Since the aza-bisphosphonate-terminated neutral phosphorous dendrimers used in this work have shown anti-inflammatory properties both in vitro and in vivo by preventing NF-κB translocation to the cell nucleus [12], and neuroinflammation has been proposed as one of the possible mechanisms contributing to the pathogenesis of Alzheimer’s disease [40], we decided to study whether these neutral phosphorous dendrimers were able to inhibit neuronal excitotoxic death. This evidence concerns the gene NFKB1 and early-onset autosomal dominant Alzheimer disease.