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Published in final edited form as: J Psychiatr Res. 2024 Jan 17;171:95–98. doi: 10.1016/j.jpsychires.2024.01.019

The Effect of Intranasal Oxytocin on Neurocognition in People with Schizophrenia: A Randomized Controlled Trial

Aslıhan İmamoğlu 1, Bryan J Stiles 1, L Fredrik Jarskog 2, Cort A Pedersen 2, Tonya Elliott 2, David L Penn 3,4
PMCID: PMC10947433  NIHMSID: NIHMS1961895  PMID: 38262165

Abstract

Schizophrenia is characterized by persistent cognitive deficits that significantly impact functional outcomes. Despite the current available treatments, these deficits remain inadequately addressed, highlighting the need to explore the effect of more novel treatments on cognition. The current study examined the effect of intranasal oxytocin on cognitive functioning in people with schizophrenia by utilizing data from a 12-week, randomized controlled trial. Sixty-seven participants with schizophrenia or schizoaffective disorder were randomized to receive placebo or intranasal oxytocin. Participants completed a comprehensive neuropsychological battery at baseline and 12 weeks. The results demonstrated that intranasal oxytocin did not significantly improve cognition in people with schizophrenia compared to placebo. These findings suggest that oxytocin does not worsen or enhance cognition in people with schizophrenia. Yet, the current intervention did not standardize the timing of cognitive assessments relative to the timing of oxytocin administration, which may explain our findings. Future studies attempting to clarify this relationship would benefit from employing a more controlled approach to the timing of treatment and assessments.

Keywords: Cognition, memory, psychosis

1. Introduction

Schizophrenia is characterized by widespread cognitive deficits that are evident early in disease onset (Aas et al., 2014), remain stable throughout the course of the disorder (Bortolato et al., 2015), and robustly predict functional impairment in patients (Fett et al., 2011; Halverson et al., 2019). Additionally, these impairments are present in individuals at-risk for developing the disorder (İmamoğlu et al., 2022) and predict subsequent transition to psychosis (Demjaha et al., 2012). Thus, cognitive functioning represents an important treatment target in this population. Yet, current available treatment options do not sufficiently remedy these cognitive impairments (O’Grada & Dinan, 2007), with most patients demonstrating minimal benefit with antipsychotics (Keefe & Harvey, 2012) and only modest improvement with cognitive remediation (Lejeune et al., 2021).

In the past decade, intranasal oxytocin has been proposed as a viable treatment for schizophrenia that can alleviate both positive and negative symptoms (Feifel et al., 2010; Pedersen et al., 2011). To date, a substantial body of literature has investigated the effect of oxytocin on the cognitive functioning of people with schizophrenia. Specifically, higher levels of endogenous oxytocin are associated with better cognition, particularly in domains of processing speed and working memory (Strauss et al., 2019). Similarly, studies examining the effect of intranasal oxytocin on cognition have shown improvements in working memory after a single dose of oxytocin (Michalopoulou et al., 2015) and verbal memory after 3 weeks of twice-daily treatment (Feifel et al., 2012). However, many other studies, including single-dose (Bradley et al., 2019; Guastella et al., 2015) and multi-dose studies lasting up to 6 weeks (Cacciotti-Saija et al., 2015; Davis et al., 2014), have not found significant improvements in neurocognition following intranasal oxytocin administration in people with schizophrenia. Notably, these discrepancies may be attributed, at least in part, to the small sample sizes employed by the studies that showed a significant effect of oxytocin.

The current study clarifies these inconsistent findings by reporting secondary results from a 12-week, twice-daily randomized controlled trial (Jarskog et al., 2017). Jarskog and colleagues previously observed that while oxytocin significantly reduces the severity of negative symptoms, it does not improve social cognition (2017). The current study expands upon these prior observations by examining the effects of intranasal oxytocin on neurocognition in a large cohort of people with schizophrenia and schizoaffective disorder. To our knowledge, this represents the longest-lasting oxytocin trial to date to examine the relationship between neurocognition and oxytocin in schizophrenia.

