Death is a complex affair, at least for cells. There are several ways in which a cell can die: It might commit a form of suicide known as apoptosis, for example, or suffocate to death by necrosis. Further complicating matters is the fact that some cells that appear dead as rocks are in fact in a limbo between life and death—a state from which they might at some point return as transformed versions of their old selves.
An intriguing example of such cellular zombies was recently discovered in the lab of Paul Greengard, a Nobel Laureate and Rockefeller’s Vincent Astor Professor who passed away last year. It happened when a team of scientists were trying to figure out what goes wrong in the brains of people with Parkinson’s disease. Like many others before them, the researchers had long struggled to understand what causes so-called dopaminergic neurons in the midbrain region to perish, leading to debilitating movement problems among other symptoms.
In retrospect, they may have been asking the wrong question. As the scientists reported in Cell Stem Cell, at least some of these midbrain neurons appear not to be dead after all, but to rather be resting in the zombie-like state, known as senescence. And the results suggest that a zombie neuron may be even more damaging to the central nervous system than a dead one: By releasing inflammatory chemicals, the undead cells spread senescence to surrounding healthy neurons and make those neighbors shut down as well.
Research associate Markus Riessland says the discovery was especially surprising given that senescence is almost unheard of among neurons, although it does occur quite frequently in other parts of the body.
“Our findings shed new light on how the disease progresses,” he says “and might provide new opportunities for treatment.” For example, Riessland and his colleagues suspect that so-called senolytic drugs, which are known to remove senescent cells, might make it possible to slow the brain’s deterioration in Parkinson’s patients.