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Huart, C.

Publications and source records attributed to Huart, C..

2 recordsLinked to original sources

Beyond Onset Timing: Longer Sound Envelope Duration Enhances Neural Representation of the Musical Beat

Musical rhythm is often experienced with a periodic beat, serving as a temporal reference for coordination with the rhythm. Thus far, models of beat processing have mainly relied on representing sensory inputs as patterns of onset timing, with limited consideration of other sensory features. Here, we challenge this view by showing that the internal representation of beat is affected by other temporal features of the stimulus beyond onset timing alone. We recorded electroencephalography (EEG) while participants listened to rhythmic sequences designed to elicit a beat. Across conditions, we manipulated the duration of the tones conveying the rhythms, while keeping all other parameters identical, including overall intensity, speed, and rhythmic pattern structure. Crucially, the beat periodicity was enhanced in neural activity with increased sound duration, even though the beat periodicity was not prominent in the acoustic features, thus ruling out basic sensory confounds. These results demonstrate the preferential role of longer sound durations in fostering temporal scaffolding processes that integrate fast rhythmic inputs into behavior-relevant internal structures such as the beat. More generally, our findings are compatible with a holistic processing account whereby a range of features beyond onset timing may be integrated into a neural representation of rhythm. Graphical Abstract: Fig. 2EEG was recorded while listeners heard rhythmic sequences eliciting a beat. Sound duration (sonic duty cycle) was varied across four conditions while speed, pattern, and intensity stayed constant. Beat-related EEG responses increased with longer sounds, and were enhanced in all conditions compared to auditory nerve model envelopes, which did not show prominent energy at the beat periodicity, ruling out sensory confounds. Results support holistic rhythm processing beyond onset timing alone. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=101 SRC="FIGDIR/small/721298v1_fig2.gif" ALT="Figure 2"> View larger version (27K): org.highwire.dtl.DTLVardef@10a0599org.highwire.dtl.DTLVardef@f5a95forg.highwire.dtl.DTLVardef@42d1ceorg.highwire.dtl.DTLVardef@dc58a7_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 2.C_FLOATNO EEG and auditory nerve model output analysis based on magnitude spectrum and autocorrelation. Each row represents a duty cycle condition. The two columns on the left represent the magnitude spectrum-based analysis. The first column represents the group-level averaged magnitude spectra at a pool of fronto-central electrodes, across conditions. Beat-related frequencies are shown in red, and beat-unrelated frequencies are shown in blue. Scalp topographies of the neural activity measured at the average magnitudes of beat-related (in red circle) and unrelated (in blue circle) frequencies are represented as insets. The second column represents the normalized magnitude spectra obtained from the auditory nerve model output for each duty cycle sequence. The two columns on the right represent the autocorrelation-based analysis (for visualization purposes, only a subset of lags from 0 to 2.4 s corresponding to the pattern duration is shown). The first column represents the group-level averaged autocorrelation function measured from the same pool of fronto-central electrodes, across conditions. Beat-related lags are shown in red, and beat-unrelated lags are shown in blue. The second column represents the autocorrelation function of the auditory nerve model output for each duty cycle sequence. C_FIG

neuroscience↗

The Olfactory Epithelium: A Critical Gateway for Pathological Tau Propagation and a Target for Mitigating Tauopathy in the Central Nervous System

Olfactory impairment is a recognized early indicator of neurodegenerative diseases (NDs), such as Alzheimers disease (AD). Intracellular aggregates of hyperphosphorylated tau protein, referred to as neurofibrillary tangles (NFTs), are a hallmark of AD. NFTs are found in the olfactory bulb (OB) and entorhinal cortex (EC), both crucial for processing olfactory information. We explored the hypothesis that typical tau lesions could appear early and progress along olfactory regions to reach connected areas critically affected in AD (e.g. EC and hippocampal formation). To that end, we used transgenic PS19 mice expressing mutated human tau protein (1N4R isoform, P301S mutation). They recapitulate major phenotypes of AD, such as accumulation of NFTs, synaptic dysfunction, cognitive impairment, and neuronal loss. The presence of pathological hyperphosphorylated human tau protein (pTau) was monitored in olfactory regions: olfactory epithelium (OE), OB, piriform cortex (PC), and in connected regions of the hippocampal formation (hippocampus and EC). pTau was detected in the OEs middle stratum and in the OBs olfactory nerve layer (ONL) at 1.5 months. At 6 months of age, tau accumulations were found in the PC and EC, along with the CA3 region and dentate gyrus of the hippocampus. We found that olfactory function remained unaffected in PS19 mice, despite the presence of tau pathology in key regions of the olfactory system. Complete stripping of the OE by intranasal administration of ZnSO4 led to a significant reduction in pretangle-like tau pathology within the PC, amygdala, and EC of 6-month-old PS19 mice. Finally, we observed in human post-mortem samples that pTau signal was present in the olfactory regions (OE and OB) of patients at early Braak stages (I/II). Based on these observations, we propose that pTau could appear, due to ageing or environmental agents, in the OE and subsequently spread in a prion-like manner to the hippocampal formation along neuroanatomical connections. These findings also indicate the interest of the OE as a target for intervention aimed at mitigating the progression of tauopathy in the CNS.

neuroscience↗