Consisting with these enhanced fibrillogenic properties, Aβ4–42 has been reported to mostly localize to fibrillar Thioflavin and Congo red (+) lesions at the core of parenchymal plaques and in vascular deposits in both, AD and Down syndrome patients, as well as in a number of APP transgenic models including the widely studied Tg2576 and APP/PS1 (Cabrera et al., 2018; Masters et al., 1985; Wirths et al., 2017; Zampar et al., 2020). This evidence concerns the gene APP and Alzheimer disease.