Lithium protects cultured neurons against beta-amyloid-induced neurodegeneration

FEBS Lett. 1999 Jun 25;453(3):260-4. doi: 10.1016/s0014-5793(99)00685-7.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Cell Death*
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Lithium / pharmacology*
  • Neurons / drug effects*
  • Neuroprotective Agents / pharmacology
  • Peptide Fragments / pharmacology*
  • Phosphorylation
  • Rats
  • Rats, Wistar
  • tau Proteins / metabolism*


  • Amyloid beta-Peptides
  • Neuroprotective Agents
  • Peptide Fragments
  • amyloid beta-protein (1-40)
  • tau Proteins
  • Lithium