Distribution of Microtubule-Associated Protein MAP2-Immunoreactive Interstitial Neurons in the Parahippocampal White Matter in Subjects With Schizophrenia

Rioux, Lise; Nissanov, Jonathan; Lauber, Katherine; Bilker, Warren B.; Arnold, Steven E.

doi:10.1176/appi.ajp.160.1.149

Cited by 61 publications

(41 citation statements)

References 24 publications

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“…The results from the present study provide one mechanism that could contribute to a deficit seen in schizophrenia: failure of migration in various cortical regions (Akbarian et al, 1996;Rioux et al, 2003). Reduced NRG1 contributes to disruption of radial glia, which in turn influences the ability of neurons to migrate properly into the cerebral cortex.…”

Section: Resultsmentioning

confidence: 73%

Endogenous Neuregulin Restores Radial Glia in a (Ferret) Model of Cortical Dysplasia

Gierdalski¹,

Sardi²,

Corfas³

et al. 2005

J. Neurosci.

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Radial glia are integral components of the developing neocortex. During corticogenesis, they form an important scaffold for neurons migrating into the cortical plate. Recent attention has focused on neuregulin (NRG1), acting through erbB receptors, in maintaining their morphology. We developed a model of developmental radial glial disruption by delivering an antimitotic [methylazoxy methanol (MAM)] to pregnant ferrets on embryonic day 24 (E24). We previously found that normal ferret cortex contains a soluble factor capable of realigning the disorganized radial glia back toward their normal morphology. Characterization of the reorganizing activity in normal cortex demonstrated that the probable factor mediating these responses was a 30 -50 kDa protein. To test whether this endogenous soluble factor was NRG1, we used organotypic cultures of E24 MAM-treated ferret neocortex supplemented with the endogenous factor obtained from normal cortical implants, exogenous NRG1␤, antibodies that either blocked or stimulated erbB receptors, or a soluble erbB subtype that binds to available NRG1. We report that exogenous NRG1 or antibodies that stimulate erbB receptors dramatically improve the morphology of disrupted radial glia, whereas blockade of NRG1-erbB signaling prevents the radial glial repair. Our results suggest that NRG1 is an endogenous factor in ferret neocortex capable of repairing damaged radial glia and that it acts via one or more erbB receptors.

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Section: Resultsmentioning

confidence: 73%

Endogenous Neuregulin Restores Radial Glia in a (Ferret) Model of Cortical Dysplasia

Gierdalski¹,

Sardi²,

Corfas³

et al. 2005

J. Neurosci.

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“…The MAPT gene is associated with neurodegenerative diseases such as frontotemporal dementia and Alzheimer disease [Pittman et al, 2006]. There is substantial debate about the involvement of the microtubilin associated proteins in schizophrenia [Arnold et al, 1991;Cotter et al, 1997Cotter et al, , 2000Rioux et al, 2003;Law et al, 2004]. The association of this tau gene with non-affective schizophrenia subjects may suggest that any effect of this gene is more prominent in non-affective subgroups of schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Do mood symptoms subdivide the schizophrenia phenotype? association of the GMP6A gene with a depression subgroup

Boks

Hoogendoorn

Jungerius

et al. 2008

American J of Med Genetics Pt B

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Genetic studies of clinically defined subgroups of schizophrenia patients may reduce the phenotypic heterogeneity of schizophrenia and thus facilitate the identification of genes that confer risk to this disorder. Several latent class analyses have provided subgroups of psychotic disorders that show considerable consistency over these studies. The presence or absence of mood symptoms was found to contribute most to the delineations of these subgroups. In this study we used six previously published subtypes of psychosis derived from latent class analysis of a large sample of psychosis patients. In 280 schizophrenia patients and 525 healthy controls we investigated the associations of these subgroups with myelin related genes. After bonferroni correction we found an association of the glycoprotein M6A gene (GPM6A) with the subgroup of schizophrenia patients with high levels of depression (P-corrected = 0.006). Borderline association of the microtubulin associated protein tau (MAPT) with a primarily non-affective group of schizophrenia patients (P-corrected = 0.052) was also observed. GPM6A modulates the influence of stress on the hippocampus in animals. Thus our findings could suggest that GMP6A plays a role in the stress-induced hippocampal alterations that are found in psychiatric disorders in general and schizophrenia in particular. Overall, these finding suggests that investigating subgroups of schizophrenia based symptoms profile and particularly mood symptoms can facilitate genetic studies of schizophrenia.

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“…They found increased density of IWMNs in dorsolateral prefrontal cortex in the deficit group (n = 3) compared with the nondeficit (n = 4) as well as the control (n = 5) groups, suggestive of different pathophysiology for deficit and nondeficit schizophrenia (however, the deficit group was much older, which could also account for the differences). Finally, Rioux et al [64], using the same staining method as Kirkpatrick (see Table 3 for methodological details), also found a maldistribution of IWMNs, especially in the deeper white matter of the parahippocampal gyrus in patients with schizophrenia compared with controls.…”

Section: The Distribution Of Neurons In White Mattermentioning

confidence: 93%

Evidence for white matter abnormalities in schizophrenia

Kubicki

McCarley

Shenton

2005

Current Opinion in Psychiatry

132

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Purpose of review-The purpose of this review is to highlight important recent imaging, histological, and genetic findings relevant to white matter abnormalities in schizophrenia. It is cast within the context of research findings conducted over the last 5 years, where we analyze their importance in understanding schizophrenia, as well as discuss future directions for research.Recent findings-White matter abnormalities have long been hypothesized in schizophrenia, although only recently has it become possible to investigate them more closely. This has come about as a result of advances in neuroimaging, including new imaging techniques sensitive to white matter structure, as well as advances in computer science, with new analysis techniques making it possible to evaluate several interconnected brain regions at a time. Postmortem studies, with advances such as fluoroscopy and electron microscopy, have also led to quantifying populations of different brain cells, including myelin-forming oligodendrocytes. Moreover, molecular studies enable examination of immunoreactivity of proteins that are responsible for building myelin sheaths. Additionally, microarray genetic studies allow us to investigate myelin-related genes in schizophrenia. Taken together, these technological advances bring us closer to understanding white matter pathology in schizophrenia.Summary-Advances in new imaging techniques likely account for the renewed interest in investigating white matter abnormalities in schizophrenia, with over 30 new articles published on this topic in the last 12 months, compared with 11 the year before. We review recent imaging, histological, and genetic findings that suggest white matter abnormalities in schizophrenia.

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Distribution of Microtubule-Associated Protein MAP2-Immunoreactive Interstitial Neurons in the Parahippocampal White Matter in Subjects With Schizophrenia

Abstract: These findings indicate there is an abnormality in the residua of the cortical subplate in the anterior region of the adult parahippocampal gyrus in schizophrenia subjects.

Cited by 61 publications

References 24 publications

Endogenous Neuregulin Restores Radial Glia in a (Ferret) Model of Cortical Dysplasia

Endogenous Neuregulin Restores Radial Glia in a (Ferret) Model of Cortical Dysplasia

Do mood symptoms subdivide the schizophrenia phenotype? association of the GMP6A gene with a depression subgroup

Evidence for white matter abnormalities in schizophrenia

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