ANN ARBOR, Mich.,August 6,2025 – New research suggests that how brain cells process sugar could hold the key to preventing neurodegeneration,the progressive loss of nerve cell function. This groundbreaking study from the University of Michigan focuses on cellular metabolism as a critical factor in nerve cell survival adn the brain’s natural defence mechanisms.
Metabolism may Unlock the Secret to a Deeper Understanding of Neurodegeneration
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Understanding how neurons use sugar could reveal new pathways to protect against diseases like Alzheimer’s and Parkinson’s.
Researchers at the University of michigan have discovered a link between sugar metabolism in neurons and their ability to resist degeneration, identifying two key proteins, DLK Kinase and SARM1, involved in this process.
Neurons,the vital cells of our brain and nervous system,are unique. Unlike manny other cells in the body, they can’t easily be repaired or replaced once damaged. This fragility means that after injuries like strokes, concussions, or neurodegenerative diseases, neurons and their crucial projections, called axons, are far more prone to breaking down than to regrowing.
However, a recent study published in the August issue of Molecular Metabolism offers a fresh perspective. Researchers at the University of Michigan have uncovered insights into neurodegeneration that could pave the way for future treatments designed to protect against neurological decline. Their findings, initially observed using fruit fly models, highlight the critical role of how neurons convert sugar into energy.
How does sugar metabolism affect neuron health?
“The way the brain produces and uses energy is often affected in brain lesions and diseases like Alzheimer’s,” explained Monica Duz, a lead author of the study and associate professor at the University of Michigan, specializing in molecular, cellular, and developmental biology. “We’ve discovered that a reduction in sugar metabolism, even before significant damage occurs, can either trigger a natural protective mechanism or lead to deterioration. When this protective mechanism is activated, axons show greater resistance.”
The Key Players: DLK Kinase and SARM1
The research identified two proteins central to maintaining axon health. The first is DLK Kinase, an enzyme that senses neuron damage and activates when metabolism is disrupted. The second is SARM1, a protein long associated with axon degeneration, which appears to be activated by the DLK-induced response.
“What surprised us is that the neuroprotective response changes based on the cell’s internal conditions,” Duz added. “The signals related to how cells use energy can determine whether neurons remain resilient or start to break down.”
Typically, when neurons and axons are healthy, DLK Kinase is more active, and SARM1 activity is suppressed. Though, the researchers noted a critical nuance: prolonged DLK activation can actually lead to progressive neurodegeneration, negating its initial protective effects.
DLK kinase has emerged as a promising target for neurodegenerative disease research, but its dual function presents a challenge. It can both protect and destroy neurons, making it tough to manipulate without unintended consequences.
This dual nature of DLK kinase poses a significant hurdle for researchers aiming to develop treatments. “If we wont to slow disease progression, we need to inhibit its negative aspect,” said T.J. Waller, a postdoctoral researcher and another lead author of the study. “We must ensure we don’t block the positive aspect, which could actually help slow the disease.”
Precisely controlling molecules with opposing functions like DLK remains a complex scientific challenge. Scientists are still working to understand exactly how this enzyme transitions from a protective role to a destructive one.
Unraveling these intricate regulatory mechanisms could revolutionize how neurodegenerative diseases and brain injuries are treated, offering direct benefits to patients in clinical settings.
the study received support from the National Science Foundation, the Rita Allen Foundation, and the Klingenstein Fellowship in neuroscience.
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