Is plasma GABA level a biomarker of Post-Traumatic Stress Disorder (PTSD) severity? A preliminary study

Trousselard, Marion; Lefebvre, Bertrand; Caillet, Lionel; Andruétan, Yann; Montleau, Franck de; Denis, Jean‐Noël; Canini, Frédéric

doi:10.1016/j.psychres.2016.05.013

Cited by 23 publications

(17 citation statements)

References 52 publications

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“…Different neurotransmitter systems (e.g., glutamate, γ‐aminobutyric acid [GABA]) are altered in brain tissue following seizures, 32,33 and, although not shown to undergo concentration changes in the blood of epilepsy patients, this has been observed in the blood in other neurological conditions such as schizophrenia (glutamate) 34 and posttraumatic stress disorder (GABA) 35 . Although purines are also well known to be released in the brain during seizures, 36 whether this translates into changes in blood purine levels has, to our knowledge, not been proven to date.…”

Section: Discussionmentioning

confidence: 99%

Elevated blood purine levels as a biomarker of seizures and epilepsy

et al. 2021

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Objective There is a major unmet need for a molecular biomarker of seizures or epilepsy that lends itself to fast, affordable detection in an easy‐to‐use point‐of‐care device. Purines such as adenosine triphosphate and adenosine are potent neuromodulators released during excessive neuronal activity that are also present in biofluids. Their biomarker potential for seizures and epilepsy in peripheral blood has, however, not yet been investigated. The aim of the present study was to determine whether blood purine nucleoside measurements can serve as a biomarker for the recent occurrence of seizures and to support the diagnosis of epilepsy. Methods Blood purine concentrations were measured via a point‐of‐care diagnostic technology based on the summated electrochemical detection of adenosine and adenosine breakdown products (inosine, hypoxanthine, and xanthine; SMARTChip). Measurements of blood purine concentrations were carried out using samples from mice subjected to intra‐amygdala kainic acid‐induced status epilepticus and in video‐electroencephalogram (EEG)‐monitored adult patients with epilepsy. Results In mice, blood purine concentrations were rapidly increased approximately two‐ to threefold after status epilepticus (2.32 ± .40 µmol·L–1 [control] vs. 8.93 ± 1.03 µmol·L–1 [after status epilepticus]), and levels correlated with seizure burden and postseizure neurodegeneration in the hippocampus. Blood purine concentrations were also elevated in patients with video‐EEG‐diagnosed epilepsy (2.39 ± .34 µmol·L–1 [control, n = 13] vs. 4.35 ± .38 µmol·L–1 [epilepsy, n = 26]). Significance Our data provide proof of concept that the measurement of blood purine concentrations may offer a rapid, low‐volume bedside test to support the diagnosis of seizures and epilepsy.

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Section: Discussionmentioning

confidence: 99%

Elevated blood purine levels as a biomarker of seizures and epilepsy

et al. 2021

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“…In patients with generalized anxiety disorder, the number of GABA A receptors is reduced in the temporal lobe [26]. Patients with post-traumatic stress disorder (PTSD) also have lower levels of GABA in the medial prefrontal cortex [66]. Moreover, patients with panic disorder have reduced GABA A receptor numbers in the frontal, temporal, and parietal cortices; the left hippocampus; and the precuneus [67].…”

Section: Mature Stage Of Lifementioning

confidence: 99%

Altered GABAergic Signaling in Brain Disease at Various Stages of Life

Kim

Yoon

2017

Exp Neurobiol

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In the healthy brain, gamma-aminobutyric acid (GABA) is regulated by neurons and glia. This begs the question: what happens in the malfunctioning brain? There are many reasons why diseases occur, including genetic mutations, systemic problems, and environmental influences. There are also many ways in which GABA can become dysregulated, such as through alterations in its synthesis or release, and changes in systems that respond to it. Notably, dysregulation of GABA can have a large impact on the brain. To date, few reviews have examined brain diseases in which dysregulation of GABA is implicated as an underlying factor. Accordingly, the time is ripe for investigating alterations in GABAergic signaling that may play a role in changes in neuronal activity observed in the major brain disorders that occur during various stages of life. This review is meant to provide a better understanding of the role of GABA in brain health and contributor to social problems from a scientific perspective.

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“…11 Homogenates of human aortic endothelial cells and human umbilical vein endothelial cells converted radiolabeled [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]glutamate into [1-14 C]GABA, and incubation of living human umbilical vein endothelial cells with [1-14 C]glutamate resulted in the release of [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]GABA into the culture medium. Inhibition of GABA transaminase, which degrades GABA and, thus, limits the half-life of this amino acid, increased its release by ≈18%, whereas inhibition or siRNAmediated knockdown of GABA producing GADs decreased GABA release by ≈50%.…”

Section: Article See P 621mentioning

confidence: 99%

“…Plasma GABA level are in the range of ≤100 nmol/L as determined by Gas chromatography mass spectroscopy, with 80 nmol/L being considered normal. 12,13 The half-maximal effective concentration (EC50) of GABA receptors, however, is far >1 μmol/L, 2 rendering plasma GABA levels rather a biomarker than a physiologically important number. Obviously, GABA concentrations in synaptic transmission or close to the site of vesicle release are much higher.…”

Section: Circulation Researchmentioning

confidence: 99%

A Buttery Taste to Vascular Biology

Brandes

2016

Circulation Research

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Is plasma GABA level a biomarker of Post-Traumatic Stress Disorder (PTSD) severity? A preliminary study

Cited by 23 publications

References 52 publications

Elevated blood purine levels as a biomarker of seizures and epilepsy

Elevated blood purine levels as a biomarker of seizures and epilepsy

Altered GABAergic Signaling in Brain Disease at Various Stages of Life

A Buttery Taste to Vascular Biology

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