This study explores how pyramidal neurons in the Tg2576 mouse model of Alzheimer’s disease (AD) maintain dendritic signaling despite structural degeneration. Using morphofunctional matrices (MFM), the researchers analyzed neurons from wild-type and Tg2576 mice, focusing on dendritic morphology and membrane properties. They found that although Tg2576 neurons exhibit dendritic atrophy, this is compensated by changes in membrane properties, preserving functional output. Hypothetical neurons with Tg morphology but without adaptive membrane changes showed greater deviation, confirming the compensatory mechanism. The findings suggest that functional deficits in AD may stem more from network-level disconnection than individual neuron failure, and highlight MFM as a valuable tool in neurodegeneration research.