2. Methods

2.1. Study Design and Subjects

Sixty-seven individuals who met criteria for schizophrenia or schizoaffective disorder, as determined by the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV), participated in a double-blind, randomized treatment study between June 2011 and September 2014. Participants received either 12 weeks of twice-daily intranasal oxytocin or placebo. The study was approved by the Biomedical Institutional Review Board at the University of North Carolina at Chapel Hill. The overall sample included people with the following self-reported race/ethnicity: 34 (51%) Caucasian/White, 28 (42%) African American/Black, 3 (4%) Asian/Asian American, and 2 (3%) other. All other demographic and clinical information is presented in Table 1.

Table 1.

Demographic and clinical characteristics of the sample at baseline.

Placebo Group (n = 32) Oxytocin Group (n = 35) p-Values

Age, years 36.63 (12.47) 40.83 (11.86) 0.16
Age Range 19 – 61 21 – 64 -
Male % (N) 73.5% (25) 77.1% (27) -
Education, years 13.03 (1.97) 12.81 (1.80) 0.64
PANSS - Total 68.52 (10.09) 65.69 (12.62) 0.32
PANSS - Negative 19.10 (5.58) 18.09 (5.64) 0.47
PANSS - Positive 18.00 (5.43) 16.97 (4.90) 0.42
PANSS - General 32.81 (5.74) 31.63 (6.61) 0.45
PANSS - Social 12.03 (3.04) 11.11 (3.59) 0.27
Medications % (N)
First-generation antipsychotics 18.75 (6) 17.14 (6) 0.87
Second-generation antipsychotics 87.5 (28) 80.0 (28) 0.42

Note. PANSS = Positive and Negative Symptom Scale.

2.2. Intervention

Participants maintained their pre-study medication and dosage throughout the study period. Following training on proper administration techniques, participants self-administered the intranasal study drug twice daily, once before breakfast and once before dinner, for 12 weeks. Each dose contained approximately 24 internal units (IU) of oxytocin or placebo, following prior studies that found significant effects of acute intranasal oxytocin treatment (MacDonald & MacDonald, 2010). A more detailed description of intervention methods, adverse events, tolerability, and randomization can be found in Jarskog et al. (2017).

2.3. Neurocognitive Assessment

We assessed neurocognition by employing the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS; Randolph et al., 1998), which is a well-validated cognitive screening measure that is suitable for assessing cognition in individuals with schizophrenia (Gold et al., 1999; Wilk et al., 2002). The RBANS contains 12 subtests examining several domains of cognition. Scores on these subtests were combined to form a total summary score and five age-adjusted index scores for the following indices: immediate memory, visuospatial/constructional, attention, language, and delayed memory. Participants completed alternate forms (i.e., Form A and B) of the RBANS during two time points (i.e., baseline vs. 12-week follow-up) to minimize practice effects, with Form A always administered at baseline.

2.4. Data Analysis Plan

The statistical analyses were conducted using R (R Core Team, 2022). We used mixed effects models from the lme4 package that included subjects as random intercept effects and Treatment Condition and Time as fixed effects (Bates et al., 2015). Post hoc comparisons utilized the Tukey method from the emmeans package (Lenth et al., 2022). 95% confidence intervals (95% CI) were calculated using the confint.merMod function from the lme4 package. The level for significance was set at α = .05. While 14 participants had missing data either at baseline or follow-up, they were included in the analyses to maximize statistical power. The analysis script is available on the Open Science Framework: https://osf.io/sebmr/?view_only=0027aabab2f74caca879acc9fb20221e

3. Results

There was a significant main effect of Time on immediate memory (B = 6.80, SE = 2.28, 95% CI [2.34; 11.29], p < .01), visuospatial/constructional abilities (B = −3.70, SE = 1.54, 95% CI [−6.73; −0.70], p = .02), attention (B = 4.75, SE = 2.07, 95% CI [.69; 8.82], p = .03), and total summary scores (B = 3.52, SE = 1.07, 95% CI [1.44; 5.61], p < .01). There was no significant effect of Time on language abilities (B = 5.05, SE = 2.76, 95% CI [−.33; 10.47], p = .07) and delayed memory (B = 4.12, SE = 2.53, 95% CI = [−.83; 9.07], p = .11).

