Chronic Schizophrenia Subjects Research Articles

Analysis of networks in the dorsolateral prefrontal cortex in chronic schizophrenia: Relevance of altered immune response.

The dorsolateral prefrontal cortex (DLPFC) has a crucial role in cognitive functioning and negative symptoms in schizophrenia. However, limited information of altered protein networks is available in this region in schizophrenia. We performed a proteomic analysis using single-shot liquid chromatography-tandem mass spectrometry of grey matter of postmortem DLPFC in chronic schizophrenia subjects (n = 20) and unaffected subjects (n = 20) followed by bioinformatic analysis to identify altered protein networks in schizophrenia (PXD024939 identifier in ProteomeXchange repository). Our results displayed a proteome profile in the DLPFC of 1989 proteins. 43 proteins were found significantly altered in schizophrenia. Analysis of this panel showed an enrichment of biological processes implicated in vesicle-mediated transport, processing and antigen presentation via MHC class II, intracellular transport and selenium metabolism. The enriched identified pathways were MHC class II antigen presentation, vesicle-mediated transport, Golgi ER retrograde transport, Nef mediated CD8 downregulation and the immune system. All these enriched categories were found to be downregulated. Furthermore, our network analyses showed crosstalk between proteins involved in MHC class II antigen presentation, membrane trafficking, Golgi-to-ER retrograde transport, Nef-mediated CD8 downregulation and the immune system with only one module built by 13 proteins. RAB7A showed eight interactions with proteins of all these pathways. Our results provide an altered molecular network involved in immune response in the DLPFC in schizophrenia with a central role of RAB7A. These results suggest that RAB7A or other proteins of this network could be potential targets for novel pharmacological strategies in schizophrenia for improving cognitive and negative symptoms.

DNA methylation levels of RELN promoter region in ultra-high risk, first episode and chronic schizophrenia cohorts of schizophrenia

The essential role of the Reelin gene (RELN) during brain development makes it a prominent candidate in human epigenetic studies of Schizophrenia. Previous literature has reported differing levels of DNA methylation (DNAm) in patients with psychosis. Therefore, this study aimed to (1) examine and compare RELN DNAm levels in subjects at different stages of psychosis cross-sectionally, (2) analyse the effect of antipsychotics (AP) on DNAm, and (3) evaluate the effectiveness and applicability of RELN promoter DNAm as a possible biological-based marker for symptom severity in psychosis.. The study cohort consisted of 56 healthy controls, 87 ultra-high risk (UHR) individuals, 26 first-episode (FE) psychosis individuals and 30 chronic schizophrenia (CS) individuals. The Positive and Negative Syndrome Scale (PANSS) was used to assess Schizophrenia severity. After pyrosequencing selected CpG sites of peripheral blood, the Average mean DNAm levels were compared amongst the 4 subgroups. Our results showed differing levels of DNAm, with UHR having the lowest (7.72 ± 0.19) while the CS had the highest levels (HC: 8.78 ± 0.35; FE: 7.75 ± 0.37; CS: 8.82 ± 0.48). Significantly higher Average mean DNAm levels were found in CS subjects on AP (9.12 ± 0.61) compared to UHR without medication (UHR(−)) (7.39 ± 0.18). A significant association was also observed between the Average mean DNAm of FE and PANSS Negative symptom factor (R2 = 0.237, ß = −0.401, *p = 0.033). In conclusion, our findings suggested different levels of DNAm for subjects at different stages of psychosis. Those subjects that took AP have different DNAm levels. There were significant associations between FE DNAm and Negative PANSS scores. With more future experiments and on larger cohorts, there may be potential use of DNAm of the RELN gene as one of the genes for the biological-based marker for symptom severity in psychosis.

