Mitochondria, the energy powerhouses of cells, play a crucial role in maintaining cellular health. Recently, researchers have discovered that a decline in mitochondrial levels in axons, the long extensions of neurons, can lead to abnormal protein accumulation, a hallmark of neurodegenerative diseases like Alzheimer’s.
Using fruit flies as a model organism, researchers found that genetically suppressing the production of a protein involved in mitochondrial transport along axons resulted in protein buildup in neurons. This buildup was attributed to a breakdown in autophagy, the process by which cells recycle damaged proteins.
Further analysis revealed that the depletion of mitochondria in axons caused a significant upregulation of eIF2β, a protein involved in regulating protein production. By artificially suppressing eIF2β levels, researchers were able to restore autophagy and improve neuron function.
These findings highlight the importance of maintaining mitochondrial health in neurons to prevent protein accumulation and neurodegeneration. As the population ages and the prevalence of neurodegenerative diseases increases, these discoveries could pave the way for new therapeutic approaches.