Notably, we observed a significant effect of Treatment on visuospatial/constructional abilities, (B = −7.51, SE = 2.87, 95% CI [−13.12; −1.91], p < .01) as well as a significant Time × Treatment interaction, (B = 4.92, SE = 2.29, 95% CI [.44; 9.39], p = .04). Pairwise comparisons revealed that the placebo group demonstrated lower visuospatial scores over time, t(51.3) = 3.70, p = .02, while the oxytocin group did not significantly change, t(55.0) = −1.23, p = .47. No other significant main effects of Treatment or Time × Treatment interaction were detected, ps > .05 (see Table 2).

Table 2.

Treatment group comparisons for outcome variables at each time point.

Outcome Variable Time Point (weeks) Placebo Oxytocin

Mean (SE) Mean (SE) p-Values

Immediate Memory 0 77.06 (3.17) 73.90 (3.05) 0.47
12 83.86 (3.24) 80.20 (3.28) 0.43
Visuospatial/constructional 0 75.56 (2.07) 68.05 (1.99) 0.01
12 71.87 (2.12) 69.28 (2.17) 0.40
Attention 0 76.60 (3.23) 75.52 (3.11) 0.81
12 81.34 (3.29) 79.78 (3.30) 0.74
Language 0 83.06 (2.27) 85.21 (2.20) 0.50
12 88.11 (2.38) 89.67 (2.60) 0.66
Delayed Memory 0 74.25 (3.26) 70.03 (3.14) 0.35
12 78.37 (3.34) 72.27 (3.41) 0.20
Total Summary Scores 0 71.44 (2.31) 68.06 (2.21) 0.29
12 74.96 (2.33) 72.71 (2.30) 0.49

Note. We report estimated marginal means, standard errors (SE), and p-values. Raw means are available on the Open Science Framework.

4. Discussion

The current study demonstrated that intranasal oxytocin administration has little effect on the neurocognitive functioning of people with schizophrenia over a 12-week period. These results are largely consistent with prior studies assessing the effectiveness of intranasal oxytocin on general neurocognition performance (Bradley et al., 2019; Cacciotti-Saija et al., 2015; Davis et al., 2014; Guastella et al., 2015). However, at least two studies have demonstrated that varying doses of oxytocin can improve working (Michalopoulou et al., 2015) and verbal memory (Feifel et al., 2012) in people with schizophrenia. The current study extends on the existing literature by reporting results from the longest duration randomized controlled trial to date to explore the relationship between oxytocin and neurocognition in people with schizophrenia and schizoaffective disorder.

We observed that both groups, irrespective of the effect of oxytocin, improved in their overall cognition over time. This observation is consistent with prior studies examining the effect of oxytocin on neurocognition in placebo-controlled studies (Cacciotti-Saija et al., 2015; Guastella et al., 2015). Specifically, we observed that participants showed significant improvements in domains of immediate memory and attention. Unlike many other cognitive batteries, the RBANS has been shown to be less affected by practice effects (Kraus & Keefe, 2007; Wilk et al., 2002). Our study design further minimized the possibility of encountering practice effects by administering alternate versions of the RBANS at different time points. Thus, both placebo and intranasal oxytocin may have been beneficial to neurocognition over time, suggesting the presence of a placebo effect. Nevertheless, it does remain plausible that the observed improvements can be partially attributed to practice effects. Future studies could explore these possibilities by comparing the cognitive improvements observed in the placebo and oxytocin groups to those in a control group that receives no intervention.

