Endogenous protectant kynurenic acid in amyotrophic lateral sclerosis
Article first published online: 20 MAY 2003
Acta Neurologica Scandinavica
Volume 107, Issue 6, pages 412–418, June 2003
How to Cite
Iłżecka, J., Kocki, T., Stelmasiak, Z. and Turski, W. A. (2003), Endogenous protectant kynurenic acid in amyotrophic lateral sclerosis. Acta Neurologica Scandinavica, 107: 412–418. doi: 10.1034/j.1600-0404.2003.00076.x
- Issue published online: 20 MAY 2003
- Article first published online: 20 MAY 2003
- Accepted for publication September 17, 2002
- amyotrophic lateral sclerosis;
- kynurenic acid;
Objectives – Excitotoxicity may play a role in neurodegeneration in amyotrophic lateral sclerosis (ALS). Kynurenic acid (KYNA), an endogenous antagonist of excitatory amino acid receptors, may inhibit excitotoxic lesions. The aim of this study was to determine the concentration of KYNA in ALS patients.
Material and methods – KYNA was measured by high-performance liquid chromatography in the serum and cerebrospinal fluid (CSF) from ALS and control patients.
Results – Our study revealed that CSF KYNA concentration was significantly higher in patients with bulbar onset of ALS compared to controls, and compared to patients with limb onset of the disease. CSF KYNA was also higher in patients with severe clinical status compared to controls. Serum KYNA was significantly lower in ALS patients with severe clinical status compared to controls, and compared to patients with mild clinical status. There were no significant differences in CSF and serum KYNA concentration between the whole ALS group of patients and controls. There was no difference in CSF KYNA concentration between males and females, and there was no correlation between KYNA concentration and age of patients, and duration of ALS.
Conclusions – An increased CSF KYNA concentration in patients with bulbar onset of ALS and in patients with severe clinical status may indicate neuroprotective role of KYNA against excitotoxicity. The difference of KYNA concentration in CSF of patients with bulbar and limb onset of ALS suggests that these two variants of motor neuron disease may have different etiopathogenetic mechanisms.