Nicotine and Behavioral Markers of Risk for Schizophrenia A Double-Blind, Placebo-Controlled, Cross-Over Study

Dépatie, Lana

doi:10.1016/s0893-133x(02)00372-x

Cited by 161 publications

(155 citation statements)

References 82 publications

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“…Our findings are consistent with other studies that have demonstrated improvement in pre-attentional and attentional tasks with nicotine administration in individuals with schizophrenia (Adler et al, 1993;Levin et al, 1996b;Kumari et al, 2001;Depatie et al, 2002;Sherr et al, 2002;Olincy et al, 2003;Harris et al, 2004;Jacobsen et al, 2004;Smith et al, 2006). Two previous studies investigated the effects of nicotine on attention in schizophrenia using the CPT-IP (Depatie et al, 2002;Sherr et al, 2002).…”

Section: Discussionsupporting

confidence: 92%

“…Two previous studies investigated the effects of nicotine on attention in schizophrenia using the CPT-IP (Depatie et al, 2002;Sherr et al, 2002). In one study (Depatie et al, 2002), a 14 mg nicotine patch application improved the number of correct hits to a greater extent in smokers with schizophrenia than in controls. We found no effect of nicotine on correct hits, however, a high correct-hit rate at baseline in our sample may have contributed to the difference in findings in the two studies.…”

Section: Discussionmentioning

confidence: 99%

“…Deficient P50 auditory sensory gating has been linked to polymorphisms at the site of the a7nAChR gene on chromosome 15q14 and is transiently reversed by nicotine administration in smokers with schizophrenia and in nonsmoking first-degree relatives of patients with schizophrenia (Adler et al, 1992(Adler et al, , 1993Freedman et al, 1997;Leonard et al, 2002). Nicotine also improves diseaseassociated deficits in prepulse inhibition (PPI) of the acoustic startle response (Kumari et al, 2001) and oculomotor function, with improvements reported in smooth pursuit eye movement (SPEM) and antisaccade error rates (Olincy et al, 1998(Olincy et al, , 2003Depatie et al, 2002;Sherr et al, 2002;Avila et al, 2003). These findings, combined with the observation that the prevalence of cigarette smoking is much higher in schizophrenia compared with the general population, (Hughes, 1986;de Leon et al, 2002) have led to the hypothesis that smoking represents a form of self-medication for patients with psychiatric illness, particularly schizophrenia (Glassman, 1993;Dalack et al, 1998;Kumari and Postma, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…There is increasing evidence that nAChR stimulation has beneficial effects on cognitive function in schizophrenia, possibly via presynaptic modulation of dopamine and/or glutamate release (McGehee et al, 1995;George et al, 2000;Picciotto et al, 2000;Wonnacott et al, 2000). The administration of both short-and long-acting preparations of nicotine to individuals with schizophrenia has been associated with improved neuropsychological performance (Levin et al, 1996b;Depatie et al, 2002;Smith et al, 2002Smith et al, , 2006Harris et al, 2004;Jacobsen et al, 2004;Myers et al, 2004). Acute administration of the selective a7nAChR partial agonist, DMXB-A, improved P50 gating compared with placebo (Olincy et al, 2006) and administration of the nAChR antagonist, mecamylamine, blocked smoking-associated improvements in performance on attentional and visuospatial working memory (VSWM), implying that nAChR activation mediates smoking-related cognitive enhancement (Sacco et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…We, therefore, performed the following study to investigate the acute effects of nicotine on cognition in nonsmokers with schizophrenia and healthy controls. We selected a measure of attention as our primary outcome as the nAChR system is thought to play an integral role in the regulation of attentional processes (Mansvelder et al, 2006) and several previous studies have reported an improvement in this cognitive domain following nicotine administration in individuals with schizophrenia (Depatie et al, 2002;Harris et al, 2004;Sacco et al, 2005;Smith et al, 2006). Our primary hypothesis was that nicotine would enhance attention in nonsmokers with schizophrenia and controls; and the secondary hypothesis was that nicotine-associated improvements in cognition would be greater in the schizophrenia group compared with controls.…”

Section: Introductionmentioning

confidence: 99%

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The Effects of Transdermal Nicotine on Cognition in Nonsmokers with Schizophrenia and Nonpsychiatric Controls

