Researchers have identified a potential mechanism by which the Alzheimer’s risk gene APOE4 disrupts brain function years before the onset of memory problems. The study, conducted on mice, revealed that APOE4 increases levels of a protein called Nell2, leading to neuron shrinkage and heightened activity in memory circuits. This early hyperactivity appears to correlate with later memory impairment.
The research team found that in mice, APOE4 increased a protein called Nell2. This increase resulted in shrinking neurons and unusually active memory circuits. Importantly, the study demonstrated that this early hyperactivity predicted worse memory performance later in life. This suggests that the changes caused by APOE4 aren’t simply a consequence of Alzheimer’s pathology, but may actively contribute to its development.
Furthermore, the researchers were able to reverse these abnormal changes in adult mice by reducing Nell2 levels. This finding offers a promising avenue for potential interventions aimed at preventing or delaying the progression of Alzheimer’s disease. The study suggests that targeting Nell2 could be a viable strategy to protect brain cells and preserve cognitive function before symptoms manifest. The researchers state that this provides hope for a new way to intervene before Alzheimer’s progresses.
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