Conversely, pathways essential for neuronal development and synaptic organization, including axonogenesis, axon guidance, and postsynaptic density, showed marked downregulation (Fig. 4b), represented by negatively-associated proteins (PTPRN2, PNOC, EPHA5, VGF, CDH8, BDNF, NPTXR, NPTX2, SCG2, PCDH, CX3CL1), indicating that as disease progresses to AD Dementia, biological resources increasingly divert toward compensatory survival mechanisms, while synaptic and neuronal processes progressively weaken. The gene discussed is PTPRN2; the disease is Alzheimer disease.