ERBB4 in excitatory neurons could ignite the Alzheimer's cascade
Researchers identify a subset of excitatory neurons that abnormally express ERBB4, triggering hyperactivity, synaptic loss, glial reactivity, and amyloid buildup—driving Alzheimer's pathology in mice; suppressing ERBB4 mitigates these effects and improves memory, while activating ERBB4 in healthy mice induces Alzheimer’s-like changes. In human data, higher ERBB4 in excitatory neurons correlates with amyloid, tau pathology, and cognitive decline, pointing to an ERBB4-to-mTOR signaling axis as an early, multi-faceted intervention target rather than a single hallmark.