Tokyo Metropolitan University researchers have linked protein accumulation in neurons, a hallmark of neurodegenerative diseases like Alzheimer's, to mitochondrial depletion in axons.

In studies using fruit flies, scientists found that hindering mitochondrial transport protein production led to abnormal neuronal protein build-up due to disrupted autophagy.

An increase in the protein eIF2β, which initiates protein production, was observed in the presence of mitochondrial depletion.

Suppressing eIF2β was shown to restore autophagy and improve neuron function, suggesting a potential therapeutic target for neurodegenerative disease treatment.

The findings indicate that mitochondrial depletion in axons can directly cause protein accumulation, enhancing understanding of neurodegenerative disease mechanisms.

This research, which offers hope for new treatments, is particularly relevant as the global population ages, increasing the prevalence of neurodegenerative diseases.