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Aim:The aim of this study is to assess the neuropsychological profiles of chronic schizophrenia and alcohol-dependent subjects.Materials and Methods:This hospital-based cross-sectional study included 30 chronic schizophrenia patients, 30 alcohol-dependent patients and 30-matched normal controls. Demographic and clinical data were collected on a self-designed proforma. Positive and Negative Syndrome Scale (PANSS) and Severity of Alcohol Dependence Questionnaire (SADQ-C) were administered to chronic schizophrenia and alcohol-dependent patients, respectively. The AIIMS Comprehensive Neuropsychological Battery in Hindi (Adult Form) was used to assess neuropsychological dysfunctions.Results:Neuropsychological dysfunctions were found in 83.3% of chronic schizophrenia patients, 36.7% alcohol dependents and none of the normal subjects. In comparison to normal subjects, schizophrenia patients had significantly more dysfunctions in neuropsychological-domains such as motor, tactile, visual, receptive and expressive speech, reading, writing, arithmetic, memory, and intellectual processes. A significant positive correlation was found between the PANSS total score and T scores of most of the clinical scales except motor and visual scales; the PANSS general psychopathology score and T scores of most of the clinical scales except motor visual and pathognomonic scales; the PANSS negative score and T scores of most of the clinical scales except visual scale; and the PANSS positive score and T scores of receptive speech, arithmetic, and memory scales. In comparison to normal subjects, the alcohol dependents had significantly more dysfunctions in neuropsychological-domains such as motor, tactile, visual, receptive and expressive speech, reading, writing, arithmetic, and memory. A significant positive correlation was found between the SADQ total scale and T scores of clinical scales such as expressive speech, writing, arithmetic, intellectual processes, left hemisphere, and total battery scales.Conclusions:Neuropsychological dysfunction was significantly more common and severe in chronic schizophrenia patients than in alcohol-dependent patients. In comparison to alcohol dependents, the chronic schizophrenia patients had more dysfunctions in neuropsychological-domains such as tactile, arithmetic, memory, and intellectual processes.

Calcium-binding proteins are altered in the cerebellum in schizophrenia

Alterations in the cortico-cerebellar-thalamic-cortical circuit might underlie the diversity of symptoms in schizophrenia. However, molecular changes in cerebellar neuronal circuits, part of this network, have not yet been fully determined. Using LC-MS/MS, we screened altered candidates in pooled grey matter of cerebellum from schizophrenia subjects who committed suicide (n = 4) and healthy individuals (n = 4). Further validation by immunoblotting of three selected candidates was performed in two cohorts comprising schizophrenia (n = 20), non-schizophrenia suicide (n = 6) and healthy controls (n = 21). We found 99 significantly altered proteins, 31 of them previously reported in other brain areas by proteomic studies. Transport function was the most enriched category, while cell communication was the most prevalent function. For validation, we selected the vacuolar proton pump subunit 1 (VPP1), from transport, and two EF-hand calcium-binding proteins, calmodulin and parvalbumin, from cell communication. All candidates showed significant changes in schizophrenia (n = 7) compared to controls (n = 7). VPP1 was altered in the non-schizophrenia suicide group and increased levels of parvalbumin were linked to antipsychotics. Further validation in an independent cohort of non-suicidal chronic schizophrenia subjects (n = 13) and non-psychiatric controls (n = 14) showed that parvalbumin was increased, while calmodulin was decreased in schizophrenia. Our findings provide evidence of calcium-binding protein dysregulation in the cerebellum in schizophrenia, suggesting an impact on normal calcium-dependent synaptic functioning of cerebellar circuits. Our study also links VPP1 to suicide behaviours, suggesting a possible impairment in vesicle neurotransmitter refilling and release in these phenotypes.

DISTINCT AND SHARED CONTRIBUTIONS OF DIAGNOSIS AND SYMPTOM DOMAINS TO COGNITIVE PERFORMANCE IN SEVERE MENTAL ILLNESS

The objective of the study was to examine the cognitive profile of Spanish patients with a first episode of schizophrenia (FESz) and to compare that to the profile of patients with a chronic schizophrenia (CSz) and non-psychiatric (NP) control subjects. The study included 106 FESz, 293 CSz, and 210 NP, assessed with the Spanish version of the MATRICS Consensus Cognitive Battery (MCCB). The MCCB cognitive profile in a Spanish sample of FESz was similar to the cognitive profile of CSz with some discrepancies in select domains. The scores of both patient samples were about 1–2 SD below the scores of non-psychiatric control subjects.

MCCB cognitive profile in Spanish first episode schizophrenia patients

The objective of the study was to examine the cognitive profile of Spanish patients with a first episode of schizophrenia (FESz) and to compare that to the profile of patients with a chronic schizophrenia (CSz) and non-psychiatric (NP) control subjects. The study included 106 FESz, 293 CSz, and 210 NP, assessed with the Spanish version of the MATRICS Consensus Cognitive Battery (MCCB). The MCCB cognitive profile in a Spanish sample of FESz was similar to the cognitive profile of CSz with some discrepancies in select domains. The scores of both patient samples were about 1–2 SD below the scores of non-psychiatric control subjects.

