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A breakthrough study led by researchers at Indiana University’s College of Arts and Sciences has uncovered a crucial missing link that plays a pivotal role in protecting the brain from aging. The team, led by Professor Hui-Chen Lu, identified the enzyme Nicotinamide Nucleotide Adenylyl Transferase 2 (NMNAT2) as a key player in providing energy to axons independently of mitochondria. Axons are thin fibers connecting nerve cells, vulnerable to damage and often the first sign of neurodegenerative diseases.
The study, published in Molecular Neurodegeneration, reveals that NMNAT2 propels glycolysis, a process breaking down glucose to generate energy, offering axons the required energy for carrying out nerve impulses. This crucial function contributes to the health and functionality of axons, delaying neurodegeneration. The newfound understanding could be vital in combating neurodegenerative diseases such as ALS, Alzheimer’s, Huntington’s, and Parkinson’s as individuals age.
Axons, being thin and prone to damage from various factors like inflammation, trauma, reduced blood flow, and infection, are critical for rapid information transmission throughout the body. NMNAT2, previously recognized for its role in providing nicotinamide adenine dinucleotide (NAD) for the brain, emerges as a potential target for therapeutic interventions.
“This new finding showcases the importance of neuron-intrinsic glycolysis in supporting axonal transport, essential for the establishment and maintenance of neuronal circuitry,” explained Professor Hui-Chen Lu. The researchers suggest that the next step could involve designing drugs targeting NMNAT2 to enhance its expression or activity during pre-symptomatic stages of neurodegeneration.
The study builds upon previous research from Lu’s laboratory, which highlighted the association between higher NMNAT2 levels and increased resistance to cognitive decline in aging individuals. The team also discovered compounds, including caffeine, capable of boosting NMNAT2 production in the body, providing insights into potential therapeutic strategies against neurodegenerative diseases.
Note: The findings offer significant implications for future drug development and intervention strategies targeting NMNAT2 to combat neurodegenerative diseases.
