# Traumatic brain injury induces DNA damage in Drosophila

## TL;DR

This study shows that traumatic brain injury causes DNA damage in fruit flies, with older flies experiencing more severe and prolonged damage.

## Contribution

The study identifies a second phase of DNA damage after TBI in Drosophila and demonstrates age-related differences in DNA damage severity.

## Key findings

- DNA damage occurs within 4 hours of TBI in both young and older fruit flies.
- Older flies show increased DNA damage over time, suggesting aging enhances DNA damage mechanisms.
- DNA damage reappears weeks after injury, indicating a second phase of genomic instability.

## Abstract

Traumatic brain injury (TBI) is a major public health concern, affecting millions of people worldwide each year. Older individuals who experience a TBI face a higher risk of cognitive decline, disability, and mortality compared with younger individuals. A well-documented molecular consequence of TBI in both humans and rodent models is DNA damage. We used a
Drosophila melanogaster
(fruit fly) TBI model to investigate when DNA damage occurs following injury and whether age at the time of injury affects its severity. Using a Comet assay, which quantifies DNA damage in individual cells, we found that damage in the brain occurred within 4 hours of injury in both young and older flies. Levels of damage remained stable in young flies at 6 hours post-injury, but increased in older flies, indicating that aging processes enhance the post-TBI DNA damage mechanism. Although DNA damage initially resolved within 24 hours of injury; likely through DNA repair, loss of damaged cells, or death of flies with damage; it reappeared weeks later, revealing a previously unrecognized second phase of genomic instability following TBI. These findings establish Drosophila as a valuable model for studying TBI-induced DNA damage, a model that offers powerful genetic tools to investigate underlying mechanisms and to test whether genetic background affects the severity of DNA damage and contributes to individual variation in TBI outcomes.