Our findings showed that the placebo group exhibited a decline in visuospatial performance over time, while the oxytocin group did not exhibit a significant change. These results, although preliminary, suggest that intranasal oxytocin may serve as a resilience factor against schizophrenia-related decline in visuospatial abilities. However, this observation is inconsistent with prior studies that employed the same neurocognitive battery to study the effect of intranasal oxytocin after both a single dose (Guastella et al., 2015) and a 6-week long administration (Cacciotti-Saija et al., 2015). This inconsistency may be attributed to our study’s larger sample size and longer study duration. Nevertheless, further research is needed to clarify the role of intranasal oxytocin in visuospatial/constructional abilities in schizophrenia.

Prior studies reported an amnesic effect of oxytocin, with non-clinical adults treated with oxytocin showing reduced memory after treatment (Fehm-Wolfsdorf et al., 1984; Heinrichs et al., 2004). While we did not observe an oxytocin-exclusive benefit on memory, we also found no evidence of an amnesic effect of oxytocin on memory. These results suggest that while oxytocin may have a negative effect on memory, these effects are not observed in people with schizophrenia after a 12-week long treatment. The effect of oxytocin on memory may exhibit variability across different populations, thus contributing to the observed discrepancy.

Several limitations should be considered when interpreting the findings of the current study. While the data presented here come from one of the largest treatment studies of oxytocin in schizophrenia (Jarskog et al., 2017), our sample size was too small to investigate the potential impact of different types of antipsychotic and other psychotropic medication on overall cognition. Additionally, the duration of the intervention may have been too short to capture longer term effects of intranasal oxytocin on neurocognition.

Furthermore, since we only collected neurocognition data at two time points (i.e., baseline and 12-week follow-up), we could not determine if the effect of oxytocin on cognitive performance fluctuated over the course of the intervention. Prior research indicates that the timing of oxytocin administration relative to when assessments are completed can impact the effect of intranasal oxytocin (Bradley & Woolley, 2017). In the current intervention, the timing of assessments was not standardized, thereby introducing a source of variability that may have influenced the effects of intranasal oxytocin on cognitive performance. To address this limitation, future studies should employ a more controlled approach to the timing of assessments. Finally, the intranasal delivery method may have increased individual variability to drug absorption and thereby daily dosage (Guastella et al., 2013).

Overall, the findings of the current study indicate that intranasal oxytocin, when compared with placebo, did not result in significant improvements in cognitive functioning among people with schizophrenia and schizoaffective disorder. The results presented here provide valuable insights into the relationship between oxytocin and cognition in schizophrenia as these results come from the longest-lasting oxytocin trial to date to characterize the relationship between neurocognition and oxytocin in schizophrenia. The extended duration and larger sample size of our study further clarifies the effect of oxytocin on cognition, while addressing the file-drawer problem documented in oxytocin research (Lane et al., 2016).

