Published : 17 Sep 2026, 06:08 PM
Updated : 17 Sep 2026, 06:08 PM
Scientists may have found a critical clue to one of Alzheimer's disease's longest-standing mysteries -- how abnormal protein build-up in the brain eventually leads to memory loss.
A study from the Institute of Basic Science in South Korea identifies a receptor protein called ERBB4 as a possible missing link between the early cellular chaos of Alzheimer's and the cognitive decline that follows, reports The Independent.
Alzheimer's has long been associated with amyloid plaques and tau tangles -- abnormal protein clumps that damage nerve cells, disrupt connections and trigger runaway brain activity.
But scientists have struggled to explain precisely how these changes translate into lost memories.
The new research points to ERBB4, a receptor that allows nerve cells to respond to external signals. In healthy brains, it is found mainly in neurons that slow down brain activity.
In Alzheimer's patients, researchers found it appearing in excitatory neurons -- the cells that drive brain activity -- throwing the brain's signalling system off balance.
This shift, researchers say, may set off a cascade of problems.
Supporting brain cells known as astrocytes and microglia, which normally clear away unwanted connections, began stripping healthy ones instead, according to The Independent.
The balance between signals that accelerate and brake nerve activity broke down -- a disruption that can appear before cognitive symptoms become obvious.
When researchers used gene-editing to remove ERBB4 from excitatory neurons in the hippocampus -- the brain region central to memory -- the results were striking.
Overactive nerve cells quieted down, plaque build-up declined, and the mice performed better on memory and spatial cognition tests.
Crucially, the reverse also held: activating ERBB4 in excitatory neurons of otherwise healthy mice produced excessive brain activity and cognitive impairment.
The findings suggest Alzheimer's does not simply destroy neurons -- it may push some into an abnormal state, states The Independent.
And a single intervention targeting ERBB4 was enough to address multiple symptoms at once, raising hopes for a more unified treatment approach.
