Decreased platelet glutamate uptake and genetic risk factors in patients with Parkinson's disease

Neurol Sci. 2001 Feb;22(1):65-6. doi: 10.1007/s100720170049.

Abstract

Genetic risk factors seem to play a role in sporadic Parkinson's disease (PD), maybe triggering oxidative stress and excitotoxicity within substantia nigra. However, genetic factors act at systemic level: reduced activity of mitochondrial enzymes and decreased glutamate uptake have been shown in platelets from PD patients. In this study we investigated glutamate uptake in platelets from 38 sporadic PD patients, 13 patients with parkinsonian syndromes and 28 controls and assessed polymorphisms of alpha-synuclein and ApoE genes. A 48% reduction of glutamate uptake p)<0.0001) was observed in PD patients which, with respect to control groups, correlated with the disease severity (r = -0.44, p < 0.05). Genetic studies of this population did not show differences between PD and controls, nor correlations with platelet glutamate uptake.

MeSH terms

  • Apolipoproteins E / genetics
  • Blood Platelets / metabolism*
  • Brain / metabolism*
  • Brain / physiopathology
  • Cell Death / genetics
  • Energy Metabolism / genetics
  • Gene Frequency / genetics
  • Genetic Markers / genetics
  • Genetic Predisposition to Disease / genetics*
  • Genotype
  • Glutamic Acid / metabolism*
  • Humans
  • Mitochondria / genetics
  • Mitochondria / metabolism
  • Nerve Tissue Proteins / genetics
  • Oxidative Stress / physiology
  • Parkinson Disease / blood*
  • Parkinson Disease / genetics*
  • Polymorphism, Genetic / genetics
  • Risk Factors
  • Synucleins
  • alpha-Synuclein

Substances

  • Apolipoproteins E
  • Genetic Markers
  • Nerve Tissue Proteins
  • SNCA protein, human
  • Synucleins
  • alpha-Synuclein
  • Glutamic Acid