Altered homeostasis of metals in the brain has previously been identified as a factor in AD, but the physiological roles of these metals and their interactions with AD pathogenesis are unclear. In the new study, Bruce Yankner and his team focused on lithium after he had previously recognized its potential in AD.

"Several years ago, I became convinced that we were missing something fundamental in our understanding of the ageing brain and AD," explains Yankner. "At that time, we were looking at the effects of lithium as a neuroprotective agent and I was struck that this one metal appeared to be able to reverse all the pathological and behavioural manifestations of AD in mouse models and in vitro at high doses. It occurred to me that perhaps lithium itself was part of the disease mechanism."