Researchers at the University of Michigan published a groundbreaking study in the journal Molecular Metabolism, revealing that a neuron’s survival after injury depends heavily on how it processes sugar. While most cells can regenerate, neurons typically collapse after a stroke or concussion. However, senior author Monica Dus and lead researcher TJ Waller discovered that by “dialing down” sugar metabolism in an already injured neuron, they could preemptively activate a protective program that allows axons, the brain’s electrical wiring, to hold on longer rather than breaking down.
Scientists found a survival switch inside brain cells
Findings could create new opportunities to treat and study neurodegenerative diseasesScientists discovered that sugar metabolism plays a surprising role in whether injured neurons collapse or cling to life. By activating…
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The team identified two key proteins acting as the brain’s “survival switch.” The first, DLK (dual leucine zipper kinase), acts as a damage sensor that is triggered by metabolic shifts. It works in tandem with SARM1, a protein long blamed for nerve decay. The study found that when DLK is briefly activated, it restrains SARM1 and protects the cell. However, there is a catch: if DLK remains “on” for too long, it reverses its role and accelerates neurodegeneration. This “double-edged sword” nature makes DLK a complex but vital target for future drug development.
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These findings, primarily observed in fruit fly models, offer a “new perspective” on treating Alzheimer’s and traumatic brain injuries. Instead of simply trying to block damage, scientists can now focus on reinforcing the brain’s existing internal defense systems. By mastering this metabolic code, researchers hope to eventually create treatments that “flip the switch” toward healing in human patients.
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