Despite indisputable progress in the molecular and genetic aspects of amyotrophic lateral sclerosis (ALS), a mechanistic comprehension of the neurodegenerative processes typical of this disorder is still missing and no effective cures to halt the progression of this pathology have yet been developed. Therefore, it seems that a substantial improvement of the outcome of ALS treatments may depend on a better understanding of the molecular mechanisms underlying neuronal pathology and survival as well as on the establishment of novel etiological therapeutic strategies. Noteworthy, a convergence of recent data from multiple studies suggests that, in cellular and animal models of ALS, a complex pathological interplay subsists between motor neurons and their non-neuronal neighbours, particularly glial cells. These observations not only have drawn attention to the physiopathological changes glial cells undergo during ALS progression, but they have moved the focus of the investigations from intrinsic defects and weakening of motor neurons to glia-neuron interactions. In this review, we summarize the growing body of evidence supporting the concept that different glial populations are critically involved in the dreadful chain of events leading to motor neuron sufferance and death in various forms of ALS. The outlined observations strongly suggest that glial cells can be the targets for novel therapeutic interventions in ALS. © 2013 Springer Basel

Valori, C., Brambilla, L., Martorana, F., Rossi, D. (2014). The multifaceted role of glial cells in amyotrophic lateral sclerosis. CELLULAR AND MOLECULAR LIFE SCIENCES, 71(2), 287-297 [10.1007/s00018-013-1429-7].

The multifaceted role of glial cells in amyotrophic lateral sclerosis

Martorana, Francesca;
2014

Abstract

Despite indisputable progress in the molecular and genetic aspects of amyotrophic lateral sclerosis (ALS), a mechanistic comprehension of the neurodegenerative processes typical of this disorder is still missing and no effective cures to halt the progression of this pathology have yet been developed. Therefore, it seems that a substantial improvement of the outcome of ALS treatments may depend on a better understanding of the molecular mechanisms underlying neuronal pathology and survival as well as on the establishment of novel etiological therapeutic strategies. Noteworthy, a convergence of recent data from multiple studies suggests that, in cellular and animal models of ALS, a complex pathological interplay subsists between motor neurons and their non-neuronal neighbours, particularly glial cells. These observations not only have drawn attention to the physiopathological changes glial cells undergo during ALS progression, but they have moved the focus of the investigations from intrinsic defects and weakening of motor neurons to glia-neuron interactions. In this review, we summarize the growing body of evidence supporting the concept that different glial populations are critically involved in the dreadful chain of events leading to motor neuron sufferance and death in various forms of ALS. The outlined observations strongly suggest that glial cells can be the targets for novel therapeutic interventions in ALS. © 2013 Springer Basel
Articolo in rivista - Articolo scientifico
Amyotrophic lateral sclerosis; Astrocytes; Glia; Microglia; Neurodegeneration; Transgenic animals; Amyotrophic Lateral Sclerosis; Animals; Astrocytes; DNA-Binding Proteins; Disease Models, Animal; Humans; Microglia; Oligodendroglia; RNA-Binding Protein FUS; Superoxide Dismutase; Transcription Factor TFIIIA; Cell Biology; Molecular Biology; Molecular Medicine; Pharmacology; Cellular and Molecular Neuroscience
English
2014
71
2
287
297
none
Valori, C., Brambilla, L., Martorana, F., Rossi, D. (2014). The multifaceted role of glial cells in amyotrophic lateral sclerosis. CELLULAR AND MOLECULAR LIFE SCIENCES, 71(2), 287-297 [10.1007/s00018-013-1429-7].
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/105746
Citazioni
  • Scopus 72
  • ???jsp.display-item.citation.isi??? 66
Social impact