Necrotic cell death and neurodegeneration

  title={Necrotic cell death and neurodegeneration},
  author={Kostoula Troulinaki and Nektarios Tavernarakis},
  pages={176 - 181}
Necrosis, one of the two main types of cell death, contributes critically in many devastating pathological conditions in human, including stroke, ischemia, trauma and neurodegenerative diseases. However, unlike apoptosis, the molecular mechanisms underlying necrotic cell death and neurodegeneration are poorly understood. Caenorhabditis elegans offers a powerful platform for a thorough and systematic dissection of the molecular basis of necrotic cell death. Similarly to humans, neuronal necrosis… 

Necrotic Cell Death in Caenorhabditis elegans

This chapter surveys necrosis paradigms that have been characterized in the nematode and outlines the cellular and molecular mechanisms implicated in mediating cell demise, and discusses experimental approaches that utilize C. elegans to elucidate the molecular underpinnings of devastating human disorders that entail necrosis.

Necrotic cell death in Caenorhabditis elegans.

The Role of Ca2+ Signaling in Aging and Neurodegeneration: Insights from Caenorhabditis elegans Models

The evidence obtained using this model organism to understand the role of Ca2+ signaling in aging and neurodegeneration is summarized.

Transcriptomic Analyses Reveal Differential Gene Expression of Immune and Cell Death Pathways in the Brains of Mice Infected with West Nile Virus and Chikungunya Virus

Evidence for a strong inflammatory response was found in mice infected with WNV and CHIKV and strong overlap with the mRNA profile described in the literature for other viral neuroinvasive diseases was measured.

The emerging roles of protein homeostasis‐governing pathways in Alzheimer's disease

Targeting the components of proteostasis pathways may be a promising therapeutic strategy against Alzheimer's disease.

Lysosomal storage disorders and neurodegenerative disease; related mechanisms of pathogenesis and identification of novel therapeutic targets

The study of models of Huntington’s disease have implicated the Niemann-Pick type C1 protein (NPC1) in the pathogenesis of this disease and identified ways in which this could be therapeutically targeted and new therapeutic targets have been identified by these studies.

Bacillus thuringiensis Crystal Protein Cry6Aa Triggers Caenorhabditis elegans Necrosis Pathway Mediated by Aspartic Protease (ASP-1)

This is the first demonstration that deficiency in necrosis pathway confers tolerance to Bt crystal protein, and that Cry6A triggers necrosis represents a newly added necrosis paradigm in the C. elegans model, which could lead to new strategies for nematode control.



Endocytosis and intracellular trafficking contribute to necrotic neurodegeneration in C. elegans

A prominent role for endocytosis in cellular destruction during neurodegeneration is demonstrated, which is likely conserved in metazoans.

Ischemic cell death in brain neurons.

A major unifying thread of the review is a consideration of how the changes occurring during and after ischemia conspire to produce damaging levels of free radicals and peroxynitrite to activate calpain and other Ca(2+)-driven processes that are damaging, and to initiate the apoptotic process.

Autophagy and cell death in Caenorhabditis elegans.

Comparative analysis suggests that the involvement of autophagy in cell death is evolutionary conserved in metazoans, and interfering with the autophagic process may facilitate therapeutic intervention in human pathologies where aberrant cellDeath is a contributing factor.

Lysosomal biogenesis and function is critical for necrotic cell death in Caenorhabditis elegans

A genetically encoded fluorescent marker is used to follow lysosome fate during neurodegeneration in vivo and demonstrates a prominent role in cellular destruction during necrotic cell death, which is likely conserved in metazoans.

The biochemistry of neuronal necrosis: rogue biology?

The mechanisms that are implicated in necrosis are reviewed and the events that transform them to catastrophic for cell survival are discussed, which are crucial to the damage that injury and disease inflict on the nervous system.

Autophagy is required for necrotic cell death in Caenorhabditis elegans

It is found that excessive autophagosome formation is induced early during necrotic cell death in C. elegans, demonstrating that autophagy contributes to cellular destruction during necrosis.

Non‐apoptotic cell death in Caenorhabditis elegans

The literature on the various types of non‐apoptotic cell death in C. elegans is reviewed and the implications, relevant to pathological conditions in humans are discussed.

Neuropathology of Degenerative Cell Death in Caenorhabditis elegans

The ultrastructural changes in these deaths suggest that enhanced membrane cycling precedes vacuolation and cell swelling, and shares features with that of genetic disorders with alterations in channel subunits, such as hypokalemic periodic paralysis in humans and the weaver mouse.

Specific aspartyl and calpain proteases are required for neurodegeneration in C. elegans

It is reported that neuronal degeneration inflicted by various genetic lesions in C. elegans requires the activity of the calcium-regulated CLP-1 and TRA-3 calpain proteases and aspartyl proteases ASP-3 and ASP-4 and suggested that perturbation of intracellular concentrations of calcium may initiate neuronal degenerations by deregulating proteolysis.