Abnormalities of oligodendrocyte clusters in supra- and infragranular layers of the prefrontal cortex in schizophrenia

A deficit of cortical gray matter myelination in the frontal lobes has been reported in schizophrenia in neuroimaging studies. Previously the decrease in the numerical density (Nv) of oligodendrocytes (NvOl) in layers 3 and 5 in area 10 of the prefrontal cortex (PFC) has been reported in schizophrenia. Oligodendrocyte progenitors proliferate in the adult human brain and form oligodendrocyte clusters for functional-dependent adaptive myelination. We aimed to estimate the NvOl and Nv of oligodendrocyte clusters (NvOlC) in supra- and infragranular sublayers of the PFC in schizophrenia and healthy controls. 17 chronic schizophrenia subjects and 20 healthy matched controls were studied in Nissl-stained sections in sublayers 3a- 3c and 5a of the PFC by stereological optical dissector method. The NvOl and the NvOlC were significantly decreased in supra- (32%, p<0.02) and infragranular sublayers (50%, p<0.001) of the PFC in the schizophrenia group as compared to controls. The Nv OlC/Nv Ol ratio decreased significantly in the schizophrenia group only in sublayers 3a (p=0.015) and 5a (p<0.001). In the control group, the NvOlC was positively correlated with the NvOl in sublayers 3b, 3c and 5a (R≥0.59; p≤0.006). In the schizophrenia group, a significant correlation between the parameters was found only in sublayer 5a (R=0.8; p<0.001). The deficit of oligodendrocyte clusters might be associated with altered proliferation and/or maturation of oligodendrocyte progenitors in schizophrenia. Specific alterations of the Nv OlC/Nv Ol ratio might be due to different connectivity of supra- and infragranular sublayers of the PFC and their disturbances in schizophrenia.

Differences in gut microbiome composition between persons with chronic schizophrenia and healthy comparison subjects

Intestinal microbiome and gut-brain axis have been receiving increasing attention for their role in the regulation of brain/behavior and possible biological basis of psychiatric disorders. Several recent clinical studies have linked the microbiome with neuropsychiatric conditions, although the literature on schizophrenia is quite limited. This study investigated gut microbiome composition in 50 individuals, including 25 persons with chronic schizophrenia and 25 demographically-matched non-psychiatric comparison subjects (NCs). Stool samples were collected and assayed using 16S rRNA sequencing of the V4 region. Examination of unweighted UniFrac and Bray-Curtis dissimilarity revealed significant community-level separation in microbiome composition between the two subject groups. At the phylum level, Proteobacteria were found to be relatively decreased in schizophrenia subjects compared to NCs. At the genus level, Anaerococcus was relatively increased in schizophrenia while Haemophilus, Sutterella, and Clostridium were decreased. Within individuals with schizophrenia, abundance of Ruminococcaceae was correlated with lower severity of negative symptoms; Bacteroides was associated with worse depressive symptoms; and Coprococcus was related to greater risk for developing coronary heart disease. Our findings provide evidence of altered gut microbial composition in persons with chronic schizophrenia and suggest a need for larger and longitudinal studies of microbiome in schizophrenia.

Reduced oligodendrocyte density in layer 5 of the prefrontal cortex in schizophrenia.

Neuroimaging and post-mortem studies have implicated altered myelin integrity and oligodendrocyte abnormalities in the dysfunction of neuronal network in schizophrenia, including the prefrontal cortex, Brodmann area (BA) 10. Pyramidal neurons in layer 5 of BA10 are the important link of reciprocal frontal cortical-basal ganglia-thalamic circuits altered in schizophrenia. Previously, we found ultrastructural dystrophic and degenerative alterations of oligodendrocytes in layer 5 of BA10 in schizophrenia. The aim of the study was to estimate the numerical density (Nv) of oligodendrocytes in layer 5 of BA10 in schizophrenia as compared to normal controls. 17 chronic schizophrenia subjects and 22 healthy matched controls were studied in Nissl-stained sections using optical disector method. Group differences were analyzed using ANCOVA followed by post hoc Duncan's test. The Nv of oligodendrocytes was significantly lower (- 32%, p < 0.001) in the schizophrenia group as compared to the control group. Young controls (age < 50years old) showed significantly higher Nv of oligodendrocytes as compared to elderly controls (age > 50years old). Young and elderly schizophrenia subgroups did not differ significantly. Both control subgroups have significantly higher Nv of oligodendrocytes as compared to the schizophrenia subgroups. Decreased Nv of oligodendrocytes found in layer 5 of BA10 may be the result of dystrophic and destructive alterations and/or disrupted development of oligodendrocytes in schizophrenia.

