Death Spreads From Cell To Cell In A Wave: How New Findings Show Old-Age Deaths Happen From Multiple Processes Breaking Down
In contrast to cell death, the processes leading to an organism's systemic collapse are less understood. This has prompted researchers to examine the nature of death in one organism's cells as the necrosis propagates throughout its entire body, the findings for which could shed considerable light on how human death takes place, especially in old age.
The new study, which comes from the Institute of Health Aging at University College London, paints death as a wave of cell necrosis that spreads across the body like a cascade. Using nematodes as the basis for their study, researchers examined the way a unique molecule emitted a fluorescent blue light as the worms' cells died. This molecule is similar to a product of oxidative damage in mammals that have died of old age.
"In the nematode Caenorhabditis elegans, intestinal lysosome-related organelles (or "gut granules") contain a bright blue fluorescent substance of unknown identity," wrote the researchers. "This has similar spectral properties to lipofuscin, a product of oxidative damage known to accumulate with age in postmitotic mammalian cells."
The researchers' theory assumes that people in old-age could have multiple processes whose cell pathways are dying and that age-related deaths are effectively the result of parallel waves of cell deaths. Despite not knowing which processes are taking place simultaneously, the findings bode well for understanding the nature of death as a gradual wave because of multiple processes, not a consequence of accumulated molecular damage.
"We've identified a chemical pathway of self-destruction that propagates cell death in worms, which we see as this glowing blue fluorescence traveling through the body," David Gems, the study's lead author, told Discovery News. "It's like a blue grim reaper, tracking death as it spreads throughout the organism until all life is extinguished."
The implications for such a finding suggest the ability to delay death, or even stop it, in cases where infections cause mass necrosis. Old-age death works in ways that are less well-known, so the technique cannot apply.
"We found that when we blocked this pathway, we could delay death induced by a stress such as infection, but we couldn't slow death from old-age," Gems said, referring to the stress cells undergo when they're required to perform at higher intensities than a body is equipped for — extreme temperatures being one example. "This suggests that aging causes death by a number of processes acting in parallel."
Gems expressed great optimism for the future of studying cell death as it applies to old-age necrosis, as the parallel processes not yet understood could provide groundbreaking opportunities for fighting infections and preserving life into old-age.
"Inhibition of necrosis pathway components can delay stress-induced death, supporting its role as a driver of organismal death," the researchers concluded. "This necrotic cascade provides a model system to study neurodegeneration and organismal death."
Source: Coburn C, Allman E, Mahanti P. Anthranilate Fluorescence Marks a Calcium-Propagated Necrotic Wave That Promotes Organismal Death in C. elegans. PLoS Biology. 2013.