Decreased left frontal lobe N-acetylaspartate in schizophrenia

Deicken, Raymond F.; Zhou, Ling; Corwin, Faith; Vinogradov, Sophia; Weiner, Michael W.

doi:10.1176/ajp.154.5.688

Cited by 74 publications

(3 citation statements)

References 16 publications

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“…Unlike many studies of adult subjects with schizophrenia, schizophreniform disorder, or at risk for schizophrenia (Bertolino et al, 1996; Bertolino et al, 1998; Bertolino and Weinberger, 1999; Bertolino et al, 2001; Bertolino et al, 2003; Block et al, 2000; Bustillo et al, 2001; Callicott et al, 2000; Cecil et al, 1999; Choe et al, 1994; Deicken et al, 1997; Heimberg et al, 1998; Jessen et al, 2006; Lim et al, 1998; Molina et al, 2005; Molina et al, 2006), but similar to several other studies (Bartha et al, 1999; Rusch et al, 2008; Sigmundsson et al, 2003; Szulc et al, 2005; Wood et al, 2003), we did not observe below-normal tNAA in the middle frontal gyri. Findings are also inconsistent in the few pediatric studies of subjects with or at risk for schizophrenia or schizophreniform disorders (reviewed in (Mehler and Warnke, 2002)) with five finding below-normal tNAA (Bertolino et al, 1998; Brooks et al, 1998; Hagino et al, 2002; Pae et al, 2004; Stanley et al, 2007) and three reporting no abnormality (Bartha et al, 1999; Wood et al, 2006; Wood et al, 2003).…”

Section: Discussionsupporting

confidence: 77%

“…For example, the frontal cortical tNAA deficits in several studies (Block et al, 2000; Deicken et al, 1997; Heimberg et al, 1998; Jessen et al, 2006; Pae et al, 2004) included regions outside of the middle frontal gyrus. Regarding tissue composition, in many cases (Brooks et al, 1998; Choe et al, 1994; Lim et al, 1998; Molina et al, 2005; Molina et al, 2006) the voxel included white matter.…”

Section: Discussionmentioning

confidence: 99%

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Proton magnetic resonance spectroscopy and thought disorder in childhood schizophrenia

Seese

O’Neill

Hudkins

et al. 2011

Schizophrenia Research

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Objective Although magnetic resonance spectroscopy has identified metabolic abnormalities in adult and childhood schizophrenia, no prior studies have investigated the relationship between neurometabolites and thought disorder. This study examined this association in language-related brain regions using proton magnetic resonance spectroscopic imaging (1H MRSI). Method MRSI was acquired bilaterally from 28 youth with childhood-onset schizophrenia and 34 healthy control subjects in inferior frontal, middle frontal, and superior temporal gyri at 1.5 T and short echo time (TR/TE=1500/30 ms). CSF-corrected “total NAA” (tNAA; N-acetyl-aspartate+N-acetyl-aspartyl-glutamate), glutamate+glutamine (Glx), creatine+phosphocreatine (Cr+PCr), choline compounds (Cho), and myo-inositol (mI) were assayed in manually drawn regions-of-interest partitioned into gray matter, white matter, and CSF and then coregistered with MRSI. Speech samples of all subjects were coded for thought disorder. Results In the schizophrenia group, the severity of formal thought disorder correlated significantly with tNAA in the left inferior frontal and superior temporal gyri and with Cr+PCr in left superior temporal gyrus. Conclusions Neurometabolite concentrations in language-related brain regions are associated with thought disorder in childhood-onset schizophrenia.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Proton magnetic resonance spectroscopy and thought disorder in childhood schizophrenia

Seese

O’Neill

Hudkins

et al. 2011

Schizophrenia Research

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“…Thus, from these studies it appears that one consequence of early life Pb 2+ exposure is the possible loss of neurons or neuronal elements such as axons and dendrites in the brain. The decrease in the NAA signal in the brain of Pb 2+ -exposed children is consistent with what is observed in the brain of schizophrenia subjects (Deicken et al, 1997; Bertolino et al, 1998). Although no apparent structural abnormalities were present in the brain of these Pb 2+ -exposed children, it may have been too early in the developmental process for measurable changes to occur in brain size and it is possible that at a latter age structural abnormalities may be apparent [See studies below].…”

Section: Neuroimaging Studies Of Brain Volume and Chemistrysupporting

confidence: 88%

Is lead exposure in early life an environmental risk factor for Schizophrenia? Neurobiological connections and testable hypotheses

2012

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Schizophrenia is a devastating neuropsychiatric disorder of unknown etiology. There is general agreement in the scientific community that schizophrenia is a disorder of neurodevelopmental origin in which both genes and environmental factors come together to produce a schizophrenia phenotype later in life. The challenging questions have been which genes and what environmental factors? Although there is evidence that different chromosome loci and several genes impart susceptibility for schizophrenia; and epidemiological studies point to broad aspects of the environment, only recently there has been an interest in studying gene × environment interactions. Recent evidence of a potential association between prenatal lead (Pb2+) exposure and schizophrenia precipitated the search for plausible neurobiological connections. The most promising connection is that in schizophrenia and in developmental Pb2+ exposure there is strong evidence for hypoactivity of the N-methyl-d-aspartate (NMDA) subtype of excitatory amino acid receptors as an underlying neurobiological mechanism in both conditions. A hypofunction of the NMDA receptor (NMDAR) complex during critical periods of development may alter neurobiological processes that are essential for brain growth and wiring, synaptic plasticity and cognitive and behavioral outcomes associated with schizophrenia. We also describe on-going proof of concept gene-environment interaction studies of early life Pb2+ exposure in mice expressing the human mutant form of the disrupted in schizophrenia 1 (DISC-1) gene, a gene that is strongly associated with schizophrenia and allied mental disorders.

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Decreased Dendritic Spine Density on Prefrontal Cortical Pyramidal Neurons in Schizophrenia

Glantz¹,

Lewis²

2000

Arch Gen Psychiatry

1,460

987

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Decreased left frontal lobe N-acetylaspartate in schizophrenia

Cited by 74 publications

References 16 publications

Proton magnetic resonance spectroscopy and thought disorder in childhood schizophrenia

Proton magnetic resonance spectroscopy and thought disorder in childhood schizophrenia

Is lead exposure in early life an environmental risk factor for Schizophrenia? Neurobiological connections and testable hypotheses

Decreased Dendritic Spine Density on Prefrontal Cortical Pyramidal Neurons in Schizophrenia

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