In cognitively healthy elderly individuals with suspected non-Alzheimer's disease pathophysiology (SNAP) or in patients with amnestic MCI, cholinergic basal forebrain neurons may be viable, although dysregulated, but do not display a massive and frank loss making them a valuable target of NGF-based therapeutic approaches aimed to prevent and/or delay the cognitive deterioration starting from the earliest stages of symptomology (Mufson et al., 2008). This evidence concerns the gene NGF and early-onset autosomal dominant Alzheimer disease.