia (PSA) have rarely been directly compared in detail. Rather previous studies have compared certain subtypes (e.g., semantic variants) or have focussed on a specific cognitive/linguistic task (e.g., reading). This study assessed a large range of linguistic and cognitive tasks across the full spectra of PSA and PPA. We applied varimax-rotated principal component analysis to explore the underlying structure of the variance in the assessment scores. Similar phonological, semantic and fluency-related components were found for PSA and PPA. A combined principal component analysis across the two aetiologies revealed graded intragroup and intergroup variations on all four extracted components. Classification analysis was employed to test, formally, whether there were any categorical boundaries for any subtypes of PPA or PSA. Semantic dementia proved to form a true diagnostic category (i.e., within group homogeneity and distinct between group differences), whereas there was considerable overlap and graded variations within and between other subtypes of PPA and PSA. These results suggest that (a) a multi-dimensional rather than categorical classification system may be a better conceptualisation of aphasia from both causes, and (b) despite the very different types of pathology, these broad classes of aphasia have considerable features in common.

neuroscience↗