Page 251 - MEGIN Book Of Abstracts - 2023

progression. However, results are mostly cross-sectional Whole-Brain Propagation Delays in Multiple
and yet contradictory as putative adaptive and mal- Sclerosis, a Combined Tractography-
adaptive mechanisms were found. Here, we aimed to Magnetoencephalography Study (2022)
explore longitudinal reorganization of brain networks
over 2-years by combining diffusion tensor imaging Sorrentino, P; Petkoski, S; Sparaco, M; Troisi Lopez,
(DTI), resting-state functional MRI (fMRI), magnetoen- E; Signoriello, E; Baselice, F; Bonavita, S; Pirozzi, M A;
cephalography (MEG), and a comprehensive neuropsy- Quarantelli, M; Sorrentino, G; Jirsa, V
chological-battery. In 37 relapsing-remitting MS (RRMS)
and 39 healthy-controls, cognition remained stable Institute of Applied Sciences and Intelligent Systems, National
over-time. We reconstructed network models based Research Council, 80078 Pozzuoli, Italy; Institut de Neurosci-
on the three modalities and analyzed connectivity in ences des Systèmes, Aix-Marseille Université, 13005 Marseille,
relation to the hierarchical topology and functional France; Department of Advanced Medical and Surgical
subnetworks. Network models were compared across Sciences, University of Campania Luigi Vanvitelli, 81100
modalities and in their association with cognition using Caserta, Italy; Department of Motor Sciences and Wellness,
linear-mixed-effect-regression models. Loss of hub Parthenope University of Naples, 80133 Naples, Italy; Depart-
connectivity and global reduction was observed on a ment of Engineering, Parthenope University of Naples, 80143
structural level over-years (p < .010), which was similar Naples, Italy; Biostructure and Bioimaging Institute, National
for functional MEG-networks but not for fMRI-networks. Research Council, 80145 Naples, Italy; Institute for Diagnosis
Structural hub connectivity increased in controls and Cure Hermitage Capodimonte, 80131 Naples, Italy; Insti-
(p = .044), suggesting a physiological mechanism of tut de Neurosciences des Systèmes, Aix-Marseille Université,
healthy aging. Despite a general loss in structural 13005 Marseille, France [email protected]
connectivity in RRMS, hub connectivity was preserved [email protected]
(p = .002) over-time in default-mode-network (DMN).
MEG-networks were similar to DTI and weakly corre- ABSTRACT Two structurally connected brain regions
lated with fMRI in MS (p < .050). Lower structural (β be- are more likely to interact, with the lengths of the
tween .23-.33) and both lower (β between .40-.59) and structural bundles, their widths, myelination, and the
higher functional connectivity (β = -.54) in DMN was topology of the structural connectome influencing
associated with poorer performance in attention and the timing of the interactions. We introduce an in vivo
memory in RRMS (p < .001). MEG-networks involved approach for measuring functional delays across the
no association with cognition. Here, cognitive stability whole brain in humans (of either sex) using magneto/
despite ongoing neurodegeneration might indicate a electroencephalography (MEG/EEG) and integrating
resilience mechanism of DMN hubs mimicking a physi- them with the structural bundles. The resulting topo-
ological reorganization observed in healthy aging. chronic map of the functional delays/velocities shows
that larger bundles have faster velocities. We estimated
Keywords: aging, cognition, connectivity, maladaption/ the topochronic map in multiple sclerosis patients,
adaption, relapsing remitting multiple sclerosis who have damaged myelin sheaths, and controls,
demonstrating greater delays in patients across the
Journal of neuroscience research (2023), Vol. 101, No. 1 network and that structurally lesioned tracts were
(36263462) (0 citations) slowed down more than unaffected ones. We provide
a novel framework for estimating functional transmis-
sion delays in vivo at the single-subject and single-tract
level.SIGNIFICANCE STATEMENT This article provides a
straightforward way to estimate patient-specific delays
and conduction velocities in the CNS, at the individual
level, in healthy and diseased subjects. To do so, it uses

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