Visceral obesity in the normal-weight people-comparing chronic schizophrenia and healthy control subjects

Visceral obesity in the normal-weight people-comparing chronic schizophrenia and healthy control subjects

High false-positive rate of a putative biomarker test to aid in the diagnosis of schizophrenia.

The current study determined the ability of a 51-analyte immunoassay panel to discriminate between subjects with chronic schizophrenia and healthy control subjects in an American population. Serum samples were collected from 25 subjects with a DSM-IV-TR diagnosis of schizophrenia and 50 healthy control subjects. Blinded samples were sent to the RulesBaseMedicine (RBM) laboratory, which analyzed the 51 biomarkers and converted the results into the VeriPsych score by the application of RBM-determined decision rules and returned these scores to the investigators. The VeriPsych score yields a conditional probability ranging from strongly positive to strongly negative that the sample was from someone who had schizophrenia. Sensitivity and specificity were calculated for these data. The study was conducted between February 27, 2010, and August 31, 2011. On the basis of this test, the conditional probability of having schizophrenia ranged from 35% to 98% in the subjects previously diagnosed with schizophrenia and ranged from < 12% to 99% in the healthy control subjects. The sensitivity of this 51-plex biomarker was 89% in this study, while the specificity was 34%. The current study confirms that the 51-plex test performs as expected in individuals with chronic schizophrenia (sensitivity = 89%), indicating that the abnormalities in this multiple biomarker test persist and are not affected by the number of years this illness has been present or by its treatment. However, there was a high false-positive rate in healthy control subjects in our sample, leading to a low specificity rate of 34%. Due to the high false-positive rate in our normal controls, this biomarker test was not able to discriminate between healthy control subjects and subjects with chronic schizophrenia in our sample.

Neuropsychological correlates of remission in chronic schizophrenia subjects: The role of general and task-specific executive processes

BackgroundAlthough cognitive deficits have consistently been characterized as core features of schizophrenia, they have not been incorporated into definitions of remission. Furthermore, just a few studies have examined the relationship between cognitive deficits and symptomatic remission. The main aim of the present study is to evaluate the executive functioning of nonremitted schizophrenia patients. Methods72 remitted and 42 nonremitted schizophrenia patients, and 119 healthy controls were examined. Subjects were tested with a comprehensive battery of cognitive tests, including a measure to assess the general components of executive functioning and individual tasks to tap the three specific executive dimensions assessed in the present study, namely updating, shifting and inhibition. ResultsSchizophrenia subjects performed poorly on general executive functioning and shifting tasks in comparison to healthy controls. Remitted subjects performed better than nonremitted on inhibition and updating tasks. Whereas being a male and showing decreases in updating increase the chances of being in the nonremitted schizophrenia subjects group, increases in shifting and updating enhance the odds of being in the healthy control group. ConclusionThe present findings suggest that executive function deficits are present in chronic schizophrenic patients. In addition, specific executive processes might be associated to symptom remission. Future studies examining prospectively first-episode, drug naive patients diagnosed with schizophrenia may be especially elucidative.

A decrease in protein level and a missense polymorphism of KIF17 are associated with schizophrenia

It has been shown that the dysfunction of N-methyl-d-asparate (NMDA) receptors-mediated neurotransmission plays a role in the pathophysiology of schizophrenia. Especially, GluN2B, a subunit of NMDA receptors, associated trafficking complex is altered in the prefrontal cortex of schizophrenia. The kinesin superfamily motor protein 17 (KIF17) is known as a transporter of NR2B.Previous studies showed that a structural variant of KIF17 gene is associated with a schizophrenic phenotype. Therefore, here we investigated KIF17 levels in postmortem prefrontal cortex in schizophrenia and the association of a missense polymorphism (Ile341Val) in KIF17 with schizophrenia. The protein expression of KIF17 in schizophrenic postmortem brains was significantly lower than that in controls. Next, the association of missense polymorphisms (rs631375, rs13375609, rs522496 and rs2296225) of KIF17 gene in 567 schizophrenia and 710 healthy subjects was examined. Both genotypic distribution and allelic frequency of rs2296225 polymorphism were significantly different between the chronic schizophrenia subjects and controls. However, our findings described above were not replicated with the independent subjects (555 schizophrenia and 814 healthy controls). Furthermore, the two alleles of rs2296225 polymorphism did not affect the mRNA expression of KIF17. These results suggest that the dysfunction of KIF17 might be involved in the pathophysiology of schizophrenia.

