A research team led by Associate Director Chung Won-Suk at the Center for Vascular Research within the Institute for Basic Science (IBS) has identified aberrant ERBB4 expression in excitatory neurons as an early driver of multiple Alzheimer’s disease pathologies. The researchers found that when ERBB4, a receptor normally associated mainly with inhibitory neurons, appears in excitatory neurons, it can trigger neuronal hyperactivity, abnormal synapse loss, reactive gliosis, amyloid accumulation and cognitive impairment. The research is published in the journal Nature.

Alzheimer’s disease is not one malfunction but many. Synapses—the tiny contact points through which neurons communicate—disappear. Neural circuits become unstable. Astrocytes and microglia become reactive. Amyloid plaques accumulate, and memory and thinking abilities gradually decline. Scientists have long struggled to explain why these seemingly different abnormalities emerge and worsen together.