The research (DOI 10.1038/s42255-026-01538-4) identifies *hyperglycosylation* as a significant metabolic driver of *Alzheimer’s disease (AD),* moving beyond the traditional focus on amyloid and tau. Using advanced *spatial multiomics,* the study demonstrates that both human AD brains and animal models exhibit an abnormal increase in *glycan biosynthesis.* Experimental results show that inhibiting the enzymes responsible for this process improves *cognitive function,* while introducing *glucosamine* supplements significantly worsens memory deficits. Furthermore, clinical data analysis reveals that AD patients taking glucosamine face *accelerated disease progression* and higher mortality rates. These findings establish that *excessive glycosylation* is a pathological mechanism rather than a secondary symptom. Ultimately, the work suggests that targeting *glycan metabolism* offers a promising and novel therapeutic strategy for treating neurodegeneration.
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