Interestingly, FPRL-1 and FPRL-2 are also functional receptors for Amyloid β (Aβ) 42, an important peptide in the pathophysiology of AD-related neuronal toxicity, suggesting that HN may exert its neuro-protective effects also by competitively inhibiting the access of FPRL-1 to Aβ 42 (20). This evidence concerns the gene FPR2 and Alzheimer disease.