Taking the parkin brakes off of neuronal NLRP3 drives inflammasome activation and neurodegeneration in Parkinson's disease

Kristine E Zengeler; John R Lukens

doi:10.1016/j.neuron.2022.06.015

Taking the parkin brakes off of neuronal NLRP3 drives inflammasome activation and neurodegeneration in Parkinson's disease

Neuron. 2022 Aug 3;110(15):2356-2358. doi: 10.1016/j.neuron.2022.06.015.

Authors

Kristine E Zengeler¹, John R Lukens²

Affiliations

¹ Center for Brain Immunology and Glia (BIG), Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA; Cell and Molecular Biology Training Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: kez9hf@virginia.edu.
² Center for Brain Immunology and Glia (BIG), Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA; Cell and Molecular Biology Training Program, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: jrl7n@virginia.edu.

PMID: 35926449
DOI: 10.1016/j.neuron.2022.06.015

Abstract

NLRP3 is a central driver of neurodegeneration thought to function mainly in microglia. In this issue of Neuron, Panicker et al. (2022) find that NLRP3 is a parkin substrate that contributes significantly to Parkinson's disease pathogenesis by acting in neurons.

Publication types

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MeSH terms

Humans
Inflammasomes*
Microglia / pathology
NLR Family, Pyrin Domain-Containing 3 Protein
Neurons / pathology
Parkinson Disease* / pathology
Ubiquitin-Protein Ligases / genetics

Substances

Inflammasomes
NLR Family, Pyrin Domain-Containing 3 Protein
Ubiquitin-Protein Ligases