Alzheimer’s illness (AD) pathogenesis is broadly believed to be pushed by the manufacturing and deposition of the β-amyloid peptide (Aβ). For a few years, investigators have been puzzled by the weak to nonexistent correlation between the quantity of neuritic plaque pathology within the human mind and the diploma of scientific dementia. Current advances in our understanding of the event of amyloid pathology have helped clear up this thriller. Substantial proof now signifies that the solubility of Aβ, and the amount of Aβ in numerous swimming pools, could also be extra carefully associated to illness state. The composition of those swimming pools of Aβ displays totally different populations of amyloid deposits, and has particular correlates with the scientific standing of the affected person. Imaging applied sciences, together with new amyloid imaging brokers primarily based on the chemical construction of histologic dyes, at the moment are making it attainable to trace amyloid pathology together with illness development within the residing affected person. Curiously, these approaches point out that the Aβ deposited in AD is totally different from that present in animal fashions. Generally, deposited Aβ is extra simply cleared from the mind in animal fashions, and doesn’t present the identical bodily and biochemical traits because the amyloid present in AD. This raises essential points concerning the event and testing of future therapeutic brokers.