Molecular switch ERBB4 linked to broad range of Alzheimer's pathologies
Researchers found that ERBB4 in a small subset of excitatory neurons drove hyperactivity, synapse loss and memory decline in mice.
5 Articles
5 Articles
A rogue neuronal signal may lie at the root of Alzheimer's disease
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.
Molecular switch ERBB4 linked to broad range of Alzheimer's pathologies
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.
(Seoul = Yonhap News) Reporter Cho Seung-han = Domestic researchers have identified a key factor that accelerates the vicious cycle of Alzheimer's disease.
A research team at the Institute for Basic Science has identified the role of ERBB4, a key regulatory protein that accelerates the progression of Alzheimer's disease. Using a mouse model, they confirmed that inhibiting ERBB4 improves cognitive function, thereby establishing a scientific basis for the development of next-generation treatments to prevent neuronal connectivity loss and inflammation.
[Digital Daily Reporter Baek Ji-young] Domestic researchers have identified a key regulatory factor that sequentially exacerbates Alzheimer's disease, ranging from neural circuit abnormalities to synapse loss, inflammation, and amyloid accumulation. In animal experiments, removing this factor reduced amyloid plaques by more than half and improved cognitive function. The Ministry of Science and ICT and the Institute for Basic Science (IBS) annou…
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