Plasma and platelet excitatory amino acids in psychiatric disorders

Ca, Altamura; Mc, Mauri; Ferrara, A.; Ar, Moro; D’Andrea, Giovanni; Zamberlan, F.

doi:10.1176/ajp.150.11.1731

Cited by 204 publications

(37 citation statements)

References 10 publications

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“…The result is compatible with previous reports, which showed increased serum levels of glutamate in chronic schizophrenia patients 28, 29 . A couple of reports have attempted and failed to replicate these findings 30, 31 ; however, a recent meta-analysis confirmed that the peripheral glutamate level of schizophrenia subjects was significantly higher than that of HC 24 . While these are findings pertain to chronic schizophrenia, we found increased glutamate levels in FEP.…”

Section: Discussionmentioning

confidence: 99%

Reduced Mismatch Negativity is Associated with Increased Plasma Level of Glutamate in First-episode Psychosis

Nagai¹,

Kirihara

Tada

et al. 2017

Sci Rep

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Reduced amplitude of mismatch negativity (MMN) is one of the more promising biological markers of schizophrenia. This finding holds true in both early and chronic phases of the disorder, and is compatible with the glutamatergic dysfunction hypothesis. To further establish MMN as a biomarker of aberrant glutamatergic neurotransmission, an exploration for an association with blood levels of glutamatergic amino acids is an important next step. Despite a large body of work investigating MMN in schizophrenia, no previous studies have undertaken this endeavor. Nineteen patients with first-episode psychosis (FEP), 21 ultra-high risk individuals (UHR), and 16 healthy controls (HC) participated in the study. The MMNs in response to duration change (dMMN) and frequency change (fMMN) were measured. The fasting plasma levels of glutamate, glutamine, glycine, D-serine, and L-serine were measured. dMMN amplitudes were significantly reduced in FEP and UHR, compared to HC. The plasma levels of glutamate of FEP were significantly higher than those of HC. Higher plasma levels of glutamate were associated with smaller dMMN amplitudes in the FEP and HC groups. These findings are compatible with the hypothesis that MMN is a useful biological marker of aberrant glutamatergic neurotransmission in the early stages of schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Reduced Mismatch Negativity is Associated with Increased Plasma Level of Glutamate in First-episode Psychosis

Nagai¹,

Kirihara

Tada

et al. 2017

Sci Rep

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“…Patients on second-generation antipsychotics were found to be more responsive to external cues for eating and they felt less satiated after a meal than patients who were not on second-generation antipsychotics [34]. In this meta-analysis, only four out of the 13 studies put patients on a controlled diet, thus dietary differences between patient and controls groups should be taken into consideration [17,26,27,35]. …”

Section: Discussionmentioning

confidence: 99%

“…Overall, 3 studies used the diagnostic criteria of the DSM-III-R [11,19,35], 2 studies used the diagnostic criteria of the DSM-IV [25,36] and 1 study used the diagnostic criteria of the Research Diagnostic Criteria by Schneider [17]. Schneider's Research Diagnostic Criteria is only available in German and could not be reviewed for this analysis; four studies did not report the diagnostic criteria used [4,16,26,27].…”

Section: Discussionmentioning

confidence: 99%

Peripheral Glutamate Levels in Schizophrenia: Evidence from a Meta-Analysis

Song¹,

Viggiano

Monda

et al. 2014

Neuropsychobiology

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Background: Recent research attempting to develop novel medications has turned to glutamatergic signaling pathways to find effective treatments for symptom clusters of schizophrenia. This meta-analysis was undertaken to clarify whether a difference in peripheral glutamate levels exists between patients with schizophrenia and healthy controls. Methods: The electronic databases Ovid MEDLINE, PubMed, and PsycINFO were systematically searched up to April 2013. The search was limited to case-control studies of blood glutamate levels in schizophrenia written in English. The differences in glutamate levels were evaluated by calculating standardized mean differences (SMD). Results: We found ten studies that met the inclusion criteria for a total of 320 schizophrenia patients and 294 controls. The meta-analysis showed that peripheral glutamate levels in schizophrenia patients were significantly higher overall than in controls (SMD = 0.635, p = 0.004). However, a significant effect of the method used to measure glutamate concentrations was found (F = 7.36, p = 0.01) where fluorometric assay was associated with effect sizes in the opposite direction. Conclusion: A higher blood glutamate concentration was found in patients with schizophrenia. However, given the small sample size and methodological differences among studies, this result is not conclusive. More comprehensive research is needed to understand the relationship between glutamate levels in schizophrenia in the blood and the brain.

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“…Increased activity of the glutamatergic system in the peripheral blood of depressive patients has been repeatedly shown [69,70,71], although this result could not be replicated by all groups [72]. The inconsistency of the findings, however, might be due to methodological problems [73].…”

Section: Inflammation Influences the Metabolism Of Serotonin And Noramentioning

confidence: 99%

Immunology of Major Depression

Müller¹

2014

Neuroimmunomodulation

148

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High levels of several proinflammatory components of the immune system, such as interleukin-6, C-reactive protein, tumor necrosis factor (TNF)-α, or neopterin in patients suffering from major depression (MD) point to the involvement of an inflammatory process in the pathophysiology of MD. The direct and indirect effects of cytokines on neurotransmitter storage and release - mediated by microglia cells and astrocytes - are discussed. The tryptophan/kynurenine metabolism is one of the indirect mechanisms because the enzyme indoleamine 2,3-dioxygenase - a key enzyme of this metabolism in the central nervous system - is driven by pro- and anti-inflammatory cytokines and degrades serotonin. Moreover, neuroactive kynurenines such as kynurenic acid and quinolinic acid act on the glutamatergic neurotransmission as N-methyl-D-aspartate antagonists and agonists, respectively. Alterations of the serotonergic, noradrenergic and glutamatergic neurotransmission have been shown with low-level neuroinflammation and may be involved in symptom generation. Epidemiological and clinical studies show a role for inflammation as a risk factor for MD. A large-scale epidemiological study in MD clearly demonstrates that severe infections and autoimmune disorders are lifetime risk factors for MD. The vulnerability-stress-inflammation model matches with this view as stress may increase proinflammatory cytokines and even contribute to a lasting proinflammatory state. Further support comes from the therapeutic benefit of anti-inflammatory medications such as the cyclo-oxygenase-2 inhibitors, TNF-α antagonists and others, and the anti-inflammatory and immunomodulatory intrinsic effects of antidepressants.

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Plasma and platelet excitatory amino acids in psychiatric disorders

Cited by 204 publications

References 10 publications

Reduced Mismatch Negativity is Associated with Increased Plasma Level of Glutamate in First-episode Psychosis

Reduced Mismatch Negativity is Associated with Increased Plasma Level of Glutamate in First-episode Psychosis

Peripheral Glutamate Levels in Schizophrenia: Evidence from a Meta-Analysis

Immunology of Major Depression

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