Remodeling functional connectivity in multiple sclerosis: A challenging therapeutic approach

Mario Stampanoni Bassi, Luana Gilio, Fabio Buttari, Pierpaolo Maffei, Girolama A. Marfia, Domenico A. Restivo, Diego Centonze, Ennio Iezzi

Research output: Contribution to journalShort survey

Abstract

Neurons in the central nervous system are organized in functional units interconnected to form complex networks. Acute and chronic brain damage disrupts brain connectivity producing neurological signs and/or symptoms. In several neurological diseases, particularly in Multiple Sclerosis (MS), structural imaging studies cannot always demonstrate a clear association between lesion site and clinical disability, originating the "clinico-radiological paradox." The discrepancy between structural damage and disability can be explained by a complex network perspective. Both brain networks architecture and synaptic plasticity may play important roles in modulating brain networks efficiency after brain damage. In particular, long-term potentiation (LTP) may occur in surviving neurons to compensate network disconnection. In MS, inflammatory cytokines dramatically interfere with synaptic transmission and plasticity. Importantly, in addition to acute and chronic structural damage, inflammation could contribute to reduce brain networks efficiency in MS leading to worse clinical recovery after a relapse and worse disease progression. These evidence suggest that removing inflammation should represent the main therapeutic target in MS; moreover, as synaptic plasticity is particularly altered by inflammation, specific strategies aimed at promoting LTP mechanisms could be effective for enhancing clinical recovery. Modulation of plasticity with different non-invasive brain stimulation (NIBS) techniques has been used to promote recovery of MS symptoms. Better knowledge of features inducing brain disconnection in MS is crucial to design specific strategies to promote recovery and use NIBS with an increasingly tailored approach.

Original languageEnglish
Article number710
JournalFrontiers in Neuroscience
Volume11
Issue numberDEC
DOIs
Publication statusPublished - Dec 13 2017

Fingerprint

Multiple Sclerosis
Brain
Neuronal Plasticity
Long-Term Potentiation
Therapeutics
Inflammation
Chronic Brain Damage
Neurons
Synaptic Transmission
Signs and Symptoms
Disease Progression
Central Nervous System
Cytokines
Recurrence

Keywords

  • Brain networks
  • Functional connectivity
  • Inflammation
  • Multiple sclerosis
  • Non-invasive brain stimulation
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Remodeling functional connectivity in multiple sclerosis : A challenging therapeutic approach. / Bassi, Mario Stampanoni; Gilio, Luana; Buttari, Fabio; Maffei, Pierpaolo; Marfia, Girolama A.; Restivo, Domenico A.; Centonze, Diego; Iezzi, Ennio.

In: Frontiers in Neuroscience, Vol. 11, No. DEC, 710, 13.12.2017.

Research output: Contribution to journalShort survey

@article{53d26bedfdc547ad92fc761378f00b6b,
title = "Remodeling functional connectivity in multiple sclerosis: A challenging therapeutic approach",
abstract = "Neurons in the central nervous system are organized in functional units interconnected to form complex networks. Acute and chronic brain damage disrupts brain connectivity producing neurological signs and/or symptoms. In several neurological diseases, particularly in Multiple Sclerosis (MS), structural imaging studies cannot always demonstrate a clear association between lesion site and clinical disability, originating the {"}clinico-radiological paradox.{"} The discrepancy between structural damage and disability can be explained by a complex network perspective. Both brain networks architecture and synaptic plasticity may play important roles in modulating brain networks efficiency after brain damage. In particular, long-term potentiation (LTP) may occur in surviving neurons to compensate network disconnection. In MS, inflammatory cytokines dramatically interfere with synaptic transmission and plasticity. Importantly, in addition to acute and chronic structural damage, inflammation could contribute to reduce brain networks efficiency in MS leading to worse clinical recovery after a relapse and worse disease progression. These evidence suggest that removing inflammation should represent the main therapeutic target in MS; moreover, as synaptic plasticity is particularly altered by inflammation, specific strategies aimed at promoting LTP mechanisms could be effective for enhancing clinical recovery. Modulation of plasticity with different non-invasive brain stimulation (NIBS) techniques has been used to promote recovery of MS symptoms. Better knowledge of features inducing brain disconnection in MS is crucial to design specific strategies to promote recovery and use NIBS with an increasingly tailored approach.",
keywords = "Brain networks, Functional connectivity, Inflammation, Multiple sclerosis, Non-invasive brain stimulation, Synaptic plasticity",
author = "Bassi, {Mario Stampanoni} and Luana Gilio and Fabio Buttari and Pierpaolo Maffei and Marfia, {Girolama A.} and Restivo, {Domenico A.} and Diego Centonze and Ennio Iezzi",
year = "2017",
month = "12",
day = "13",
doi = "10.3389/fnins.2017.00710",
language = "English",
volume = "11",
journal = "Frontiers in Neuroscience",
issn = "1662-4548",
publisher = "Frontiers Media S.A.",
number = "DEC",

