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Extracellular N-acetylaspartate depletion in traumatic brain injury

Extracellular N-acetylaspartate depletion in traumatic brain injury
Extracellular N-acetylaspartate depletion in traumatic brain injury
N-Acetylaspartate (NAA) is almost exclusively localized in neurons in the adult brain and is present in high concentration in the CNS. It can be measured by proton magnetic resonance spectroscopy and is seen as a marker of neuronal damage and death. NMR spectroscopy and animal models have shown NAA depletion to occur in various types of chronic and acute brain injury. We investigated 19 patients with traumatic brain injury (TBI). Microdialysis was utilized to recover NAA, lactate, pyruvate, glycerol and glutamate, at 12-h intervals. These markers were correlated with survival and a 6-month Glasgow Outcome Score. Eleven patients died and eight survived. A linear mixed model analysis showed a significant effect of outcome and of the interaction between time of injury and outcome on NAA levels (p = 0.009 and p = 0.004, respectively). Overall, extracellular NAA was 34% lower in non-survivors. A significant non-recoverable fall was observed in this group from day 4 onwards, with a concomitant rise in lactate–pyruvate ratio and glycerol. These results suggest that mitochondrial dysfunction is a significant contributor to poor outcome following TBI and propose extracellular NAA as a potential marker for monitoring interventions aimed at preserving mitochondrial function.
0022-3042
861-869
Belli, Antonio
33707b7b-b004-4245-aead-98a8e1e2b2e2
Sen, Jon
464edd7f-7891-4e3f-a86c-0675fd129828
Petzold, Axel
f7d23dac-63d2-4b0c-a0c1-0c2e60cffdc1
Russo, Salvatore
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Kitchen, Neil
f0586d86-9678-4566-a057-7164e75d56d3
Smith, Martin
355414f9-5908-4f09-8b52-138c81b3eb1e
Tavazzi, Barbara
22416dea-27d4-496d-8104-803bc0b0f13c
Vagnozzi, Roberto
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Signoretti, Stefano
55ae0833-9e5f-410a-ad3c-25f7dec233f5
Amorini, Angela Maria
aec4907d-88e9-4f09-944a-120859f43a42
Bellia, Francesco
16842653-d0d3-4ed0-a5c2-19dc55cc138c
Lazzarino, Giuseppe
2344efe0-43bc-4781-9f72-451f3d7f407d
Belli, Antonio
33707b7b-b004-4245-aead-98a8e1e2b2e2
Sen, Jon
464edd7f-7891-4e3f-a86c-0675fd129828
Petzold, Axel
f7d23dac-63d2-4b0c-a0c1-0c2e60cffdc1
Russo, Salvatore
8538ab12-e8af-4864-a74d-9c00f713e466
Kitchen, Neil
f0586d86-9678-4566-a057-7164e75d56d3
Smith, Martin
355414f9-5908-4f09-8b52-138c81b3eb1e
Tavazzi, Barbara
22416dea-27d4-496d-8104-803bc0b0f13c
Vagnozzi, Roberto
3c1c46f7-9a64-459e-82cd-50cf9ee73a2e
Signoretti, Stefano
55ae0833-9e5f-410a-ad3c-25f7dec233f5
Amorini, Angela Maria
aec4907d-88e9-4f09-944a-120859f43a42
Bellia, Francesco
16842653-d0d3-4ed0-a5c2-19dc55cc138c
Lazzarino, Giuseppe
2344efe0-43bc-4781-9f72-451f3d7f407d

Belli, Antonio, Sen, Jon, Petzold, Axel, Russo, Salvatore, Kitchen, Neil, Smith, Martin, Tavazzi, Barbara, Vagnozzi, Roberto, Signoretti, Stefano, Amorini, Angela Maria, Bellia, Francesco and Lazzarino, Giuseppe (2006) Extracellular N-acetylaspartate depletion in traumatic brain injury. Journal of Neurochemistry, 97 (3), 861-869. (doi:10.1111/j.1471-4159.2005.03602.x).

Record type: Article

Abstract

N-Acetylaspartate (NAA) is almost exclusively localized in neurons in the adult brain and is present in high concentration in the CNS. It can be measured by proton magnetic resonance spectroscopy and is seen as a marker of neuronal damage and death. NMR spectroscopy and animal models have shown NAA depletion to occur in various types of chronic and acute brain injury. We investigated 19 patients with traumatic brain injury (TBI). Microdialysis was utilized to recover NAA, lactate, pyruvate, glycerol and glutamate, at 12-h intervals. These markers were correlated with survival and a 6-month Glasgow Outcome Score. Eleven patients died and eight survived. A linear mixed model analysis showed a significant effect of outcome and of the interaction between time of injury and outcome on NAA levels (p = 0.009 and p = 0.004, respectively). Overall, extracellular NAA was 34% lower in non-survivors. A significant non-recoverable fall was observed in this group from day 4 onwards, with a concomitant rise in lactate–pyruvate ratio and glycerol. These results suggest that mitochondrial dysfunction is a significant contributor to poor outcome following TBI and propose extracellular NAA as a potential marker for monitoring interventions aimed at preserving mitochondrial function.

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Published date: February 2006

Identifiers

Local EPrints ID: 40700
URI: http://eprints.soton.ac.uk/id/eprint/40700
ISSN: 0022-3042
PURE UUID: b92ea895-7db9-44f0-a4ff-5998c0b876cb

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Date deposited: 07 Jul 2006
Last modified: 15 Jul 2019 18:58

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Contributors

Author: Antonio Belli
Author: Jon Sen
Author: Axel Petzold
Author: Salvatore Russo
Author: Neil Kitchen
Author: Martin Smith
Author: Barbara Tavazzi
Author: Roberto Vagnozzi
Author: Stefano Signoretti
Author: Angela Maria Amorini
Author: Francesco Bellia
Author: Giuseppe Lazzarino

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