Post-mortem studies of brain tissue from ALS patients reveal an abnormal form of tau is present in novel brain areas, and the tau interacts with DRP1. The tau appears to cause the brain cell's mitochondria to fragment and increase oxidative stress. Reducing tau reversed the effect, decreasing oxidative stress and mitochondrial fragmentation.
Ceramide exposure impairs the ability for neurons to make energy by directly damaging mitochondria. Additionally, ceramides force neurons to rapidly uptake glucose in order to provide cellular energy.
Researchers have developed a method of removing damaged mitochondria in fruit flies, causing the insects to become more active and increasing typical lifespan. UCLA researchers report the method could eventually be used to benefit humans and delay the onset of age-related diseases.
Inhibition of the Drp1 mitochondrial fission protein shows potential as a treatment for Parkinson's disease.