Later studies have used markers like Musashi-1, nestin and PSA-NCAM to show that neurogenic abnormalities in AD differ between phases and areas of neurogenesis and stages of AD: while hippocampal stem cells (Musashi-1) decrease, proliferation increases and differentiation/migration phase as well as axonal/dendritic targeting (DCX and β-III-tubulin) remain unchanged, suggesting an attenuation of stem cells together with compensatory increases in proliferation that, however, does not result in increases in differentiated new neurons in AD [134]. The gene discussed is NCAM1; the disease is Alzheimer disease.