Monday, May 20, 2024

Mitochondrial Decline Linked to Protein Build-Up in Neurological Disorders

Scientists at Tokyo Metropolitan University Illuminate Path to New Neurodegenerative Disease Therapies

Researchers at Tokyo Metropolitan University have unveiled a pivotal mechanism potentially driving the onset and progression of age-related neurodegenerative diseases such as Alzheimer’s and Amyotrophic Lateral Sclerosis (ALS). The study reveals that the depletion of axonal mitochondria, the energy powerhouses of cells, could directly contribute to abnormal protein accumulation in neurons, shedding light on possible therapeutic interventions.

Led by Associate Professor Dr. Kanae Ando, the research team employed Drosophila fruit flies to explore the genesis of protein aggregates. They discovered that the suppression of milton, a protein essential for mitochondrial transport in axons, led to significant protein accumulation. This finding underscores the role of mitochondrial health in neuronal function and the breakdown of autophagy, the body’s way of clearing damaged cells.

Intriguingly, the study also found that altering neuronal energy levels did not impact autophagy, suggesting that mitochondrial function in axons is specifically crucial for protein regulation. Proteomic analysis further identified an increase in eIF2β, a component of the protein synthesis initiator eIF2, linking mitochondrial loss directly to cellular protein management dysfunctions.

Moreover, the research highlights a potential therapeutic pathway; by reducing eIF2β levels, the team was able to restore some neuronal functions and autophagic activity, offering hope for interventions that could mitigate the effects of mitochondrial depletion in neurodegenerative conditions.

This breakthrough not only advances our understanding of the cellular mechanisms behind debilitating neurological diseases but also opens the door to novel strategies for combating the effects of aging on the brain. The findings from this study are set to catalyze further research into the links between mitochondrial health and neurodegeneration, potentially leading to groundbreaking treatments.

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