Increased SP4 and SP1 transcription factor expression in the postmortem hippocampus of chronic schizophrenia

Altered levels of transcription factor specificity protein 4 (SP4) and 1 (SP1) in the cerebellum, prefrontal cortex and/or lymphocytes have been reported in severe psychiatric disorders, including early psychosis, bipolar disorder, and chronic schizophrenia subjects who have undergone long-term antipsychotic treatments. SP4 transgenic mice show altered hippocampal-dependent psychotic-like behaviours and altered development of hippocampal dentate gyrus. Moreover, NMDAR activity regulates SP4 function. The aim of this study was to investigate SP4 and SP1 expression levels in the hippocampus in schizophrenia, and the possible effect of antipsychotics and NMDAR blockade on SP protein levels in rodent hippocampus. We analysed SP4 and SP1 expression levels in the postmortem hippocampus of chronic schizophrenia (n = 14) and control (n = 11) subjects by immunoblot and quantitative RT-PCR. We tested the effect of NMDAR blockade on SP factors in the hippocampus of mouse treated with an acute dose of MK801. We also investigated the effect of subacute treatments with haloperidol and clozapine on SP protein levels in the rat hippocampus. We report that SP4 protein and both SP4 and SP1 mRNA expression levels are significantly increased in the hippocampus in chronic schizophrenia. Likewise, acute treatment with MK801 increased both SP4 and SP1 protein levels in mouse hippocampus. In contrast, subacute treatment with haloperidol and clozapine did not significantly alter SP protein levels in rat hippocampus. These results suggest that SP4 and SP1 upregulation may be part of the mechanisms deregulated downstream of glutamate signalling pathways in schizophrenia and might be contributing to the hippocampal-dependent cognitive deficits of the disorder.

The extent of diffusion MRI markers of neuroinflammation and white matter deterioration in chronic schizophrenia

In a previous study we have demonstrated, using a novel diffusion MRI analysis called free-water imaging, that the early stages of schizophrenia are more likely associated with a neuroinflammatory response and less so with a white matter deterioration or a demyelination process. What is not known is how neuroinflammation and white matter deterioration change along the progression of the disorder. In this study we apply the free-water measures on a population of 29 chronic schizophrenia subjects and compare them with 25 matching controls. Our aim was to compare the extent of free-water imaging abnormalities in chronic subjects with the ones previously obtained for subjects at their first psychotic episode. We find that chronic subjects showed a limited extent of abnormal increase in the volume of the extracellular space, suggesting a less extensive neuroinflammatory response relative to patients at the onset of schizophrenia. At the same time, the chronic schizophrenia subjects had greater extent of reduced fractional anisotropy compared to the previous study, suggesting increased white matter deterioration along the progression of the disease. Our findings substantiate the role of neuroinflammation in the earlier stages of the disorder, and the effect of neurodegeneration that is worsening in the chronic phase.

EPA-1297 - Lateralization of cerebral hemodynamics in schizophrenia during the trail making test: a functional transcranial doppler sonography study

Schizophrenia is a major mental disorder, with complex symptoms involving psychosis, apathy and cognitive impairment. The Trail Making Test (TMT) is a useful tool to assess cognitive functioning. Functional transcranial Doppler sonography (fTCD) of basal cerebral arteries is a noninvasive technique that allows monitoring of cerebral hemodynamics with a high temporal resolution during cognitive tasks. We assessed cerebral hemodynamics and lateralization in the middle cerebral arteries (MCA) using fTCD while patients with chronic schizophrenia and healthy subjects performed the TMT Part A and B, as well as a control task. fTCD was used to asses bilateral mean cerebral blood flow velocity (MFV) changes in the middle (MCA) and anterior (ACA) cerebral arteries. Fifteen patients with chronic Schizophrenia and 20 healthy control subjects with similar sociodemographic characteristics performed the TMT during fTCD measurements of the MCA and ACA. Schizophrenia patients demonstrated an overall poorer performance, with a significant different lateralization pattern for both forms of TMT than healthy subjects. There was a significant slowing both forms of TMT, schizophrenia was associated with initially left sided lateralization. Healthy subjects showed a bilateral pattern. These novel results show performance and brain perfusion abnormalities in schizophrenia, supporting the idea that cognitive performance has a pathological functional correlate predominantly in the lateral hemispheres of the brain. It adds to the notion that fTCD is a valuable tool to correlate psychological paradigms with brain perfusion.

