In this model, Alzheimer's disease is suggested to be an imbalance in physiological signaling pathways that mediate synaptic maintenance vs. synaptic re-organization, mediated at least in part by APP, functioning in synaptic element interdependence, as part of a plasticity module that includes other receptors such as the common neurotrophin receptor, p75NTR and the axon guidance receptor DCC, among others [68] (see Appendix 2 regarding proposed follow-up studies). The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.