Molecular targets for treating cognitive dysfunction in schizophrenia

John Gray, Bryan L. Roth

Research output: Contribution to journalArticle

180 Citations (Scopus)

Abstract

Cognitive impairment is a core feature of schizophrenia as deficits are present in the majority of patients, frequently precede the onset of other positive symptoms, persist even with successful treatment of positive symptoms, and account for a significant portion of functional impairment in schizophrenia. While the atypical antipsychotics have produced incremental improvements in the cognitive function of patients with schizophrenia, overall treatment remains inadequate. In recent years, there has been an increased interest in developing novel strategies for treating the cognitive deficits in schizophrenia, focusing on ameliorating impairments in working memory, attention, and social cognition. Here we review various molecular targets that are actively being explored for potential drug discovery efforts in schizophrenia and cognition. These molecular targets include dopamine receptors in the prefrontal cortex, nicotinic and muscarinic acetylcholine receptors, the glutamatergic excitatory synapse, various serotonin receptors, and the γ-aminobutyric acid (GABA) system.

Original languageEnglish (US)
Pages (from-to)1100-1119
Number of pages20
JournalSchizophrenia Bulletin
Volume33
Issue number5
DOIs
StatePublished - Sep 2007
Externally publishedYes

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Schizophrenia
Cognition
Aminobutyrates
Serotonin Receptors
Dopamine Receptors
Nicotinic Receptors
Muscarinic Receptors
Drug Discovery
Prefrontal Cortex
Short-Term Memory
Synapses
gamma-Aminobutyric Acid
Antipsychotic Agents
Cognitive Dysfunction
Therapeutics

Keywords

  • Acetylcholine
  • Dopamine
  • GABA
  • Glutamate
  • NMDA
  • Serotonin

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Neuroscience(all)

Cite this

Molecular targets for treating cognitive dysfunction in schizophrenia. / Gray, John; Roth, Bryan L.

In: Schizophrenia Bulletin, Vol. 33, No. 5, 09.2007, p. 1100-1119.

Research output: Contribution to journalArticle

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