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Key Alzheimer's Trigger Found in Brain
16 Sep
Summary
- A brain molecule, ERBB4, may link abnormal nerve activity to memory loss.
- ERBB4 receptor's abnormal activation initiates Alzheimer's-related problems.
- Targeting ERBB4 receptors shows promise in treating Alzheimer's symptoms.
A groundbreaking study suggests a specific brain molecule, ERBB4, may be the key to understanding how Alzheimer's disease progresses from abnormal nerve connections to memory impairment.
Previous research identified amyloid plaques and tau tangles as primary drivers of Alzheimer's. However, the link between the resulting nerve cell dysfunction and cognitive decline remained elusive. This new research from South Korea proposes that an abnormal activation of the ERBB4 receptor in excitatory neurons initiates several Alzheimer's-related problems simultaneously.
Scientists observed that astrocytes and microglia, cells responsible for supporting neurons and clearing debris, removed increasing numbers of healthy neuron connections in mice exhibiting Alzheimer's symptoms. They also found that non-neuronal glial cells were unbalancing crucial signals for nerve activity.
Further investigation revealed that in healthy brains, ERBB4 is mainly in inhibitory neurons. However, in Alzheimer's, it appears in excitatory neurons. This shift suggests Alzheimer's can push neurons into an abnormal state. Eliminating ERBB4 receptors in the hippocampus, a memory-critical region, quieted hyperactive cells, improved glial cell function, reduced plaque buildup, and enhanced memory performance in mice.
Analysis of post-mortem human brain tissue confirmed elevated ERBB4 expression in excitatory neurons affected by Alzheimer's. The findings highlight aberrant ERBB4 expression as an early driver of Alzheimer's pathophysiology and a promising therapeutic target for neurodegenerative diseases.
