Seeing the dead causes rapid aging in flies, according to study

Gaining a better understanding of insect neural circuits can help regulate aging through targeted drug therapies in humans and slow the aging process. 

Additionally, such neural underpinnings could determine how perception could affect human physiology. 

The mechanics

A specific group of brain cells in flies, R2 and R4 neurons are activated when flies encounter other dead flies. This activation of neurons causes the fly to age more rapidly. 

The researchers observed that brain activity in those flies increased when the active flies were exposed to dead fruit flies. This advanced aging in living flies depends on serotonin receptors.

The serotonin receptor 5-HT2A represents the neural population in the ellipsoid body (EB) of the fly’s central complex, is identified as R2 and R4 neurons. Silencing the neurons have determined to be necessary for the effect.

According to the study, “neurons act as a rheostat and plays an important role in transducing sensory information about the presence of dead individuals to modulate life span.”

Death perception

The scientific research was conducted through a set of experiments. The press release states, “When these R2 and R4 neurons were artificially activated, fruit fly lifespans decreased even when the fly did not experience any death perception.”

The presence of a protein called foxo in certain neurons, as well as the production of specific insulin-like peptides, called dilp3 and dilp5 (but not dilp2), are necessary to regulate the process. It seems that dilp2 may be affected in certain cells of the brain after the activation of these specific neurons.

Furthermore, the findings suggested that peptides don't affect foxo activity directly in the R2 and R4 neurons.

This injunction is allowing researchers to compare the driving forces behind the physiological effects of death exposure and the biological mechanisms in animals.

The study aims to understand animals' biological responses to relevant sensory inputs.

Comprehending the animal control system could help modulate lifespan in humans, the study claims, "Our results may provide insight for treating individuals who are routinely exposed to stressful situations surrounding death, including active combat soldiers and first responders."

The study published on 13 June can be accessed here.

Abstract

Sensory perception modulates aging, yet we know little about how. An understanding of the neuronal mechanisms through which animals orchestrate biological responses to relevant sensory inputs would provide insight into the control systems that may be important for modulating lifespan. Here, we provide new awareness into how the perception of dead conspecifics, or death perception, which elicits behavioral and physiological effects in many different species, affects lifespan in the fruit fly, Drosophila melanogaster. Previous work demonstrated that cohousing Drosophila with dead conspecifics decreases fat stores, reduces starvation resistance, and accelerates aging in a manner that requires both sight and the serotonin receptor 5-HT2A. In this manuscript, we demonstrate that a discrete, 5-HT2A-expressing neural population in the ellipsoid body (EB) of the Drosophila central complex, identified as R2/R4 neurons, acts as a rheostat and plays an important role in transducing sensory information about the presence of dead individuals to modulate life- span. Expression of the insulin-responsive transcription factor foxo in R2/R4 neurons and insulin-like peptides dilp3 and dilp5, but not dilp2, are required, with the latter likely altered in median neurosecretory cells (MNCs) after R2/R4 neuronal activation. These data generate new insights into the neural underpinnings of how perceptive events may impact aging and physiology across taxa.