Antiglutamatergic therapy in Alzheimer's disease--effects of lamotrigine. Short communication

J Neural Transm (Vienna). 1998;105(2-3):295-303. doi: 10.1007/s007020050059.

Abstract

It has been proposed that excitotoxic damage by glutamatergic hyperactivity is responsible for neurodegeneration in Alzheimer's disease. Lamotrigine (LTG) inhibits presynaptic glutamate release and is considered to be effective in treatment of other neurodegenerative disorders by its cerebroprotective properties. We used LTG in 11 patients with the diagnosis of probable Alzheimer's disease. 300 mg/day administration of LTG improved word recognition, naming and depressed mood on Alzheimer Disease Assessment Scale (ADAS).

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Aged
  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / pathology
  • Alzheimer Disease / psychology
  • Biological Availability
  • Brain / diagnostic imaging
  • Brain / pathology
  • Cross-Over Studies
  • Double-Blind Method
  • Excitatory Amino Acid Antagonists / adverse effects
  • Excitatory Amino Acid Antagonists / pharmacokinetics
  • Excitatory Amino Acid Antagonists / therapeutic use*
  • Female
  • Humans
  • Lamotrigine
  • Magnetic Resonance Imaging
  • Male
  • Middle Aged
  • Psychiatric Status Rating Scales
  • Tomography, Emission-Computed, Single-Photon
  • Triazines / adverse effects
  • Triazines / pharmacokinetics
  • Triazines / therapeutic use*

Substances

  • Excitatory Amino Acid Antagonists
  • Triazines
  • Lamotrigine