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62 reviewsSUMMARYThe molecular mechanisms underlying the pathogenesis of Alzheimer’s disease (AD), the most common form ofdementia, remain poorly understood. Proteomics offers a crucial approach to elucidating AD pathogenesis, asalterations in protein expression are more directly linked to phenotypic outcomes than changes atthe genetic ortranscriptomic level. In this study, we develop multiscale proteomic network models for AD by integrating largescale matched proteomic and genetic data from brain regions vulnerable to the disease. These models revealdetailed protein interaction structures and identify putative key driver proteins (KDPs) involved in AD progression. Notably, the network analysis uncovers an AD-associated subnetwork that captures glia-neuron interactions. AHNAK, a top KDP in this glia-neuron network, is experimentally validated in human induced pluripotentstem cell (iPSC)-based models ofAD. This systematic identification of dysregulated protein regulatory networksand KDPs lays down a foundation for developing innovative therapeutic strategies for AD.
