Free amino acids in the brain of patients with Parkinson's disease

1988 ◽  
Vol 94 (1-2) ◽  
pp. 182-186 ◽  
Author(s):  
Juha O. Rinne ◽  
Toivo Halonen ◽  
Paavo J. Riekkinen ◽  
Urpo K. Rinne
1974 ◽  
Vol 12 (1) ◽  
pp. 33-37 ◽  
Author(s):  
L.R. Gjessing ◽  
P. Gjesdahl ◽  
P. Dietrichson ◽  
J. Presthus

1966 ◽  
Vol 101 (3) ◽  
pp. 591-597 ◽  
Author(s):  
R M O'Neal ◽  
R E Koeppe ◽  
E I Williams

1. Free glutamic acid, aspartic acid, glutamic acid from glutamine and, in some instances, the glutamic acid from glutathione and the aspartic acid from N-acetyl-aspartic acid were isolated from the brains of sheep and assayed for radioactivity after intravenous injection of [2-(14)C]glucose, [1-(14)C]acetate, [1-(14)C]butyrate or [2-(14)C]propionate. These brain components were also isolated and analysed from rats that had been given [2-(14)C]propionate. The results indicate that, as in rat brain, glucose is by far the best precursor of the free amino acids of sheep brain. 2. Degradation of the glutamate of brain yielded labelling patterns consistent with the proposal that the major route of pyruvate metabolism in brain is via acetyl-CoA, and that the short-chain fatty acids enter the brain without prior metabolism by other tissue and are metabolized in brain via the tricarboxylic acid cycle. 3. When labelled glucose was used as a precursor, glutamate always had a higher specific activity than glutamine; when labelled fatty acids were used, the reverse was true. These findings add support and complexity to the concept of the metabolic; compartmentation' of the free amino acids of brain. 4. The results from experiments with labelled propionate strongly suggest that brain metabolizes propionate via succinate and that this metabolic route may be a limited but important source of dicarboxylic acids in the brain.


Amino Acids ◽  
2008 ◽  
Vol 36 (2) ◽  
pp. 303-308 ◽  
Author(s):  
M. Sato ◽  
S. Tomonaga ◽  
D. M. Denbow ◽  
M. Furuse

1960 ◽  
Vol 5 (4) ◽  
pp. 339-348 ◽  
Author(s):  
S. S. Barkulis ◽  
A. Geiger ◽  
Y. Kawakita ◽  
V. Aguilar

Author(s):  
Y. E. Razvodovsky ◽  
V. Y. Smirnov ◽  
Ye. M. Doroshenko ◽  
N. Ye. Maksimovich ◽  
I. N. Semenenya

Mechanisms of development of ischemic stroke are complex and have not been fully established. The aim of this study was to estimate the changes in the pool of free amino acids and biogenic animes in the brain cortex of rats with subtotal cerebral ischemia (SCI) and treated with L-NAME. Experiment was made on 18 rats: 12 animals were undergoing bilateral filament occlusion of arteries carotid, 6 of them were treated with L-NAME. The analyses of free amino acids levels in the blood plasma extracts were carried out by reversed phase HPLC.Concentrations of several amino acids were elevated during SCI including aspartate, b-alanine, valine and leucine. In contrast, the levels of glutamate, asparagine, treonine, gamma-aminobutiric acid, tyrosine and 5-hydroxiindolylacetate were decreased. The administration of L-NAME partially prevented the imbalance of the amino acids pool due to SCI by normalizing the levels of aspartate, glutamate, asparagine, methionine, gamma-aminobutiric acid, b-alanine, 5-hydroxiindolylacetate. However, the administration of L-NAME has induced an additional imbalance in the amino acids pool in the brain cortex (decrease in the levels of glutamine, histidine, taurine, tryptophan, phenylalanine, tyrosine (in comparison to SCI) and decrease in the levels of treonine and arginine. The imbalance of the amino acids pool induced by the administration of L-NAME during SCI is more severe than the imbalance caused by SCI.


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