Modeling Resilience to Damage in Multiple Sclerosis: Plasticity Meets Connectivity

Mario Stampanoni Bassi, Ennio Iezzi, Luigi Pavone, Georgia Mandolesi, Alessandra Musella, Antonietta Gentile, Luana Gilio, Diego Centonze, Fabio Buttari

Research output: Contribution to journalReview articlepeer-review

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by demyelinating white matter lesions and neurodegeneration, with a variable clinical course. Brain network architecture provides efficient information processing and resilience to damage. The peculiar organization characterized by a low number of highly connected nodes (hubs) confers high resistance to random damage. Anti-homeostatic synaptic plasticity, in particular long-term potentiation (LTP), represents one of the main physiological mechanisms underlying clinical recovery after brain damage. Different types of synaptic plasticity, including both anti-homeostatic and homeostatic mechanisms (synaptic scaling), contribute to shape brain networks. In MS, altered synaptic functioning induced by inflammatory mediators may represent a further cause of brain network collapse in addition to demyelination and grey matter atrophy. We propose that impaired LTP expression and pathologically enhanced upscaling may contribute to disrupting brain network topology in MS, weakening resilience to damage and negatively influencing the disease course.

Original languageEnglish
JournalInternational Journal of Molecular Sciences
Volume21
Issue number1
DOIs
Publication statusPublished - Dec 24 2019

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