Figure 2. Excitatory neuronal ERBB4 as a common driver of Alzheimer’s disease pathology (IMAGE)
Caption
Schematic illustration of the proposed disease mechanism whereby aberrant ERBB4 upregulation in excitatory neurons promotes neuronal hyperactivity, synaptic imbalance, reactive gliosis, amyloid accumulation, and subsequent memory and cognitive decline. Selective suppression of ERBB4 in excitatory neurons attenuates these interconnected pathological changes, restores synaptic and circuit function, reduces amyloid burden and glial reactivity, and improves memory, identifying excitatory neuronal ERBB4 as a potential regulatory point—and one “root of the problem”—in the Alzheimer’s disease cascade.
Credit
Institute for Basic Science
Usage Restrictions
Attribution Required
License
Original content