Year: 1999
Type: article
Abstract: The deposition of beta-amyloid peptide (A beta), the hyperphosphorylation of tau protein and the death of neurons in certain brain regions are characteristic features of Alzheimer's disease. It has been proposed that the accumulation of aggregates of A beta is the trigger of neurodegeneration in this disease. In support of this view, several studies have demonstrated that the treatment of cultured neurons with A beta leads to the hyperphosphorylation of tau protein and neuronal cell death. Here we report that lithium prevents the enhanced phosphorylation of tau protein at the sites recognized by antibodies Tau-1 and PHF-1 which occurs when cultured rat cortical neurons are incubated with A beta. Interestingly, lithium also significantly protects cultured neurons from A beta-induced cell death. These results raise the possibility of using chronic lithium treatment for the therapy of Alzheimer's disease.
Source: FEBS Letters
Authors: Gema Alvarez, Juan Ramón Muñoz-Montaño, Jorgina Satrústegui, Jesús Avila, Elena Bogónez, Javier Dı́az-Nido
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: bronze
Funder: Medical Research Council
OpenAlex ID: W1982947429
