The NLRP3 inflammasome protects the host against microbial infections. In this study, Malireddi et al. demonstrate the critical role of TAK1 in restricting RIPK1 signaling to inhibit spontaneous NLRP3 inflammasome activation and cell death, which may be targeted for treatment of myeloid proliferation.

Neuronal cell death in the central nervous system has always been a challenging process to decipher. In physiological condition, neuronal cell death is restricted in the adult brain even as people ages. However, in pathological conditions of various neurodegenerative diseases, the cell death and shrinkage of a specific brain region represent a fundamental pathological feature across different neurodegenerative diseases. In this review, we will briefly go through the general pathways of cell death and describe the evidence of the cell deaths in the context of common neurodegenerative diseases individually, discussing our current understandings of cell death in connecting with the renowned pathogenic proteins, including tau, amyloid-beta, alpha-synuclein, huntingtin, and TDP-43.