CD2AP is an adapter protein primarily functioning to link membrane proteins to the actin cytoskeleton 1. It plays critical roles in multiple biological contexts: in renal podocytes, CD2AP is expressed as a component of the slit diaphragm and anchors it to the actin cytoskeleton 2, with CD2AP mutations causing focal segmental glomerulosclerosis 3. In immune cells, CD2AP regulates cytoskeleton organization and protein trafficking 4. CD2AP is notably enriched in microglia, where it regulates phagocytic responses to amyloid-beta 4. In neuronal contexts, CD2AP facilitates endosomal-lysosomal degradation of amyloid precursor protein (APP) by promoting APP-CD2AP interaction, thereby reducing amyloid-beta generation 5. Genetic variants in CD2AP are associated with Alzheimer's disease risk 16, with evidence suggesting microglial CD2AP deficiency paradoxically protects against amyloid pathology and cognitive decline in AD models 4. This protection may occur through reduced microglial activation and altered phagocytic responses to pathological substrates. CD2AP thus represents a convergence point between kidney and brain pathophysiology, highlighting a potential kidney-brain axis in neurodegeneration 3.