Thus, the altered relationships between Ng and BACE1 in both A+ groups could reflect compromised pre- and postsynaptic integrity when expressed as a ratio.17 In summary, the differential expression of BACE1 and Ng along the Alzheimer’s disease continuum may relate to pathological changes at both pre-and post-synaptic terminals and is consistent with synapse degradation and altered neuron-glia interactions at more advanced stages. This evidence concerns the gene NRGN and Alzheimer disease.