Proteins are 'action molecules' and their functioning is dependent upon acquiring the correct 3D shape. Proteins can mis-fold into the wrong shape in disease, and as a consequence can clump into aggregates that clog cellular functions. Two common protein-folding diseases of the brain are Alzheimer’s Disease (AD) and Parkinson’s Disease. In AD a small protein called amyloid beta (Aβ) is prone to misfolding, while in Parkinson’s the culprit is called α-synuclein. AD is very common, and while not transmissible, a close relationship between prion disease and AD is demonstrated by common misfolding to β-sheet enriched structures, shared sporadic and genetic manifestations, and some overlaps in pathology. Some labs have gone further and suggested functional relationships between PrP and Aβ proteolysis, or toxic effects of Aβ mediated by binding to normal prion proteins. These overlaps are of interest to us, because AD may open new windows on prion disease, and vice versa. AD research activities are pursued by the Westaway, Allison and Kar labs. The Alberta Alzheimer Consortium represents a team effort by the Westaway, Jhamandas, Dixon, and Kar labs, with the involvement of Alberta-based Gerontologists and Neurologists.