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.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system characterized by demyelination and neurodegeneration
These data show that inflammation in MS is associated with a profound alteration of synaptic plasticity mainly characterized by impaired long-term potentiation (LTP) and overexpressed synaptic upscaling
Acute optic neuritis has been associated with reduced FC in the visual system and altered connectivity between visual and non-visual networks, indicating rapid connectivity changes in response to focal inflammation [79]; in addition, both reduced and increased FC has been reported in clinically isolated syndrome (CIS) patients without brain lesions [64], suggesting that central nervous system (CNS) inflammation may represent a prominent cause of connectivity dysfunction in MS [7]
Summary
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system characterized by demyelination and neurodegeneration. Different mechanisms contribute to this “clinico-radiological paradox” and both synaptic plasticity and brain networks architecture may play an important role, influencing resilience to damage. A growing number of studies have demonstrated that the organization of brain networks is highly specialized and reveals specific features evolved to improve efficiency, containing the wiring cost. This architecture protects networks from random attacks and is useful for optimal reorganization after damage [8,9]. Experimental and clinical studies have clearly shown that the efficiency of synaptic plasticity mechanisms, of long-term potentiation (LTP), influences the chances of recovery after damage [10,11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
