A rogue neuronal signal lies at the root of Alzheimer’s disease
Peer-Reviewed Publication
Updates every hour. Last Updated: 28-Oct-2026 17:17 ET (28-Oct-2026 21:17 GMT/UTC)
What if amyloid plaques are not the whole story of Alzheimer’s disease? New research suggests that a broad range of Alzheimer’s pathologies may be orchestrated by a molecular switch called ERBB4 when it turns on in the wrong neurons. Once activated, this misplaced signal can set off a chain reaction that disrupts brain circuits, eliminates synapses, activates glial cells, increases amyloid pathology and impairs memory.
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.New research found that adverse childhood experiences, particularly negative relationships between a child and parent, were linked to more frequent drinking during periods of extreme heat.
A research team has uncovered fundamental molecular mechanisms governing the formation of tendons and ligaments, which are essential for musculoskeletal integration. Understanding these mechanisms could pave the way for the regeneration of tendons, ligaments, and their attachment sites, known as entheses, which have limited capacity for functional repair after injury because of their poor vascularization.