Increased Vertical Axon Numbers in Cingulate Cortex of Schizophrenics

Beneš, Francine M.; Majocha, Ronald E.; Bird, Edward D.; Marotta, Charles A.

doi:10.1001/archpsyc.1987.01800230097015

Cited by 139 publications

(56 citation statements)

References 30 publications

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“…This is in keeping with previous functional neuroimaging studies (Andreasen et al, 1992;Dolan et al, 1995) as well as neurophysiological data, suggesting schizophrenia-related abnormalities in anterior cingulate cortex (Benes et al, 1987(Benes et al, , 1992. The suggested roles for this region in attention (Corbetta et al, 1991;Bench et al, 1993) and performance monitoring (Carter et al, 1998) are compatible with the pattern of cognitive deficits in attention (McGhie and Chapman, 1961) and working memory (Park and Holzman, 1992) reported in association with the disease.…”

Section: Fig 1 Left Panelsupporting

confidence: 91%

Abnormal Cingulate Modulation of Fronto-Temporal Connectivity in Schizophrenia

Fletcher¹,

McKenna

Friston³

et al. 1999

NeuroImage

246

113

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Functional neuroimaging provides a novel means of exploring neurophysiological function in schizophrenia. However, most of the studies that have been carried out report their findings in terms of regionally localized abnormalities. In this paper we propose an alternative method of data analysis that emphasizes global integration rather than isolated regional changes in response to psychological tasks. In doing so, we suggest that brain abnormalities in schizophrenia are best characterized as a disturbance in the integration of activity across a number of brain regions. Using a hypothesis-led analysis, we show that the condition is associated with a disruption of the normal anterior cingulate modulation of prefrontotemporal integration. This analytical technique, we suggest, provides a conceptually powerful approach to the imaging of abnormal brain function in psychopathological conditions.

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Section: Fig 1 Left Panelsupporting

confidence: 91%

Abnormal Cingulate Modulation of Fronto-Temporal Connectivity in Schizophrenia

Fletcher¹,

McKenna

Friston³

et al. 1999

NeuroImage

246

113

View full text Add to dashboard Cite

show abstract

“…Deficits in these pathways could result in the disarray of neuronal orientation and abnormal axon projections seen in schizophrenics. 5,6 (d) Glial secreted factors such as Wnt and TNF-a also play an important role in synaptogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…1 Although the aetiology of the disease remains unknown, several lines of evidence based on neuropathological, pharmacological and genetic data suggest that schizophrenia is a disease of the synapse. 2 Post mortem and brain imaging studies of schizophrenics reveal neuroanatomical pathologies such as smaller neuropil size, decreased number of dendritic spines and arborisations, 3,4 abnormal neuronal migration and orientation, [4][5][6] decreased number of synaptic proteins, 7,8 enlarged ventricles and decreased brain volumes. 2,9 These impairments suggest that abnormal or reduced synaptic connectivity may result from improper neurodevelopment culminating from an underlying genetic predisposition and/or early environmental insult.…”

Section: Introductionmentioning

confidence: 99%

Disrupted in Schizophrenia 1 Interactome: evidence for the close connectivity of risk genes and a potential synaptic basis for schizophrenia

et al. 2006

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Disrupted in Schizophrenia 1 (DISC1) is a schizophrenia risk gene associated with cognitive deficits in both schizophrenics and the normal ageing population. In this study, we have generated a network of protein-protein interactions (PPIs) around DISC1. This has been achieved by utilising iterative yeast-two hybrid (Y2H) screens, combined with detailed pathway and functional analysis. This so-called 'DISC1 interactome' contains many novel PPIs and provides a molecular framework to explore the function of DISC1. The network implicates DISC1 in processes of cytoskeletal stability and organisation, intracellular transport and cellcycle/division. In particular, DISC1 looks to have a PPI profile consistent with that of an essential synaptic protein, which fits well with the underlying molecular pathology observed at the synaptic level and the cognitive deficits seen behaviourally in schizophrenics. Utilising a similar approach with dysbindin (DTNBP1), a second schizophrenia risk gene, we show that dysbindin and DISC1 share common PPIs suggesting they may affect common biological processes and that the function of schizophrenia risk genes may converge.

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“…Merely poorer average performance would not necessarily be expected to change the correlation matrix if schizo phrenics performed the task using the same cast of brain regions linked in the same way. Brain areas could be less activated due to neurotransmitter abnormalities such as excess of inhibitory dopamine release or abnormalities in local networks of interneurons [60]. The use of tasks on which schizophrenics and normals performed equally might well result in identical correlation matrices if brain areas unaffected in schizophrenia were used.…”

Section: Discussionmentioning

confidence: 99%

Correlational Patterns of Cerebral Glucose Metabolism in Never-Medicated Schizophrenics

et al. 1996

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We studied 18 never-medicated schizophrenic patients and 22 normal control subjects with ¹⁸F-deoxyglucose (FDG) positron emission tomography. Patients and controls performed the continuous performance test during FDG uptake. Cortical and subcortical structures comprising two circuits selected on the basis of several theoretical models of schizophrenia were examined. The correlation of glucose metabolic rate (GMR) for each structure in each circuit with connected structures was calculated and tested for two-tailed significance. Schizophrenics showed significantly different patterns of intercorrela-tions for both circuits. The largest difference was in the correlation of GMR in the anterior thalamus with the frontal cortex, a key element in the thalamo-cortical-striatal circuit suggested to be abnormal in some models of schizophrenia. Correlations of the frontal lobe with other regions were also more positive in normal controls than schizophrenics; controls had three correlational paths from the frontal cortex (to temporal cortex, ventral anterior thalamus, and dorsal medial thalamus) with significantly more positive correlations than schizophrenics, perhaps consistent with other findings of frontal cortical dysfunction in schizophrenia. Normal controls also had both more significant positive and more significant negative correlations between the occipital cortex and other brain areas than schizophrenics. Correlations between homologous areas in the right and left hemispheres were prominent in both groups.

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Increased Vertical Axon Numbers in Cingulate Cortex of Schizophrenics

Cited by 139 publications

References 30 publications

Abnormal Cingulate Modulation of Fronto-Temporal Connectivity in Schizophrenia

Abnormal Cingulate Modulation of Fronto-Temporal Connectivity in Schizophrenia

Disrupted in Schizophrenia 1 Interactome: evidence for the close connectivity of risk genes and a potential synaptic basis for schizophrenia

Correlational Patterns of Cerebral Glucose Metabolism in Never-Medicated Schizophrenics

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