Arif et al. [112] reported that BMAA causes tau hyper-phosphorylation in hippocampal primary neurons, metabolically active brain slices and in vivo (i.c.v.infusion) potentially by inhibiting PP2A activity which is responsible for dephosphorylating most of the hyper-phosphorylated sites of tau [113] and is often compromised in the AD brain [114]. This evidence concerns the gene PTPA and Alzheimer disease.