Dysfunctional neural networks associated with impaired social interactions in early psychosis: an ICA analysis

The "default mode", or baseline of brain function is a topic of great interest in schizophrenia research. Recent neuroimaging studies report that the symptoms of chronic schizophrenia subjects are associated with temporal frequency alterations as well as with the disruption of local spatial patterns in the default mode network (DMN). Previous studies both on chronic and medicated subjects with psychosis suffered from limitations; on this basis, it was hypothesized that the default mode network showed abnormal activation and connectivity in young and neuroleptic-naïve patients with first-episode psychosis. This study investigated emotional responses to pleasant and unpleasant/disgusting visual stimuli by a resting-state analysis of fMRI-data from 12 untreated first-episode psychosis patients with prevalently negative symptomatology versus 12 healthy subjects. We chose this experimental task to explore the functional link between default mode network and hedonic processing which has been proposed as a marker of cerebral dysfunction in psychotic disorder and implicated in its pathophysiology. Independent Component Analysis (ICA) was used to identify the default mode component. Both healthy and first-episode subjects showed significant spatial differences in the default mode network. In first-episode subjects, medial frontal hypoactivity and cerebellar hyperactivity were correlated with the severity of negative symptoms.

Human blood analysis reveals differences in gene expression of catecholamine-regulated protein 40 (CRP40) in schizophrenia

Heat shock proteins (HSPs) are important players in neurodegeneration and psychiatric disorders. We previously reported significant reductions of a 40-kDa Catecholamine Regulated Protein (CRP40) in schizophrenia post-mortem brain specimens. This study investigated whether gene expression of CRP40 is altered in living subjects with schizophrenia. CRP40 mRNA was analyzed in white blood cells of first episode and chronic/treated schizophrenia subjects compared to healthy controls. Significant reductions in CRP40 mRNA were found among first episode schizophrenia subjects and chronic schizophrenia subjects compared to healthy controls (p<0.05 for both). These results suggest a possible functional role of CRP40 in the pathogenesis of schizophrenia.

Fractional anisotropy and radial diffusivity: Diffusion measures of white matter abnormalities in the anterior limb of the internal capsule in schizophrenia

IntroductionHigher cognitive functioning is mediated by frontal-subcortical cognitive and limbic feedback sub-loops. The thalamo-cortical projection through the anterior limb of the internal capsule (ALIC) serves as the final step in these feedback sub-loops. We evaluated abnormalities in the ALIC fiber tract in schizophrenia using both structural MRI and diffusion tensor imaging (DTI). Methods20 chronic schizophrenia patients and 22 male, normal controls group matched for handedness, age, and parental SES, underwent structural and DTI brain imaging on a 1.5Tesla GE system. We manually measured ALIC volume normalized for intracranial contents (ICC) using structural brain images and then registered these high resolution structural brain scan derived ALIC label maps to DTI space allowing for the measurement in the ALIC of diffusion indices including, fractional anisotropy (FA) mean diffusivity (MD), radial diffusivity (RD), and axial diffusivity (AD). ResultsWe found in the ALIC of chronic schizophrenia subjects, compared with normal controls, bilaterally lower FA and bilaterally higher RD, but no differences in AD, MD, or relative volume. Cognitive correlations in schizophrenia patients showed, in particular, that higher left ALIC FA correlated positively with better verbal and nonverbal declarative/episodic memory performance. DiscussionUsing a novel approach to assess both diffusion and volume measures in the ALIC in schizophrenia, we found abnormalities in measures of diffusion, but not volume, supporting their importance as sensitive indices of abnormalities in white matter fiber bundles in schizophrenia. Our findings also support the role of ALIC white matter tract FA abnormalities in declarative/episodic memory in schizophrenia.

Differences in the levels of superoxide dismutase and brain-derived neurotrophic factor in first-episode schizophrenia, chronic schizophrenia and normal control subjects

Differences in the levels of superoxide dismutase and brain-derived neurotrophic factor in first-episode schizophrenia, chronic schizophrenia and normal control subjects