Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting the motor nervous system. Despite the mechanism underlying motor neuron death is not yet clarified, multiple pathogenic processes have been proposed to account for ALS. Among these, inflammatory/immune responses have recent...

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Main Authors: Giovanna Morello, Antonio Gianmaria Spampinato, Sebastiano Cavallaro
Format: Article
Language:English
Published: Hindawi Limited 2017-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2017/7070469
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spelling doaj-186aa9abacdf442993049d00b5957f8c2020-11-24T22:48:13ZengHindawi LimitedMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/70704697070469Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic TargetsGiovanna Morello0Antonio Gianmaria Spampinato1Sebastiano Cavallaro2Institute of Neurological Sciences, Italian National Research Council, Catania, ItalyInstitute of Neurological Sciences, Italian National Research Council, Catania, ItalyInstitute of Neurological Sciences, Italian National Research Council, Catania, ItalyAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting the motor nervous system. Despite the mechanism underlying motor neuron death is not yet clarified, multiple pathogenic processes have been proposed to account for ALS. Among these, inflammatory/immune responses have recently gained particular interest, although there are conflicting reports on the role of these processes in ALS pathogenesis and treatment. This apparent discrepancy may be due to the absence of an effective stratification of ALS patients into subgroups with markedly different clinical, biological, and molecular features. Our research group recently described genome-wide characterization of motor cortex samples from sporadic ALS (SALS) patients, revealing the existence of molecular and functional heterogeneity in SALS. Here, we reexamine data coming from our previous work, focusing on transcriptomic changes of inflammatory-related genes, in order to investigate their potential contribution in ALS. A total of 1573 inflammatory genes were identified as differentially expressed between SALS patients and controls, characterizing distinct topological pathways and networks, suggestive of specific inflammatory molecular signatures for different patient subgroups. Besides providing promising insights into the intricate relationship between inflammation and ALS, this paper represents a starting point for the rationale design and development of novel and more effective diagnostic and therapeutic applications.http://dx.doi.org/10.1155/2017/7070469
collection DOAJ
language English
format Article
sources DOAJ
author Giovanna Morello
Antonio Gianmaria Spampinato
Sebastiano Cavallaro
spellingShingle Giovanna Morello
Antonio Gianmaria Spampinato
Sebastiano Cavallaro
Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets
Mediators of Inflammation
author_facet Giovanna Morello
Antonio Gianmaria Spampinato
Sebastiano Cavallaro
author_sort Giovanna Morello
title Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets
title_short Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets
title_full Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets
title_fullStr Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets
title_full_unstemmed Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets
title_sort neuroinflammation and als: transcriptomic insights into molecular disease mechanisms and therapeutic targets
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2017-01-01
description Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting the motor nervous system. Despite the mechanism underlying motor neuron death is not yet clarified, multiple pathogenic processes have been proposed to account for ALS. Among these, inflammatory/immune responses have recently gained particular interest, although there are conflicting reports on the role of these processes in ALS pathogenesis and treatment. This apparent discrepancy may be due to the absence of an effective stratification of ALS patients into subgroups with markedly different clinical, biological, and molecular features. Our research group recently described genome-wide characterization of motor cortex samples from sporadic ALS (SALS) patients, revealing the existence of molecular and functional heterogeneity in SALS. Here, we reexamine data coming from our previous work, focusing on transcriptomic changes of inflammatory-related genes, in order to investigate their potential contribution in ALS. A total of 1573 inflammatory genes were identified as differentially expressed between SALS patients and controls, characterizing distinct topological pathways and networks, suggestive of specific inflammatory molecular signatures for different patient subgroups. Besides providing promising insights into the intricate relationship between inflammation and ALS, this paper represents a starting point for the rationale design and development of novel and more effective diagnostic and therapeutic applications.
url http://dx.doi.org/10.1155/2017/7070469
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