Footnotes

Declarations of interest: none

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References

  1. Aas M, Dazzan P, Mondelli V, Melle I, Murray RM, & Pariante CM (2014). A systematic review of cognitive function in first-episode psychosis, including a discussion on childhood trauma, stress, and inflammation. Frontiers in Psychiatry, 4, 182. 10.3389/fpsyt.2013.00182 [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Bates D, Mächler M, Bolker B, & Walker S (2015). Fitting Linear Mixed-Effects Models Using lme4. Journal of Statistical Software, 67(1), 1–48. 10.18637/jss.v067.i01 [DOI] [Google Scholar]
  3. Bortolato B, Miskowiak KW, Köhler CA, Vieta E, & Carvalho AF (2015). Cognitive dysfunction in bipolar disorder and schizophrenia: a systematic review of meta-analyses. Neuropsychiatric Disease and Treatment, 3111–3125. 10.2147/NDT.S76700 [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Bradley ER, van Nieuwenhuizen A, Abram S, Niles AN, & Woolley JD (2019). Oxytocin does not improve working memory in schizophrenia. Schizophrenia Research, 208, 486. 10.1016/j.schres.2019.01.020 [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Bradley ER, & Woolley JD (2017). Oxytocin effects in schizophrenia: reconciling mixed findings and moving forward. Neuroscience & Biobehavioral Reviews, 80, 36–56. 10.1016/j.neubiorev.2017.05.007 [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Cacciotti-Saija C, Langdon R, Ward PB, Hickie IB, Scott EM, Naismith SL, … & Guastella AJ (2015). A double-blind randomized controlled trial of oxytocin nasal spray and social cognition training for young people with early psychosis. Schizophrenia Bulletin, 41(2), 483–493. 10.1093/schbul/sbu094 [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Davis MC, Green MF, Lee J, Horan WP, Senturk D, Clarke AD, & Marder SR (2014). Oxytocin-augmented social cognitive skills training in schizophrenia. Neuropsychopharmacology, 39(9), 2070–2077. 10.1038/npp.2014.68 [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Demjaha A, Valmaggia L, Stahl D, Byrne M, & McGuire P (2012). Disorganization/cognitive and negative symptom dimensions in the at-risk mental state predict subsequent transition to psychosis. Schizophrenia Bulletin, 38(2), 351–359. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Fehm-Wolfsdorf G, Born J, Voigt KH, & Fehm HL (1984). Human memory and neurohypophyseal hormones: opposite effects of vasopressin and oxytocin. Psychoneuroendocrinology, 9(3), 285–292. 10.1016/0306-4530(84)90007-6 [DOI] [PubMed] [Google Scholar]
  10. Feifel D, MacDonald K, Cobb P, & Minassian A (2012). Adjunctive intranasal oxytocin improves verbal memory in people with schizophrenia. Schizophrenia Research, 139(1–3), 207–210. 10.1016/j.schres.2012.05.018 [DOI] [PubMed] [Google Scholar]
  11. Feifel D, Macdonald K, Nguyen A, Cobb P, Warlan H, Galangue B, … & Hadley A (2010). Adjunctive intranasal oxytocin reduces symptoms in schizophrenia patients. Biological Psychiatry, 68(7), 678–680. 10.1016/j.biopsych.2010.04.039 [DOI] [PubMed] [Google Scholar]
  12. Fett AKJ, Viechtbauer W, Penn DL, van Os J, & Krabbendam L (2011). The relationship between neurocognition and social cognition with functional outcomes in schizophrenia: a meta-analysis. Neuroscience & Biobehavioral Reviews, 35(3), 573–588. 10.1016/j.neubiorev.2010.07.001 [DOI] [PubMed] [Google Scholar]
  13. Gold JM, Queern C, Iannone VN, & Buchanan RW (1999). Repeatable battery for the assessment of neuropsychological status as a screening test in schizophrenia, I: Sensitivity, reliability, and validity. American Journal of Psychiatry, 156(12), 1944–1950. 10.1176/ajp.156.12.1944 [DOI] [PubMed] [Google Scholar]
  14. Guastella AJ, Hickie IB, McGuinness MM, Otis M, Woods EA, Disinger HM, … & Banati RB (2013). Recommendations for the standardisation of oxytocin nasal administration and guidelines for its reporting in human research. Psychoneuroendocrinology, 38(5), 612–625. 10.1016/j.psyneuen.2012.11.019 [DOI] [PubMed] [Google Scholar]
