It has recently been discovered that SGR retro-inserts novel genomic complementary DNA into neuronal genomes and becomes dysregulated in AD, producing numerous APP variant genes, transcripts, and AβP that would remain in the brain in various potential forms (e.g., plaques, fibrils, prions, and soluble products) and may not be recognized by specific Aβ-antibodies used in the therapeutic attempts to target AβP [156,157]. This evidence concerns the gene APP and Alzheimer disease.