Génpolimorfizmusok és génexpresszió szkizofréniában.

Translated title of the contribution: Gene polymorphism and gene expression in schizophrenia

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The author reviews relevant data on the neuropathology and molecular genetics of schizophrenia. Anatomical alterations are localized mainly in the hippocampus, dorsal thalamus and dorsolateral prefrontal cortex, and involve the morphology and molecular structure of the neurons and synapses. Several susceptibility genes [including COMT, dysbindin, neuregulin, DISCI, RGS4, GRM3, G72, PPP3CC, CHRNA7, PRODH2, Aktl, 5qGABA(A)] having physiological function in the brain have been identified and this supports the view of schizophrenia as a disorder of cerebral synaptic function. NMDA receptor-mediated glutamate transmission may be particularly involved, but disturbances of dopamine and GABA signalling seem to be linked as well. Based on recent data, an agreement is emerging between the roles of the genes on the molecular and synaptic levels and the understanding of the disorder at the neural systems level.

Original languageHungarian
Pages (from-to)404-412
Number of pages9
JournalPsychiatria Hungarica : A Magyar Pszichiátriai Társaság tudományos folyóirata
Volume21
Issue number6
Publication statusPublished - 2006

Fingerprint

Schizophrenia
Neuregulins
Gene Expression
Prefrontal Cortex
Molecular Structure
N-Methyl-D-Aspartate Receptors
Thalamus
Synapses
gamma-Aminobutyric Acid
Genes
Molecular Biology
Glutamic Acid
Hippocampus
Dopamine
Neurons
Brain
Neuropathology

ASJC Scopus subject areas

  • Psychiatry and Mental health

Cite this

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abstract = "The author reviews relevant data on the neuropathology and molecular genetics of schizophrenia. Anatomical alterations are localized mainly in the hippocampus, dorsal thalamus and dorsolateral prefrontal cortex, and involve the morphology and molecular structure of the neurons and synapses. Several susceptibility genes [including COMT, dysbindin, neuregulin, DISCI, RGS4, GRM3, G72, PPP3CC, CHRNA7, PRODH2, Aktl, 5qGABA(A)] having physiological function in the brain have been identified and this supports the view of schizophrenia as a disorder of cerebral synaptic function. NMDA receptor-mediated glutamate transmission may be particularly involved, but disturbances of dopamine and GABA signalling seem to be linked as well. Based on recent data, an agreement is emerging between the roles of the genes on the molecular and synaptic levels and the understanding of the disorder at the neural systems level.",
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