Atrophic and Static (Neurodevelopmental) Schizophrenic Psychoses Premorbid Functioning, Symptoms and Neuroleptic Response

Garver, David L.; Nair, Thamilarasi R.; Christensen, James; Holcomb, Jennifer; Ramberg, Jane E.; Kingsbury, Steven J.

doi:10.1016/s0893-133x(98)00138-9

Cited by 29 publications

(9 citation statements)

References 30 publications

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“…Subtyping schizophrenia A Jablensky 823 205 Prepulse inhibition of the startle reflex [206][207][208] Deficient gating of the auditory evoked response (P50) [209][210][211] P300 amplitude reduction and latency delay 212 N400 amplitude reduction (semantic context underutilization) 213 Mismatch negativity (MMN) [214][215][216][217] Smooth pursuit eye movement dysfunction (SPEM) [218][219][220][221] Antisaccade error rate (AS) [222][223][224] Composite inhibitory phenotype (P50, AS, SPEM) 225 Multivariate electrophysiological endophenotype (MMN, P50, P300, AS) 226 Neuroimaging markers and endophenotypes Fronto-thalamic-cerebellar gray matter deficit 227 Fronto-striato-thalamic gray matter deficit 228 MRI-derived three-factor phenotype 229 MRI whole-brain nonlinear pattern classification 230 Frontal hypoactivation in response to cognitive tasks (hypofrontality) 231 Atrophic and static (neurodevelopmental) schizophrenia endophenotypes 232 Cognitive markers and endophenotypes Continuous performance tests (CPT, signal/noise ratio) [233][234][235] Attention and vigilance-based subtype 18 Verbal dysmnesic subtype 18 Verbal memory deficit, cortical or subcortical type 236,237 Dysexecutive subtype 18 Prefrontal executive/working memory phenotype 238 Frontal/abstraction deficit profile 239 Spatial working memory 240...…”

Section: Molecular Psychiatrymentioning

confidence: 99%

Subtyping schizophrenia: implications for genetic research

2006

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Phenotypic variability and likely extensive genetic heterogeneity have been confounding the search for the causes of schizophrenia since the inception of the diagnostic category. The inconsistent results of genetic linkage and association studies using the diagnostic category as the sole schizophrenia phenotype suggest that the current broad concept of schizophrenia does not demarcate a homogeneous disease entity. Approaches involving subtyping and stratification by covariates to reduce heterogeneity have been successful in the genetic study of other complex disorders, but rarely applied in schizophrenia research. This article reviews past and present attempts at delineating schizophrenia subtypes based on clinical features, statistically derived measures, putative genetic indicators, and intermediate phenotypes, highlighting the potential utility of multidomain neurocognitive endophenotypes.

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Section: Molecular Psychiatrymentioning

confidence: 99%

Subtyping schizophrenia: implications for genetic research

2006

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“…Therefore, it is quite possible that cytokine abnormalities may also be present in the brain and associated with the pathophysiology of SZ. The initial evidence that abnormalities of cytokines may be present in the brain is substantiated by the reports of abnormal levels of cytokines in the cerebrospinal fluid (CSF) of SZ patients (el-Mallakh et al, 1993; Garver et al, 1999; Garver et al, 2003; Soderlund et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Abnormal gene and protein expression of inflammatory cytokines in the postmortem brain of schizophrenia patients

Pandey

Rizavi

Zhang

et al. 2018

Schizophrenia Research

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Immune function abnormalities have been implicated in the pathophysiology of schizophrenia (SZ). This is primarily based on the observation that the levels of proinflammatory cytokines are significantly increased in the serum of SZ patients compared with normal control (NC) subjects. However, it is not known if similar cytokines abnormalities are also present in the brain of SZ patients. To further examine the involvement of inflammatory cytokines in the brain of SZ patients, we determined the protein and mRNA levels of TNF-α, IL-1β, IL-2, IL-6, IL-8, IL-10, IL-13, LTA and IL-1RA in the prefrontal cortex (PFC, Brodmann area 9) of SZ patients. We found that the protein and mRNA expression levels of the cytokines TNF-α and IL-6 are significantly increased and those of IL-10 are significantly decreased in the PFC of SZ patients. No difference in the protein and mRNA levels of IL-1β, IL-13, and IL-1RA was observed between SZ patients and NC subjects. The protein expression levels of IL-8 were significantly decreased and those of LTA were significantly increased in SZ patients, but no significant difference in the mRNA levels of IL-8 and LTA was observed between SZ patients and NC subjects. The levels of IL-2 were undetectable or very low in the postmortem brain of either SZ or NC subjects. These results suggest abnormalities of specific pro- and anti-inflammatory cytokines in the postmortem brain of SZ patients. These observations may have important implications in understanding the role of inflammatory cytokines in the pathophysiology of SZ.

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“…In contrast, when the 5-HT 2C R is edited, its coupling to G-proteins and its affinity for serotonin are drastically reduced. The extent of editing correlates with 5-HT 2C R functional activity: more highly edited isoforms exhibit the least function (Fitzgerald et al 1999; Herrick-Davis et al 1999; Niswender et al 1999; Wang et al 2000b; Quirk et al 2001; Berg et al 2001; Marion et al 2004). …”

Section: Introductionmentioning

confidence: 99%