ACHE and early-onset autosomal dominant Alzheimer disease: Furthermore, in vivo studies have demonstrated how trans-crocetin, i.e., a biologically active metabolite of crocin, is able to prevent the formation of senile plaques and neurofibrillary tangles (NFTs) and intracellular aggregations of hyperphosphorylated tau protein, namely the protein commonly known as the primary biomarker causing Alzheimer’s disease, through the suppression of acetylcholinesterase (AChE) activity [65,66].