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Vidailhet, M.

Publications and source records attributed to Vidailhet, M..

4 recordsLinked to original sources

Saccadic network dysfunction underlies eye-movement variability in early Parkinson's disease

Parkinsons disease is a neurodegenerative disorder characterized by altered subcortical-cortical connectivity, leading to motor and cognitive deficits. Saccadic eye movement abnormalities are among the earliest and most persistent markers of the disease, serving as sensitive indicators of disrupted oculomotor and cognitive control. While changes in average saccadic behavioral measures are widely reported in Parkinson's disease, intra-individual variability in saccadic performance and the underlying network dysfunction remain poorly understood. Here, we quantified intra-individual saccadic variability in early-stage Parkinsons disease and identified its functional correlates within the resting-state saccadic network. We analyzed data from 91 patients with early-stage Parkinsons disease and 46 healthy controls who underwent oculomotor testing and resting-state functional magnetic resonance imaging. First, at the behavioral level, we assessed intra-individual variability in saccadic performance within each group using the coefficient of variation of reaction time and normalized peak velocity across trials. Second, at the brain level, we assessed group differences in static and dynamic functional connectivity across 39 regions comprising the saccadic network. We examined the relationship between network connectivity and saccadic variability using partial least squares analysis. We also quantified network organization using graph-theory measures of global efficiency and clustering coefficient. Finally, we tested the relevance of intra-individual saccadic variability and network features in distinguishing patients from healthy controls using a multivariate Mahalanobis classifier. Our results showed that, compared to HC, patients had higher intra-individual variability in saccadic behavioral measures of reaction time (pHolm = 0.012) and normalized peak velocity (pHolm = 0.012). Interestingly, patients had (i) reduced static and dynamic connectivity within the saccadic network and (ii) weaker associations between network connectivity and intra-individual saccadic variability of specifically normalized peak velocity. These results were particularly driven by regions within the cognitive saccade network. The classifier that integrated intra-individual saccadic variability and network connectivity achieved 95.62% accuracy in distinguishing patients from healthy controls, with dynamic connectivity contributing more strongly to classification performance than static connectivity. We demonstrate that elevated intra-individual variability of saccades, underpinned by altered functional connectivity within cognitive-oculomotor networks, is a prominent feature of early-stage Parkinsons disease. Emerging as a promising physiological marker of disease pathophysiology, intra-individual variability offers a powerful new framework to refine early diagnosis and improve the tracking of neurodegeneration before severe clinical milestones are reached.

neuroscience↗

The role of dopaminergic, cholinergic and noradrenergic networks in hyposmia in Parkinson's disease

BackgroundOlfactory impairment is frequently observed in Parkinsons disease (PD) before motor symptom onset. Patients with isolated rapid eye movement sleep behaviour disorder (iRBD) are at risk to develop PD and present olfactory dysfunction. Subcortical neuromodulatory nuclei including the substantia nigra, the nucleus basalis of Meynert, and the locus coeruleus, may all contribute to olfactory dysfunction. ObjectiveThe objective of this study was to understand the network alterations underlying olfactory dysfunction in PD and in the early prodromal iRBD patients using multimodal MRI. MethodsPD (n = 107), iRBD patients (n = 35) and healthy controls (HC, n = 39) were recruited from the ICEBERG cohort for a cross-sectional study. We separated subjects in Healthy Controls, iRBD patients, and PD patients with or without RBD and with or without anosmia. Olfactory, motor, and cognitive scores were assessed and combined with multimodal imaging. ResultsWe found that olfaction positively correlated with (i) striatal DaT signal in PD patients; (ii) neuromelanin contrast in the locus coeruleus and (iii) Nucleus Basalis of Meynert grey matter (GM) volume in all patients. These signals were uncorrelated with motor and cognitive scores. Functional connectivity was reduced in regions of the cholinergic olfactory network in anosmic patients. Functional connectivity was also reduced in the noradrenergic network of patients with RBD. DiscussionOur results indicate the implication of the cholinergic network in PD patients with anosmia and a contribution of the noradrenergic network to olfactory dysfunction, only in patients with RBD.

neuroscience↗

Longitudinal neuromelanin changes in prodromal and early Parkinson's disease in humans and rat model

Studies in animal models of Parkinsons disease (PD) suggested that the accumulation of the neuromelanin (NM), a pigment contained in nigral dopaminergic neurons, could trigger neurodegeneration above a pathogenic threshold. Here we investigated this hypothesis using NM-sensitive MRI in rodents and in patients with isolated rapid eye movement sleep disorders (iRBD) subjects, a prodromal phase of parkinsonism, and early PD. We first combined NM-sensitive MRI and histology to study NM accumulation and neurodegeneration in a humanized rat model of PD. NM-MRI signal changes were biphasic with an initial increase due to the accumulation of NM in dopaminergic neurons, followed signal decrease due to neurodegeneration. In healthy subjects and patients with iRBD, NM-MRI signal increased initially and then decreased similarly as in rodents after reaching a similar maximum signal intensity in both groups. In early PD and converted iRBD patients, NM-MRI signal drop was greater than in healthy individuals. Results in animals and humans show that NM-sensitive MRI is a marker of the intracellular NM accumulation up to a threshold then of neuronal degeneration beyond this threshold and agree with the hypothesis of a pathogenic threshold of NM triggering neurodegeneration.

neuroscience↗

Loss of floor plate Netrin-1 impairs midline crossing of corticospinal axons and leads to mirror movements

In human, execution of unimanual movements requires lateralized activation of the primary motor cortex, which then transmits the motor command to the contralateral hand through the crossed corticospinal tract (CST). Mutations in NETRIN-1 alter motor control lateralization, leading to congenital mirror movements. To address the role of midline Netrin-1 on CST development and subsequent motor control, we analyzed the morphological and functional consequences of floor-plate Netrin-1 depletion in conditional knock-out mice (Shh::cre;Ntn1lox/lox mice). Here, we show that depletion of floor plate Netrin-1 critically disrupts midline crossing of the CST, whereas the other commissural systems are mostly preserved. The CST defect results in abnormal but functional ipsilateral projections, and is associated with abnormal symmetric movements. Therefore, our study reveals a new role for Netrin-1 in CST development. It also describes a unique mouse model recapitulating characteristics of human congenital mirror movements, through abnormal CST decussation.

neuroscience↗