Specific metabolites in the medial prefrontal cortex are associated with the neurocognitive deficits in schizophrenia: A preliminary study

Shirayama, Yukihiko; Obata, Takayuki; Matsuzawa, Daisuke; Nonaka, Hiroi; Kanazawa, Yôko; Yoshitome, Eiji; Ikehira, Hiroo; Hashimoto, Kenji; Iyo, Masaomi

doi:10.1016/j.neuroimage.2009.10.031

Cited by 91 publications

(99 citation statements)

References 81 publications

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“…Altered glutamatergic neurotransmission leads to altered levels of glutamine, glutamate and most notably of glutamine-to-glutamate ratio, as observed in 1 H NMR spectra from anterior brain areas of schizophrenia patients (Shirayama et al, 2010;Bustillo et al, 2009;Tayoshi et al, 2009;Lutkenhoff et al, 2008), and similar observations have been reported in experimental models of schizophrenia. A recent study reported elevated glutamine to glutamate ratio and changed energy metabolism in prefrontal cortex of rats with NMDA receptor hypofunction, a rodent model that mimics schizophrenia symptoms (Iltis et al, 2009).…”

Section: Schizophreniasupporting

confidence: 75%

“…For example, impaired neurotransmission and excitotoxicity after an ischemic insult lead to transient glutamate decrease and glutamine accumulation Lei et al, 2009). In line with this idea, disturbed glutamatergic neurotransmission in anterior regions of the schizophrenic brain leads to altered levels of glutamine, glutamate and most notably of glutamine to glutamate ratio, as observed in clinical 1 H NMR spectroscopy studies (Bustillo et al, 2009;Lutkenhoff et al, 2008;Shirayama et al, 2010;Tayoshi et al, 2009).…”

Section: Neurotransmitter Metabolismmentioning

confidence: 65%

“…Schizophrenia patients display brain metabolic alterations, particularly increased glutamine and glutamate in anterior regions of the cortex (Shirayama et al, 2010;Bustillo et al, 2009;Tayoshi et al, 2009;Lutkenhoff et al, 2008). Other reports suggested altered NAA, creatine and choline in the thalamus (Yoo et al, 2009) and hippocampus (Lutkenhoff et al, 2008).…”

Section: Schizophreniamentioning

confidence: 99%

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The neurochemical profile quantified by in vivo 1H NMR spectroscopy

et al. 2012

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Section: Schizophreniasupporting

confidence: 75%

Section: Neurotransmitter Metabolismmentioning

confidence: 65%

Section: Schizophreniamentioning

confidence: 99%

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The neurochemical profile quantified by in vivo 1H NMR spectroscopy

et al. 2012

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“…For example, impaired neurotransmission and excitotoxicity after an ischemic insult lead to transient glutamate decrease and glutamine accumulation (Berthet et al, 2011;Lei et al, 2009). In line with this idea, disturbed glutamatergic neurotransmission in schizophrenia leads to altered levels of glutamine, glutamate, and most notably of Gln/Glu, as observed in translational and clinical 1 H MRS studies (Bustillo et al, 2009;Hashimoto et al, 2005;Lutkenhoff et al, 2008;Shirayama et al, 2010;Tayoshi et al, 2009). …”

Section: Discussionmentioning

confidence: 67%

Longitudinal neurochemical modifications in the aging mouse brain measured in vivo by 1H magnetic resonance spectroscopy

Duarte

Gruetter

2014

Neurobiology of Aging

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H MRS Brain Metabolism a b s t r a c tAlterations to brain homeostasis during development are reflected in the neurochemical profile determined noninvasively by 1 H magnetic resonance spectroscopy. We determined longitudinal biochemical modifications in the cortex, hippocampus, and striatum of C57BL/6 mice aged between 3 and 24 months . The regional neurochemical profile evolution indicated that aging induces general modifications of neurotransmission processes (reduced GABA and glutamate), primary energy metabolism (altered glucose, alanine, and lactate) and turnover of lipid membranes (modification of choline-containing compounds and phosphorylethanolamine), which are all probably involved in the frequently observed age-related cognitive decline. Interestingly, the neurochemical profile was different in male and female mice, particularly in the levels of taurine that may be under the control of estrogen receptors. These neurochemical profiles constitute the basal concentrations in cortex, hippocampus, and striatum of healthy aging male and female mice.

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“…These results did not appear related to a more ventral [23][24][25] or dorsal frontal placement. [26][27][28][29][30] However, the quality of the spectral fits is not always clear in these reports (except for [27][28][29] ) and the samples were small (9 to 30 for the schizophrenia groups 6 ). More recent studies reported increases, [31][32][33][34][35] reductions 25,[36][37][38] and no differences 39 in Glx or glutamate.…”

Section: Discussionmentioning

confidence: 99%

Glutamatergic and Neuronal Dysfunction in Gray and White Matter: A Spectroscopic Imaging Study in a Large Schizophrenia Sample

Bustillo

Jones

Chen

et al. 2016

SCHBUL

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Glutamine plus glutamate (Glx), as well as N-acetylaspartate compounds (NAAc, N-acetylaspartate plus N-acetyl-aspartyl-glutamate), a marker of neuronal viability, can be quantified with proton magnetic resonance spectroscopy ( 1 H-MRS). We used 1 H-MRS imaging to assess Glx and NAAc, as well as totalcholine (glycerophospho-choline plus phospho-choline), myo-inositol and total-creatine (creatine plus phosphocreatine) from an axial supraventricular slab of gray matter (GM, medial-frontal and medial-parietal) and white matter (WM, bilateral-frontal and bilateralparietal) voxels. Schizophrenia subjects (N = 104) and healthy controls (N = 97) with a broad age range (16 to 65) were studied. In schizophrenia, Glx was increased in GM (P < .001) and WM (P = .01), regardless of age. However, with greater age, NAAc increased in GM (P < .001) but decreased in WM (P < .001) in schizophrenia. In patients, total creatine decreased with age in WM (P < .001). Finally, overall cognitive score correlated positively with WM neurometabolites in controls but negatively in the schizophrenia group (NAAc, P < .001; and creatine [only younger], P < .001). We speculate the results support an ongoing process of increased glutamate metabolism in schizophrenia. Later in the illness, disease progression is suggested by increased cortical compaction without neuronal loss (elevated NAAc) and reduced axonal integrity (lower NAAc). Furthermore, this process is associated with fundamentally altered relationships between neurometabolite concentrations and cognitive function in schizophrenia.

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Specific metabolites in the medial prefrontal cortex are associated with the neurocognitive deficits in schizophrenia: A preliminary study

Cited by 91 publications

References 81 publications

The neurochemical profile quantified by in vivo 1H NMR spectroscopy

The neurochemical profile quantified by in vivo 1H NMR spectroscopy

Longitudinal neurochemical modifications in the aging mouse brain measured in vivo by 1H magnetic resonance spectroscopy

Glutamatergic and Neuronal Dysfunction in Gray and White Matter: A Spectroscopic Imaging Study in a Large Schizophrenia Sample

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