As there was a trend towards increased full-length Ng in CU-AP compared to controls as measured by WB, it is possible that the CU-AP individuals are able to respond to the pathological changes and counteract or compensate for the cognitive decline these would otherwise cause, perhaps by increasing the numbers of synapses or simply producing more full-length Ng thus providing them with the means of a cognitive reserve. The gene discussed is NRGN; the disease is Mental deterioration.