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 language | English |
|---|---|
| Article number | 710 |
| Journal | Frontiers in Neuroscience |
| Volume | 11 |
| Issue number | DEC |
| DOIs | |
| Publication status | Published - Dec 13 2017 |
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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 journal › Short survey
}
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
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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 -