}

TY - JOUR

T1 - Remodeling functional connectivity in multiple sclerosis

T2 - A challenging therapeutic approach

AU - Bassi, Mario Stampanoni

AU - Gilio, Luana

AU - Buttari, Fabio

AU - Maffei, Pierpaolo

AU - Marfia, Girolama A.

AU - Restivo, Domenico A.

AU - Centonze, Diego

AU - Iezzi, Ennio

PY - 2017/12/13

Y1 - 2017/12/13

N2 - Neurons in the central nervous system are organized in functional units interconnected to form complex networks. Acute and chronic brain damage disrupts brain connectivity producing neurological signs and/or symptoms. In several neurological diseases, particularly in Multiple Sclerosis (MS), structural imaging studies cannot always demonstrate a clear association between lesion site and clinical disability, originating the "clinico-radiological paradox." The discrepancy between structural damage and disability can be explained by a complex network perspective. Both brain networks architecture and synaptic plasticity may play important roles in modulating brain networks efficiency after brain damage. In particular, long-term potentiation (LTP) may occur in surviving neurons to compensate network disconnection. In MS, inflammatory cytokines dramatically interfere with synaptic transmission and plasticity. Importantly, in addition to acute and chronic structural damage, inflammation could contribute to reduce brain networks efficiency in MS leading to worse clinical recovery after a relapse and worse disease progression. These evidence suggest that removing inflammation should represent the main therapeutic target in MS; moreover, as synaptic plasticity is particularly altered by inflammation, specific strategies aimed at promoting LTP mechanisms could be effective for enhancing clinical recovery. Modulation of plasticity with different non-invasive brain stimulation (NIBS) techniques has been used to promote recovery of MS symptoms. Better knowledge of features inducing brain disconnection in MS is crucial to design specific strategies to promote recovery and use NIBS with an increasingly tailored approach.

AB - Neurons in the central nervous system are organized in functional units interconnected to form complex networks. Acute and chronic brain damage disrupts brain connectivity producing neurological signs and/or symptoms. In several neurological diseases, particularly in Multiple Sclerosis (MS), structural imaging studies cannot always demonstrate a clear association between lesion site and clinical disability, originating the "clinico-radiological paradox." The discrepancy between structural damage and disability can be explained by a complex network perspective. Both brain networks architecture and synaptic plasticity may play important roles in modulating brain networks efficiency after brain damage. In particular, long-term potentiation (LTP) may occur in surviving neurons to compensate network disconnection. In MS, inflammatory cytokines dramatically interfere with synaptic transmission and plasticity. Importantly, in addition to acute and chronic structural damage, inflammation could contribute to reduce brain networks efficiency in MS leading to worse clinical recovery after a relapse and worse disease progression. These evidence suggest that removing inflammation should represent the main therapeutic target in MS; moreover, as synaptic plasticity is particularly altered by inflammation, specific strategies aimed at promoting LTP mechanisms could be effective for enhancing clinical recovery. Modulation of plasticity with different non-invasive brain stimulation (NIBS) techniques has been used to promote recovery of MS symptoms. Better knowledge of features inducing brain disconnection in MS is crucial to design specific strategies to promote recovery and use NIBS with an increasingly tailored approach.

KW - Brain networks

KW - Functional connectivity

KW - Inflammation

KW - Multiple sclerosis

KW - Non-invasive brain stimulation

KW - Synaptic plasticity

UR - http://www.scopus.com/inward/record.url?scp=85037977924&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85037977924&partnerID=8YFLogxK

U2 - 10.3389/fnins.2017.00710

DO - 10.3389/fnins.2017.00710

M3 - Short survey

AN - SCOPUS:85037977924

VL - 11

JO - Frontiers in Neuroscience

JF - Frontiers in Neuroscience

SN - 1662-4548

IS - DEC

M1 - 710

ER -