Barr

Culhane

Jubelt

et al. 2007

Neuropsychopharmacol

215

151

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Abundant evidence indicates that the neuronal nicotinic acetylcholine receptor (nAChR) system is integral to regulation of attentional processes and is dysregulated in schizophrenia. Nicotinic agonists may have potential for the treatment of cognitive impairment in this disease. This study investigated the effects of transdermal nicotine on attention in individuals with schizophrenia (n ¼ 28) and healthy controls (n ¼ 32). All participants were nonsmokers in order to eliminate confounding effects of nicotine withdrawal and reinstatement that may occur in the study of smokers. Subjects received 14 mg transdermal nicotine and identical placebo in a randomized, placebocontrolled, crossover design. A cognitive battery was conducted before and 3 h after each patch application. The primary outcome measure was performance on the Continuous Performance Test Identical Pairs (CPT-IP) Version. Nicotine significantly improved the performance on the CPT-IP as measured by hit reaction time, hit reaction time standard deviation and random errors in both groups. In addition, nicotine reduced commission errors on the CPT-IP and improved the performance on a Card Stroop task to a greater extent in those with schizophrenia vs controls. In summary, nicotine improved attentional performance in both groups and was associated with greater improvements in inhibition of impulsive responses in subjects with schizophrenia. These results confirm previous findings that a single dose of nicotine improves attention and suggest that nicotine may specifically improve response inhibition in nonsmokers with schizophrenia.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Effects of Transdermal Nicotine on Cognition in Nonsmokers with Schizophrenia and Nonpsychiatric Controls

Barr

Culhane

Jubelt

et al. 2007

Neuropsychopharmacol

215

151

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Effects of Moderate-Dose Treatment With Varenicline on Neurobiological and Cognitive Biomarkers in Smokers and Nonsmokers With Schizophrenia or Schizoaffective Disorder

Hong¹,

Thaker

McMahon

et al. 2011

Arch Gen Psychiatry

110

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Context Nicotine administration transiently improves many neurobiological and cognitive functions in schizophrenia. It is not yet clear which nAChR subtype(s) is responsible for these seemingly pervasive nicotinic effects in schizophrenia. Objective α4β2 is a key nAChR subtype for nicotinic actions. We investigated the effect of varenicline, a relatively specific α4β2 partial agonist/antagonist, on key biomarkers that are associated with schizophrenia and are previously shown to be responsive to nicotinic challenge in humans. Design double-blind, parallel, randomized, placebo controlled trial in schizophrenia patients to examine effects of varenicline on biomarkers at short-term (2 week) and long-term (8 week), using a slow titration and moderate dosing strategy for retaining α4β2 specific effect while minimizing side effects. Setting Outpatients. Participants 69 smoking and nonsmoking patients randomized; 64 completed week 2; 59 completed week 8. Intervention(s) varenicline. Main Outcome Measure(s) prepulse inhibition, sensory gating, antisaccade, spatial working memory, eyetracking, processing speed, and sustained attention. Results Moderate dose of varenicline 1) reduced P50 sensory gating deficit after a long-term (p=0.006) but not short-term treatment; significant in nonsmokers but not in smokers; 2) reduced startle reactivity (p=0.015) regardless of baseline smoking status; and 3) improved executive function by reducing antisaccade error rate (p=0.034) regardless of smoking status. Moderate dose varenicline had no significant effect on spatial working memory, predictive and maintenance pursuit, processing speed, or sustained attention by Connor’s CPT. Clinically, there was no evidence of exacerbation of psychiatric symptoms, psychosis, depression, or suicidality using a gradual titration, 1 mg daily dose. Conclusions Moderate dose varenicline has a unique treatment profile on core schizophrenia related biomarkers. Further development is warranted for specific nAChR compounds and dosing/duration strategy to target subgroup of schizophrenia patients with specific biological deficits. ClinicalTrials.gov Identifier: NCT00492349

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Effects of Cigarette Smoking on Spatial Working Memory and Attentional Deficits in Schizophrenia

Sacco¹,

Termine²,

Seyal³

et al. 2005

Arch Gen Psychiatry

319

270

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Nicotine and Behavioral Markers of Risk for Schizophrenia A Double-Blind, Placebo-Controlled, Cross-Over Study

Cited by 161 publications

References 82 publications

The Effects of Transdermal Nicotine on Cognition in Nonsmokers with Schizophrenia and Nonpsychiatric Controls

The Effects of Transdermal Nicotine on Cognition in Nonsmokers with Schizophrenia and Nonpsychiatric Controls

Effects of Moderate-Dose Treatment With Varenicline on Neurobiological and Cognitive Biomarkers in Smokers and Nonsmokers With Schizophrenia or Schizoaffective Disorder

Effects of Cigarette Smoking on Spatial Working Memory and Attentional Deficits in Schizophrenia

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