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...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2017-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/7070469 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832567566483062784 |
|---|---|
| author | Giovanna Morello Antonio Gianmaria Spampinato Sebastiano Cavallaro |
| author_facet | Giovanna Morello Antonio Gianmaria Spampinato Sebastiano Cavallaro |
| author_sort | Giovanna Morello |
| collection | DOAJ |
| 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. |
| format | Article |
| id | doaj-art-186aa9abacdf442993049d00b5957f8c |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-186aa9abacdf442993049d00b5957f8c2025-02-03T01:01:11ZengWileyMediators 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 |
| spellingShingle | Giovanna Morello Antonio Gianmaria Spampinato Sebastiano Cavallaro Neuroinflammation and ALS: Transcriptomic Insights into Molecular Disease Mechanisms and Therapeutic Targets Mediators of Inflammation |
| title | 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_short | 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 |
| url | http://dx.doi.org/10.1155/2017/7070469 |
| work_keys_str_mv | AT giovannamorello neuroinflammationandalstranscriptomicinsightsintomoleculardiseasemechanismsandtherapeutictargets AT antoniogianmariaspampinato neuroinflammationandalstranscriptomicinsightsintomoleculardiseasemechanismsandtherapeutictargets AT sebastianocavallaro neuroinflammationandalstranscriptomicinsightsintomoleculardiseasemechanismsandtherapeutictargets |