Axonal Degeneration: RIPK1 Multitasking in ALS

Kristin Politi; Serge Przedborski

doi:10.1016/j.cub.2016.08.052

Axonal Degeneration: RIPK1 Multitasking in ALS

Curr Biol. 2016 Oct 24;26(20):R932-R934. doi: 10.1016/j.cub.2016.08.052.

Authors

Kristin Politi¹, Serge Przedborski²

Affiliations

¹ Departments of Pathology & Cell Biology, Columbia University Medical Center, 630 West 168(th) Street, New York, NY 10032, USA; The Center for Motor Neuron Biology and Disease, Columbia University Medical Center, 630 West 168(th) Street, New York, NY 10032, USA.
² Departments of Pathology & Cell Biology, Columbia University Medical Center, 630 West 168(th) Street, New York, NY 10032, USA; The Center for Motor Neuron Biology and Disease, Columbia University Medical Center, 630 West 168(th) Street, New York, NY 10032, USA; Department of Neurology, Columbia University Medical Center, 630 West 168(th) Street, New York, NY 10032, USA. Electronic address: [email protected].

PMID: 27780064
DOI: 10.1016/j.cub.2016.08.052

Abstract

A recent study reports that microglia and oligodendrocytes promote motor neuron degeneration by inducing inflammation and necroptosis in a manner dependent on receptor-interacting kinase 1 (RIPK1). These findings could be significant for our understanding of the neurobiology and treatment of neurodegenerative diseases like amyotrophic lateral sclerosis.

Publication types

Comment

MeSH terms

Amyotrophic Lateral Sclerosis*
Apoptosis
Humans
Inflammation
Neurodegenerative Diseases*
Receptor-Interacting Protein Serine-Threonine Kinases

Substances

RIPK1 protein, human
Receptor-Interacting Protein Serine-Threonine Kinases

Supplementary concepts

Amyotrophic Lateral Sclerosis 2, Juvenile