Free D- and L-amino acids in ventricular cerebrospinal fluid from Alzheimer and normal subjects
Department of Chemistry, Barry University, Miami Shores, Florida, USA. Amino Acids
(Impact Factor: 3.29).
09/1998; 15(3):263-9. DOI: 10.1007/BF01318865
Free D-Ser, D-Asp and total D-amino acids were significantly higher (p < 0.05) in Alzheimer (AD) ventricular CSF than in normal CSF. There was no significant difference in the total L-amino acids between AD and normal CSF, but L-Gln and L-His were significantly higher (p < 0.05) in AD-CSF. The higher concentrations of these D- and L-amino acids in AD ventricular CSF could reflect the degenerative process that occurs in Alzheimer's brain since ventricular CSF is the repository of amino acids from the brain.
Available from: Enrico D'Aniello
- "Hence, given that Alzheimer's patients possess a reduced cognitive activity, we have deduced that D-Asp could also be involved in human learning and memory. Intriguingly, further research in this field revealed that in human ventricular cerebrospinal fluid obtained from the third ventricle (Fisher et al. 1994), and from the spinal cerebral fluid of Alzheimer's subjects (Fisher et al. 1998), the concentration of D-Asp is significantly higher than that found in the same tissue of healthy control subjects. A tentative explanation toward this phenomenon is that, for unknown reasons, in Alzheimer's disease, D-Asp is transferred from the brain to the ventricular and then to the spinal cerebral fluid. "
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ABSTRACT: D-Aspartic acid (D-Asp) is an endogenous amino acid present in neuroendocrine systems. Here, we report evidence that D-Asp in the rat is involved in learning and memory processes. Oral administration of sodium D-aspartate (40 mM) for 12-16 days improved the rats' cognitive capability to find a hidden platform in the Morris water maze system. Two sessions per day for three consecutive days were performed in two groups of 12 rats. One group was treated with Na-D-aspartate and the other with control. A significant increase in the cognitive effect was observed in the treated group compared to controls (two-way ANOVA with repeated measurements: F ((2, 105)) = 57.29; P value < 0.001). Five further sessions of repeated training, involving a change in platform location, also displayed a significant treatment effect [F ((2, 84)) = 27.62; P value < 0.001]. In the hippocampus of treated rats, D-Asp increased by about 2.7-fold compared to controls (82.5 +/- 10.0 vs. the 30.6 +/- 5.4 ng/g tissue; P < 0.0001). Moreover, 20 randomly selected rats possessing relatively high endogenous concentrations of D-Asp in the hippocampus were much faster in reaching the hidden platform, an event suggesting that their enhanced cognitive capability was functionally related to the high levels of D-Asp. The correlation coefficient calculated in the 20 rats was R = -0.916 with a df of 18; P < 0.001. In conclusion, this study provides corroborating evidence that D-aspartic acid plays an important role in the modulation of learning and memory.
Amino Acids 11/2009; 38(5):1561-9. DOI:10.1007/s00726-009-0369-x · 3.29 Impact Factor
Available from: Mar Gil-Diaz
- "(referred to by Cesapó, Cesapó-Kiss, Stefler, Martín, & Némethy, 1995; Hamase, Morikawa, & Zaitsu, 2002). Although disagreements exist about the toxicity of D-AA (Fisher et al., 1998; Goltsov et al., 2006; Rubio-Barroso, Santos-Delgado, Martín-Olivar, & Polo-Díez, 2006), there is no doubt that food quality decreases. "
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ABSTRACT: Potential racemization of L-amino acids (AA) in ready-to-eat (RTE) cooked ham after hygienization by electron-beam irradiation between 1 and 8kGy was studied. An indirect chiral method based on the derivatization reaction of AA with o-phthaldialdehyde and N-acetyl-L-cysteine followed by reversed-phase HPLC and fluorimetric detection was applied to detect ten enantiomeric pairs of free AA (Asp, Ser, Thr, Ala, Tyr, Val, Trp, Phe and Leu). Five of the D-AA were not found in any of the samples analyzed; the other five remaining D-AA (D-Asp, D-Ser, D-Ala, D-Val and D-Leu) were detected both in irradiated and non-irradiated cooked ham samples, their content being in the range 1.25-13.79μg/g. Although significant differences appeared for a few of the samples and doses, no positive correlation between the D-AA content and the irradiation doses was observed. Therefore, the electron-beam irradiation technique could be useful for sanitation of packed RTE cooked ham at doses allowed by WHO and EU, since it remains chemically safe to eat.
Meat Science 12/2008; 82(1):24-9. DOI:10.1016/j.meatsci.2008.11.019 · 2.62 Impact Factor
Available from: Shengzhou Wu
- "Indeed, we found that A induces D-serine release from microglia through increased expression of serine racemase, and D-serine contributes to the neurotoxicity *Address correspondence to this author at the Reynolds Institute on Aging, 629 Jack Stephens Dr., Little Rock AR 72205, USA; Tel: 501-526-5811; Fax: 501-526-5830; E-mail: firstname.lastname@example.org of A . This is consistent with the elevation of D-serine in Alzheimer ventricular cerebrospinal fluid . "
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ABSTRACT: Alzheimer's disease (AD) involves neuronal loss and reduction of synaptic density in specific brain region. Some of the neuronal deaths are associated with excitotoxicity. We previously reported that amyloid beta-peptide (Abeta) induced release of N-methyl-D-aspartate receptor (NMDA-R) co-agonists, including glutamate and D-serine. The induction of D-serine production by Abeta involves transcriptional and/or translational regulation of serine racemase gene. Similarly, we report here that conditioned medium from microglia treated with secreted amyloid precursor protein (sAPP) contained elevated levels of D-serine. In microglia, sAPP increased the steady-state dimeric protein level of serine racemase. Promoter-reporter and mRNA analyses suggested that serine racemase is transcriptionally induced by sAPP. These data extend the link between excitotoxicity and neuroinflammation. D-serine may cooperate with glutamate to link neuroinflammation with excitotoxicity, suggesting a pathogenic mechanism applicable to neuronal death in AD and other neurodegenerative diseases.
Current Alzheimer Research 08/2007; 4(3):243-51. DOI:10.2174/156720507781077241 · 3.89 Impact Factor
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