Lithium protects cultured neurons against beta-amyloid-induced neurodegeneration

The deposition of beta-amyloid peptide (A beta), the hyperphosphorylation o f tau protein and the death of neurons in certain brain regions are charact eristic features of Alzheimer's disease. It has been proposed that the accu mulation of aggregates of A beta is the trigger of neurodegeneration in thi s disease. In support of this view, several studies have demonstrated that the treatment of cultured neurons with A beta leads to the hyperphosphoryla tion of tau protein and neuronal cell death. Here we report that lithium pr events the enhanced phosphorylation of tau protein at the sites recognized by antibodies Tau-1 and PHF-1 which occurs when cultured rat cortical neuro ns are incubated with A beta. Interestingly, lithium also significantly pro tects cultured neurons from A beta-induced cell death. These results raise the possibility of using chronic lithium treatment for the therapy of Alzhe imer's disease. (C) 1999 Federation of European Biochemical Societies.