Neurobiology of Schizophrenia: Search for the Elusive Correlation with Symptoms

Mathalon, Daniel H.; Ford, Judith M.

doi:10.3389/fnhum.2012.00136

Cited by 69 publications

(44 citation statements)

References 42 publications

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“…This type of variability may, in part, be due to small sample sizes, difficulty getting valid reports from patients during clinical interviews, and/or symptom attenuation following treatment with antipsychotic medication (Mathalon & Ford, 2012). …”

Section: Discussionmentioning

confidence: 99%

Equivalent mismatch negativity deficits across deviant types in early illness schizophrenia-spectrum patients

Hay

Roach

Srihari

et al. 2015

Biological Psychology

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Neurophysiological abnormalities in auditory deviance processing, as reflected by the mismatch negativity (MMN), have been observed across the course of schizophrenia. Studies in early schizophrenia patients have typically shown varying degrees of MMN amplitude reduction for different deviant types, suggesting that different auditory deviants are uniquely processed and may be differentially affected by duration of illness. To explore this further, we examined the MMN response to 4 auditory deviants (duration, frequency, duration + frequency “double deviant”, and intensity) in 24 schizophrenia-spectrum patients early in the illness (ESZ) and 21 healthy controls. ESZ showed significantly reduced MMN relative to healthy controls for all deviant types (p < 0.05), with no significant interaction with deviant type. No correlations with clinical symptoms were present (all ps > 0.05). These findings support the conclusion that neurophysiological mechanisms underlying processing of auditory deviants are compromised early in illness, and these deficiencies are not specific to the type of deviant presented.

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Section: Discussionmentioning

confidence: 99%

Equivalent mismatch negativity deficits across deviant types in early illness schizophrenia-spectrum patients

Hay

Roach

Srihari

et al. 2015

Biological Psychology

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“…The idea that schizophrenia is a brain disorder and, therefore, it is possible to study the neurobiological bases of the clinical symptoms that the diagnosis is based on, it has been translated into a paradigm shift, giving primacy to neurochemical and molecular perspectives to the detriment of those that understand it as a psychological reactions to stressful environments (Mathalon and Ford 2012). Both approaches have always been considered, in some way, incompatible and, both, largely unsuccessful.…”

Section: What Do We Know About the Neurobiology Of Schizophrenia?mentioning

confidence: 99%

Rethinking schizophrenia through the lens of evolution: shedding light on the enigma

Cariaga-Martínez¹,

Gutiérrez²,

Alelú-Paz³

2018

RIO

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Schizophrenia refers to a complex psychiatric illness characterized by the heterogenic presence of positive, negative and cognitive symptoms occurring in all human societies. The fact that the disorder lacks a unifying neuropathology, presents a decreased fecundity of the affected individuals and has a cross-culturally stable incidence rate, makes it necessary for an evolutionary explanation that fully accounts for the preservation of "schizophrenic genes" in the global human genepool, explaining the potential sex differences and the heterogeneous cognitive symptomatology of the disorder and is consistent with the neuropsychological, developmental and evolutionary findings regarding the human brain. Here we proposed a new evolutionary framework for schizophrenia that is consistent with findings presented in different dimensions, considering the disorder as a form of brain functioning that allows us to adapt to the environment and, ultimately, maintain the survival of the species. We focus on the epigenetic regulation of thalamic interneurons as a major player involved in the development of the clinical picture characteristic of schizophrenia.

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“…On the basis of papers such as this it would be easy to conclude that schizophrenia is well established as a brain disease associated with a specific biological pathway or aberrant process, even though it is widely accepted that no such resolution has been reached (Charney et al, 2002;Chou & Chouard, 2008;Mathalon & Ford, 2012). Consequently, epigenetic research in schizophrenia is tending to mirror and reproduce wider patterns of uncertainty and presumption regarding the status and character of schizophrenia as a presumed brain disease.…”

Section: Positioning Schizophrenia In Epigeneticsmentioning

confidence: 99%