Citation

Hindmarch I, Hashimoto K. Hum. Psychopharmacol. 2010; 25(3): 193-200.

Copyright

(Copyright © 2010, John Wiley and Sons)

DOI

10.1002/hup.1106

PMID

unavailable

Abstract

Cognitive impairment is a primary feature of patients with major depressive disorder (MDD) and is characterised by stress-induced neural atrophy. Via alpha-adrenergic, anti-cholinergic and anti-histaminic activities, several antidepressants can cause significant counter-therapeutic cognitive impairment. Evidence is emerging of the involvement of sigma-1 receptor agonism in the mechanism of action of some antidepressants, notably fluvoxamine. Sigma-1 receptors are abundant in areas affected by depression/stress-induced cerebral atrophy and their ligands have a unique pharmacological profile; they may promote neurogenesis and initiate adaptive neural plasticity as a protection/ reaction to stress. Fluvoxamine, as a potent sigma-1 receptor agonist, has shown ameliorating effects in animal models of psychosis, depression, stress, anxiety, obsessive-compulsive disorder (OCD) and aggression and has been shown to improve cognitive impairments. In humans, fluvoxamine may repair central nervous system (CNS) atrophy and restore cognitive function. The current review explores the mechanisms through which sigma-1 receptors can modulate cognitive function and examines how antidepressant therapy with fluvoxamine may help improve cognitive outcomes in patients with depression. Copyright © 2010 John Wiley & Sons, Ltd.

Language: en

Keywords

Humans; human; cognition; Depression; suicide; Animals; incidence; Treatment Outcome; Cognition; head injury; decision making; bipolar disorder; depression; aggression; schizophrenia; anxiety; prefrontal cortex; psychosis; stress; behavior change; major depression; hippocampus; clinical trial; treatment outcome; psychology; posttraumatic stress disorder; review; epilepsy; Fluvoxamine; Depressive Disorder; antidepressant agent; disease association; cognitive defect; fluvoxamine; paroxetine; sertraline; mitochondrion; fear; priority journal; anxiety disorder; nuclear magnetic resonance imaging; Alzheimer disease; neurotransmission; nonhuman; physiology; confusion; problem solving; learning disorder; neurochemistry; psychomotor retardation; amnesia; dose response; positron emission tomography; brain atrophy; remission; anticholinergic effect; obsessive compulsive disorder; concentration loss; brain size; metabolism; intelligence quotient; animal; single drug dose; nervous system development; binding affinity; cingulate gyrus; amygdaloid nucleus; Cognition Disorders; cerebellum; nerve cell plasticity; endoplasmic reticulum; neuroprotection; neuroanatomy; nerve growth factor; putamen; chronic stress; gray matter; cell membrane; sigma 1 opiate receptor; temporal cortex; drug effects; 1 (3,4 dimethoxyphenethyl) 4 (3 phenylpropyl)piperazine; 2 [4 methoxy 3 (2 phenylethoxy)phenyl] n,n dipropylethylamine; agonists; calcium mobilization; Neurogenesis; Receptors, sigma; sigma opiate receptor; sigma-1 receptor; Sigma-1 receptor