Neuroprotection in Schizophrenia and Its Therapeutic Implications
Psychiatry Investigation
; : 383-391, 2017.
Article
em En
| WPRIM
| ID: wpr-220954
Biblioteca responsável:
WPRO
ABSTRACT
Schizophrenia is a chronic and debilitating mental disorder. The persisting negative and cognitive symptoms that are unresponsive to pharmacotherapy reveal the impairment of neuroprotective aspects of schizophrenia. In this review, of the several neuroprotective factors, we mainly focused on neuroinflammation, neurogenesis, and oxidative stress. We conducted a narrative and selective review. Neuroinflammation is mainly mediated by pro-inflammatory cytokines and microglia. Unlike peripheral inflammatory responses, neuroinflammation has a role in various neuronal activities such as neurotransmission neurogenesis. The cross-talk between neuroinflammation and neurogenesis usually has beneficial effects in the CNS under physiological conditions. However, uncontrolled and chronic neuroinflammation exert detrimental effects such as neuronal loss, inhibited neurogenesis, and excessive oxidative stress. Neurogenesis is also a major component of neuroprotection. Adult neurogenesis mainly occurs in the hippocampal region, which has an important role in memory formation and processing. Impaired neurogenesis and an ineffective response to antipsychotics may be thought to indicate a deteriorating course of schizophrenia. Oxidative stress and excessive dopaminergic neurotransmission may create a vicious cycle and consequently disturb NMDA receptor-mediated glutamatergic neurotransmission. Based on the current evidences, several neuroprotective therapeutic approaches have been reported to be efficacious for improving psychopathology, but further longitudinal and large-sample based studies are needed.
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Texto completo:
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Base de dados:
WPRIM
Assunto principal:
Psicopatologia
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Esquizofrenia
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Antipsicóticos
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Citocinas
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N-Metilaspartato
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Microglia
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Transmissão Sináptica
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Estresse Oxidativo
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Manifestações Neurocomportamentais
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Tratamento Farmacológico
Tipo de estudo:
Diagnostic_studies
Limite:
Adult
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Humans
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article