The amino acids GABA and glutamate also act as ..

The hypothesis was that a larger difference in glutamate concentration would enhance the ..

glutamate blockers - Truth in Labeling

"In the course of the disease, the chronic releaseof glutamate and the permanently increased intracellular calciumconcentration leads to neuronal degeneration (neurodegeneration)."

Stahl's Essential Psychopharmacology - Stahl Online

"Prolonged excitation is toxic to nerve cells. Neurobiologistsrecognize that the nerve cell messenger, glutamate, can cause harm whenits messages are overwhelming. Normally glutamate is swiftly clearedfrom the nerve cell junctions to keep the messages brief. Moleculescalled transporters aid in keeping glutamate in proper concentrationsaround nerve cells. Abundant evidence points to glutamate as adestructive factor in ALS and investigators are working to find out howthis can be changed. Gene therapy approaches are under investigation todeliver glutamate transporters to cells affected by ALS. Other avenuestowards control of glutamate in ALS are also under activeinvestigation."

A number ofexperimental drugs are being investigated for Parkinsons diseasebecause they block the actions of glutamate, an amino acid that is aparticularly potent nerve cell killer. Some of these drugs block areceptor group to glutamate called N-methyl-D-aspartate (NMDA).Investigative NMDA antagonists include remacemide, memantine, riluzole,and budipine."


For a better understanding of obesity

N2 - Objective: To ascertain the specificity of alternatively spliced mRNA variants of the astroglial glutamate transporter EAAT2 for ALS. Background: An important hypothesis for ALS pathogenesis is that motor neuron injury may result from chronically elevated glutamate levels in the CNS. Supporting this idea are reports of decreased glutamate transport in ALS. This in turn has recently been suggested to be due to the presence of aberrant mRNA splice variants for EAAT2 in ALS. Methods: Postmortem human brain tissue was obtained from different brain regions of patients with ALS, normal controls (NC), and patients with AD and Lewy body dementia (LB) - neurodegenerative diseases in which motor neurons are unaffected. Brain RNA was analyzed for EAAT2 isoforms using reverse transcription PCR and cDNA cloning/sequencing methods. Results: Splice variants lacking exons 7 or 9 were present in ALS brain, as previously reported, but were also present in brains from NC, AD, and LB patients. PCR product sequence analyses from non-ALS brain show variant splicing identical to that reported for ALS. Quantitative PCR analysis shows that these isoforms may be somewhat more abundant in ALS than AD, LB, and NC brains. Conclusions: EAAT2 mRNA splice variants are found in the brains of NC and AD patients, as in ALS. The authors cannot exclude the possibility that quantitative changes in variant EAAT2 isoforms might relate directly, or indirectly, to ALS pathology. However, the qualitative presence of these 'abnormal' EAAT2 splice variants does not appear to be sufficient to explain motor neuron degeneration in ALS.

beta-Methylamino-L-alanine - Wikipedia

There are many types of chemicals that act as neurotransmitters in the human body and the way that foods may affect these chemicals is important to understanding the possible role of diet in developmental disorders.

Amyotrophic Lateral Sclerosis — NEJM

AB - Objective: To ascertain the specificity of alternatively spliced mRNA variants of the astroglial glutamate transporter EAAT2 for ALS. Background: An important hypothesis for ALS pathogenesis is that motor neuron injury may result from chronically elevated glutamate levels in the CNS. Supporting this idea are reports of decreased glutamate transport in ALS. This in turn has recently been suggested to be due to the presence of aberrant mRNA splice variants for EAAT2 in ALS. Methods: Postmortem human brain tissue was obtained from different brain regions of patients with ALS, normal controls (NC), and patients with AD and Lewy body dementia (LB) - neurodegenerative diseases in which motor neurons are unaffected. Brain RNA was analyzed for EAAT2 isoforms using reverse transcription PCR and cDNA cloning/sequencing methods. Results: Splice variants lacking exons 7 or 9 were present in ALS brain, as previously reported, but were also present in brains from NC, AD, and LB patients. PCR product sequence analyses from non-ALS brain show variant splicing identical to that reported for ALS. Quantitative PCR analysis shows that these isoforms may be somewhat more abundant in ALS than AD, LB, and NC brains. Conclusions: EAAT2 mRNA splice variants are found in the brains of NC and AD patients, as in ALS. The authors cannot exclude the possibility that quantitative changes in variant EAAT2 isoforms might relate directly, or indirectly, to ALS pathology. However, the qualitative presence of these 'abnormal' EAAT2 splice variants does not appear to be sufficient to explain motor neuron degeneration in ALS.