GAP43 and early-onset autosomal dominant Alzheimer disease: The reduction in the GAP-43 levels seen in the SPF-FB-treated animals is in line with the Rekart and coworkers findings that the elevated levels of GAP-43 leading to potentially aberrant sprouting were positively correlated with the severity of Alzheimer’s Disease, suggests that the increased expression of GAP-43 leads to a miswiring of circuits critical for memory function (Rekart et al., 2004).