Target Tau, not Amyloid, to Prevent and Treat Alzheimer’s Disease
Esiri MM.
In this article I wish to put the case for a change of emphasis in the approach to finding a prevention/treatment for Alzheimer’s disease from a focus on beta amyloid to one on tau. In particular, I make the case for aiming to prevent the spread of abnormal tau from the medial temporal lobe to widespread areas of association cortex that are anatomically linked to this critical region. I pose an analogy with cardiovascular disease in which the initiating pathology, lipid streaks, are left untreated until they are so extensive as to provoke secondary pathology, the treatment of which, in many cases, controls the effects of disease. In Alzheimer’s disease beta amyloid, if it is the initiating pathology, represents the equivalent of lipid streaks in this analogy and tau the secondary pathology that needs to be curtailed to control the disease.