The effects of tau expression on glial mitochondrial morphology in Drosophila melanogaster

Abstract

Tauopathies are a branch of neurodegenerative disorders characterized by the phosphorylation of the protein tau. These diseases are one of the leading causes of dementia, currently have no known cure, and are frequently heartbreaking to affected individuals and their families. While neurodegenerative diseases are poorly understood, studies have shown that hyperphosphorylated tau causes mitochondrial dysfunction and results in a decrease of ATP production during cellular respiration, as well as an increase in the toxic byproduct ROS, leading to apoptosis. While the effects of tau on mitochondria is established in neurons, this relationship has not been thoroughly examined in the “other” cells of the brain, known as glial cells. Glia support neuronal cellular respiration and synaptic functioning, making them potentially susceptible to mitochondrial tauopathy. This research examined whether the morphology and quantity of glial mitochondria are disrupted in the presence of tau in Drosophila melanogaster. It found that the quantity of glial mitochondria is significantly reduced in the presence of tau, but that tau had no effect on mitochondrial volume, surface area, and sphericity. These findings suggest that glial mitochondria are disrupted by tauopathy in a unique manner, and highlights their importance in future studies as therapeutic targets for neurodegenerative diseases. Given their roles in metabolic support, we further quantified age and sex differences in astrocytic mitochondria, finding that day three flies possess fewer mitochondria than days 10 and 30. These studies were employed with the goal of establishing control conditions for future studies aimed at determining astrocytic-specific effects of tau expression.