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Catching a killer: Mechanisms of programmed cell death and immune activation in Amyotrophic Lateral Sclerosis

Neel, Dylan V., Basu, Himanish, Gunner, Georgia, Chiu, Isaac M.·2022·Immunological Reviews
DOI 10.1111/imr.13083PMC PMC9489610
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Abstract

In the central nervous system (CNS), execution of programmed cell death (PCD) is crucial for proper neurodevelopment. However, aberrant activation of these pathways in adult CNS leads to neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). How a cell dies is critical, as it can drive local immune activation and tissue damage. Classical apoptosis engages several mechanisms to evoke “immunologically silent” responses, whereas other forms of programmed death such as pyroptosis, necroptosis, and ferroptosis release molecules that can potentiate immune responses and inflammation. In ALS, a fatal neuromuscular disorder marked by progressive death of lower and upper motor neurons, several cell types in the CNS express machinery for multiple PCD pathways. The specific cell types engaging PCD, and ultimate mechanisms by which neuronal death occurs in ALS are not well defined. Here, we provide an overview of different PCD pathways implicated in ALS. We also examine immune activation in ALS and differentiate apoptosis from necrotic mechanisms based on downstream immunological consequences. Lastly, we highlight therapeutic strategies that target cell death pathways in the treatment of neurodegeneration and inflammation in ALS.

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Metadata

Authors
Neel, D. V., Basu, H., Gunner, G., & Chiu, I. M.
Affiliations
Department of Immunology Harvard Medical School Blavatnik Institute Boston Massachusetts USA
ORCID
Venue
Immunological Reviews
Publisher
Wiley
Published
2022-05-07
Volume
311
Issue
1
Pages
130-150
ISSN
  • 0105-2896
  • 1600-065X
DOI
10.1111/imr.13083
PMC
PMC9489610
Cited by
22
References
28
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Funders
  • Chan Zuckerberg Initiative
  • National Institutes of Health (5R01DK127257‐02, 5R01AI130019‐05)
  • Burroughs Wellcome Fund
  • Kenneth Rainin Foundation
  • National Institute of General Medical Sciences (T32GM007753)

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