Amino acids as dietary excitotoxins: A contribution to understanding neurodegenerative disorders

  title={Amino acids as dietary excitotoxins: A contribution to understanding neurodegenerative disorders},
  author={Brian S. Meldrum},
  journal={Brain Research Reviews},
  • B. Meldrum
  • Published 1 September 1993
  • Biology, Medicine
  • Brain Research Reviews
Oxidative stress, glutamate, and neurodegenerative disorders.
Two broad mechanisms--oxidative stress and excessive activation of glutamate receptors--are converging and represent sequential as well as interacting processes that provide a final common pathway for cell vulnerability in the brain.
The Role of Excitatory Aminoacids and its Neurotoxic Impact in Severe Head Injury Patients
The impact on enzyme activities shows a clear sign on the affect of cardial enzymes due to severe head injury, which may be of vital importance in treating patients with antagonists in suppressing the levels of glutamic and aspartic acids.
A Review of Glutamate Receptors II: Pathophysiology and Pathology
The diseases in which the pathophysiology and pathology are associated, in part, with the glutamate system are explored, including epilepsy, amnesia, anxiety, hyperalgesia and psychosis.
Excitatory Amino Acids and Neurotoxicity in the Human Neocortex
The current review focuses on the role of EAAs as neurotransmitters within particular pathways of the human cortex, particularly with regard to the neocortex and comparisons with data from non-human primates.
Homocysteine induces cell death of rat astrocytes in vitro
Therapeutic Potential of AMPA Receptor Ligands in Neurological Disorders
Recent evidence suggests that antagonists at non-NMDA receptors are more effective neuroprotective agents than NMDA receptor antagonists after ischaemic attacks, and that their administration can be delayed for up to 12 hours without seriously compromising the extent of neuroprotection.
Delayed Excitotoxic Neurodegeneration Induced by Excitatory Amino Acid Agonists in Isolated Retina
It is shown that glutamate, NMDA, AMPA, and KA all cause delayed as well as acute excitotoxic damage in the retina, and brief exposure to the non‐NMDA receptor agonists, in relatively low concentrations, led to delayed LDH release.
Glutamate as a neurotransmitter in the brain: review of physiology and pathology.
Endogenous glutamate, by activating NMDA, AMPA or mGluR1 receptors, may contribute to the brain damage occurring acutely after status epilepticus, cerebral ischemia or traumatic brain injury, and may also contribute to chronic neurodegeneration in such disorders as amyotrophic lateral sclerosis and Huntington's chorea.


Excitotoxic mechanisms, and age-related susceptibility to brain damage in ischemia, hypoglycemia and toxic mussel poisoning.
Experiments utilizing excitatory amino acid antagonists at the N-methyl-d-aspartate and other subtypes of excitational receptor have shown neuronal protection, in both ischemia and hypoglycemia, which is robust enough to produce a detectable improvement in neurologic deficit on neurobehavioral testing.
Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses?
  • M. Beal
  • Biology
    Annals of neurology
  • 1992
If defective mitochondrial energy metabolism plays a role in cell death in neurodegenerative disorders, potential therapeutic strategies would be to use excitatory amino acid antagonists or agents to bypass bioenergetic defects.
The neurotoxicity of excitatory amino acids is produced by passive chloride influx
  • S. Rothman
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1985
These experiments suggest that the pathophysiology of amino acid neurotoxicity may be rather straightforward, and showed that depolarization produced by high external potassium concentrations or veratridine was also toxic, but only in the presence of external chloride.
Aminooxyacetic Acid Results in Excitotoxin Lesions by a Novel Indirect Mechanism
The results raise the possibility that a regional impairment of intracellular energy metabolism may secondarily result in excitotoxic neuronal death in chronic neurodegenerative illnesses, such as Huntington's disease.
Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid
It is demonstrated that lesions due to quinolinic acid closely resemble those of HD as they result in marked depletions of both GABA and substance P, with selective sparing of somatostatin/neuropeptide Y neurones.