Astrocyte-targeted production of IL-10 induces changes in microglial reactivity and reduces motor neuron death after facial nerve axotomy

Glia ◽  
2015 ◽  
Vol 63 (7) ◽  
pp. 1166-1184 ◽  
Author(s):  
Nàdia Villacampa ◽  
Beatriz Almolda ◽  
Antonietta Vilella ◽  
Iain L. Campbell ◽  
Berta González ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Motor Neuron ◽  
Neuron Death ◽  
Facial Nerve Axotomy ◽  
Motor Neuron Death

scholarly journals Oligodendrocytes contribute to motor neuron death in ALS via SOD1-dependent mechanism

2016 ◽  
Vol 113 (42) ◽  
pp. E6496-E6505 ◽  
Author(s):  
Laura Ferraiuolo ◽  
Kathrin Meyer ◽  
Thomas W. Sherwood ◽  
Jonathan Vick ◽  
Shibi Likhite ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Lactate Production ◽  
Chromosome 9 ◽  
Neuron Death ◽  
Motor Neuron Death ◽  
Repeat Expansions ◽  
Human Oligodendrocytes ◽  
Lateral Sclerosis ◽  
Dependent Mechanism

Oligodendrocytes have recently been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS). Here we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes induce WT motor neuron (MN) hyperexcitability and death. Moreover, we efficiently derived human oligodendrocytes from a large number of controls and patients with sporadic and familial ALS, using two different reprogramming methods. All ALS oligodendrocyte lines induced MN death through conditioned medium (CM) and in coculture. CM-mediated MN death was associated with decreased lactate production and release, whereas toxicity in coculture was lactate-independent, demonstrating that MN survival is mediated not only by soluble factors. Remarkably, human SOD1 shRNA treatment resulted in MN rescue in both mouse and human cultures when knockdown was achieved in progenitor cells, whereas it was ineffective in differentiated oligodendrocytes. In fact, early SOD1 knockdown rescued lactate impairment and cell toxicity in all lines tested, with the exclusion of samples carrying chromosome 9 ORF 72 (C9orf72) repeat expansions. These did not respond to SOD1 knockdown nor did they show lactate release impairment. Our data indicate that SOD1 is directly or indirectly involved in ALS oligodendrocyte pathology and suggest that in this cell type, some damage might be irreversible. In addition, we demonstrate that patients with C9ORF72 represent an independent patient group that might not respond to the same treatment.

Delayed selective motor neuron death and Fas antigen induction after spinal cord ischemia in rabbits

1998 ◽  
Vol 797 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Masahiro Sakurai ◽  
Takeshi Hayashi ◽  
Koji Abe ◽  
Mitsuaki Sadahiro ◽  
Koichi Tabayashi
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Spinal Cord Ischemia ◽  
Neuron Death ◽  
Fas Antigen ◽  
Motor Neuron Death

Axotomy-Induced Motor Neuron Death

1999 ◽  
pp. 181-196
Author(s):  
Jeffrey L. Elliott ◽  
William D. Snider
Keyword(s):  
Motor Neuron ◽  
Neuron Death ◽  
Motor Neuron Death

Influence of grafting a smaller target muscle on the magnitude of naturally occurring trochlear motor neuron death during development

1991 ◽  
Vol 304 (2) ◽  
pp. 187-197 ◽  
Author(s):  
G. S. Sohal ◽  
S. D. Stoney ◽  
L. R. Campbell ◽  
T. Arumugam ◽  
K. Kumaresan ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Neuron Death ◽  
Naturally Occurring ◽  
Motor Neuron Death
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