			Home About us Contact

Aspartate Levels (aspartate + level)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Frontal lobe syndrome or adolescent-onset schizophrenia?

ACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2006
A case report
Objective:, To highlight the difficulties that abound in making a clinical distinction between early-onset schizophrenia (EOS) and juvenile frontal dementia early in the course of illness. Method:, Clinical information and data from investigations in single case was collated and reviewed. Results:, A 15-year-old girl was admitted to our psychiatric unit because of cognitive decline and formal thought disorder with echopraxia, echolalia and palilalia, and a lack of flexibility in the use of cognitive and motor strategies that culminated in psychosis. A single photon emission computerized tomography scan showed marked frontal lobe hypoperfusion; however, on proton spectroscopy there was no differential in N -acetyl aspartate levels. Conclusion:, Hypofrontality in EOS is well established and the association of frontal functional alterations, neuropsychological impairment and psychotic symptomatology is suggestive of frontal lobe prodrome that precedes the onset of psychosis. [source]

NMDA receptors mediate an early up-regulation of brain-derived neurotrophic factor expression in substantia nigra in a rat model of presymptomatic Parkinson's disease

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 10 2009
Gonzalo Bustos
Abstract The clinical symptoms of Parkinson's disease (PD) appear late and only when the degenerative process at the level of the nigrostriatal dopamine (DA) pathway is quite advanced. An increase in brain-derived neurotrophic factor (BDNF) expression may be one of the molecular signals associated to compensatory and plastic responses occurring in basal ganglia during presymptomatic PD. In the present study, we used in vivo microdialysis, semiquantitative reverse transcriptase,polymerase chain reaction, and immunohistochemistry to study N-methyl- D -aspartic acid (NMDA) receptor regulation of BDNF expression in substantia nigra (SN) of adult rats after partial lesioning of the nigrostriatal DA pathway with unilateral striatal injections of 6-hydroxydopamine (6-OHDA). A time-dependent partial decrease of striatal DA tissue content as well as parallel and gradual increases in extracellular glutamate and aspartate levels in SN were found 1 to 7 days after unilateral 6-OHDA intrastriatal injection. Instead, the number of tyrosine hydroxylase,immunoreactive (IR) cells in the ipsilateral SN pars compacta remained statistically unchanged after neurotoxin injection. Intrastriatal administration of 6-OHDA also produced an early and transient augmentation of pan-BDNF, exon II,BDNF, and exon III,BDNF transcripts in the ipsilateral SN. The pan-BDNF and exon II,BDNF transcript increases were completely abolished by the prior systemic administration of MK-801, a selective antagonist of NMDA receptors. MK-801 also blocked the increase in BDNF-IR cells in SN observed 7 days after unilateral 6-OHDA intrastriatal injections. Our findings suggest that a coupling between glutamate release, NMDA receptor activation, and BDNF expression may exist in the adult SN and represent an important signal in this midbrain nucleus triggered in response to partial DA loss occurring in striatal nerve endings during presymptomatic PD. © 2009 Wiley-Liss, Inc. [source]

Effects of Acamprosate on Excitatory Amino Acids During Multiple Ethanol Withdrawal Periods

ALCOHOLISM, Issue 3 2003
Abdelkader Dahchour
Background: Our previous studies on the effects of acamprosate on enhanced locomotion during repeated withdrawals are now extended to the effects of acamprosate on excitatory amino acids in the hippocampus during repeated ethanol withdrawals. Methods: In this study, Wistar rats were made ethanol dependent by 4 weeks of vapor inhalation. After this first cycle of chronic ethanol treatment, rats underwent repeated and alternate cycles of 24 hr withdrawals and 1 week of chronic ethanol treatment. The microdialysis technique was used together with high-performance liquid chromatography and electrochemical detection to quantify different amino acids such as aspartate and glutamate. Results: An intraperitoneal administration of acamprosate (400 mg/kg) to naïve rats did not alter aspartate or glutamate levels compared with the saline groups. During the first cycle of ethanol withdrawal, the administration of acamprosate (400 mg/kg, intraperitoneally) 2 hr after the commencement of ethanol withdrawal decreased both aspartate and glutamate microdialysate levels when compared with their respective saline group. Acamprosate administration also significantly decreased glutamate levels during the third withdrawal compared with the saline group, whereas no changes were seen in aspartate levels. Conclusion: The results of this work demonstrate that acamprosate reduced the excitatory amino acid glutamate increase observed during repeated ethanol withdrawal. These effects of acamprosate may provide a protective mechanism against neurotoxicity by reducing excitatory amino acids, particularly glutamate. [source]

In vitro neurotoxic properties and excitatory aminoacids concentration in the cerebrospinal fluid of amyotrophic lateral sclerosis patients.

ACTA NEUROLOGICA SCANDINAVICA, Issue 2 2010
Relationship with the degree of certainty of disease diagnoses
Fiszman ML, Ricart KC, Latini A, Rodríguez G, Sica REP. In vitro neurotoxic properties and excitatory aminoacids concentration in the cerebrospinal fluid of amyotrophic lateral sclerosis patients. Relationship with the degree of certainty of disease diagnoses. Acta Neurol Scand: 2010: 121: 120,126. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective,,, To determine glutamate and aspartate levels in the cerebrospinal fluid (CSF) in patients with sporadic amyotrophic lateral sclerosis (SALS) grouped according to El Escorial diagnostic criteria, and to perform an in vitro assessment of the neurotoxicity of the CSF in murine cortical neurons. Methods,,, SALS patients were sorted according to El Escorial diagnostic criteria. Glutamate and aspartate were measured in the CSF using high performance liquid chromatography. Cultured cortical neuron viability was determined after exposure to CSF for 24 h. Results,,, Glutamate levels were elevated in 28 out of the 29 patients with definite, probable or possible SALS. There were no differences in glutamate concentrations when the three clinical forms of the disease were compared; neither there were significant variation across disease duration and clinical presentation. In agreement with previous reports, we concluded that CSF-SALS-induced in vitro neurotoxicity is mediated by ionotropic glutamate receptors. We found no relationship between the degree of in vitro neurotoxicity and glutamate concentration in the CSF. Conclusions,,, Glutamate but not aspartate CSF levels may contribute to ALS pathogenesis. However, glutamate levels may not influence the degree of diagnosis certainty or lesion extension. [source]