  15. Guastella AJ, Ward PB, Hickie IB, Shahrestani S, Hodge MAR, Scott EM, & Langdon R (2015). A single dose of oxytocin nasal spray improves higher-order social cognition in schizophrenia. Schizophrenia Research, 168(3), 628–633. 10.1016/j.schres.2015.06.005 [DOI] [PubMed] [Google Scholar]
  16. Halverson TF, Orleans-Pobee M, Merritt C, Sheeran P, Fett AK, & Penn DL (2019). Pathways to functional outcomes in schizophrenia spectrum disorders: Meta-analysis of social cognitive and neurocognitive predictors. Neuroscience & Biobehavioral Reviews, 105, 212–219. 10.1016/j.neubiorev.2019.07.020 [DOI] [PubMed] [Google Scholar]
  17. Heinrichs M, Meinlschmidt G, Wippich W, Ehlert U, & Hellhammer DH (2004). Selective amnesic effects of oxytocin on human memory. Physiology & Behavior, 83(1), 31–38. 10.1016/j.physbeh.2004.07.020 [DOI] [PubMed] [Google Scholar]
  18. İmamoğlu A, Foubert C, Healey MK, Langella S, Belger A, Giovanello KS, & Wahlheim CN (2022). Episodic memory impairment in children and adolescents at risk for schizophrenia: A role for context processing. Schizophrenia Research: Cognition, 28, 100241. 10.1016/j.scog.2022.100241 [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Jarskog LF, Pedersen CA, Johnson JL, Hamer RM, Rau SW, Elliott T, & Penn DL (2017). A 12-week randomized controlled trial of twice-daily intranasal oxytocin for social cognitive deficits in people with schizophrenia. Schizophrenia Research, 185, 88–95. 10.1016/j.schres.2017.01.008 [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Keefe RS, & Harvey PD (2012). Cognitive impairment in schizophrenia. Novel Antischizophrenia Treatments, 11–37. 10.1007/978-3-642-25758-2_2 [DOI] [PubMed] [Google Scholar]
  21. Kraus MS, & Keefe RS (2007). Cognition as an outcome measure in schizophrenia. The British Journal of Psychiatry, 191(S50), s46–s51. 10.1192/bjp.191.50.s46 [DOI] [PubMed] [Google Scholar]
  22. Lane A, Luminet O, Nave G, & Mikolajczak M (2016). Is there a publication bias in behavioural intranasal oxytocin research on humans? Opening the file drawer of one laboratory. Journal of Neuroendocrinology, 28(4). 10.1111/jne.12384 [DOI] [PubMed] [Google Scholar]
  23. Lejeune JA, Northrop A, & Kurtz MM (2021). A meta-analysis of cognitive remediation for schizophrenia: efficacy and the role of participant and treatment factors. Schizophrenia Bulletin, 47(4), 997–1006. 10.1093/schbul/sbab022 [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Lenth R, Singmann H, Love J, Buerkner P, & Herve M (2022). Emmeans: estimated marginal means. R package version 1.8. 2. https://CRAN.R-project.org/package=emmeans [Google Scholar]
  25. Michalopoulou PG, Averbeck BB, Kalpakidou AK, Evans S, Bobin T, Kapur S, & Shergill SS (2015). The effects of a single dose of oxytocin on working memory in schizophrenia. Schizophrenia Research, 162(1–3), 62. 10.1016/j.schres.2014.12.029 [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. O’Grada C, & Dinan T (2007). Executive function in schizophrenia: what impact do antipsychotics have?. Human Psychopharmacology: Clinical and Experimental, 22(6), 397–406. 10.1002/hup.861 [DOI] [PubMed] [Google Scholar]
  27. Pedersen CA, Gibson CM, Rau SW, Salimi K, Smedley KL, Casey RL, … & Penn DL (2011). Intranasal oxytocin reduces psychotic symptoms and improves Theory of Mind and social perception in schizophrenia. Schizophrenia Research, 132(1), 50–53. 10.1016/j.schres.2011.07.027 [DOI] [PubMed] [Google Scholar]
  28. Pinkham AE, Gur RE, & Gur RC (2007). Affect recognition deficits in schizophrenia: neural substrates and psychopharmacological implications. Expert Review of Neurotherapeutics, 7(7), 807–816. 10.1586/14737175.7.7.807 [DOI] [PubMed] [Google Scholar]
  29. R Core Team (2020). R: A language and environment for statistical computing. R Foundation for Statistical Computing. https://www.R-project.org/. [Google Scholar]
  30. Randolph C, Tierney MC, Mohr E, & Chase TN (1998). The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS): preliminary clinical validity. Journal of Clinical and Experimental Neuropsychology, 20(3), 310–319. 10.1076/jcen.20.3.310.823 [DOI] [PubMed] [Google Scholar]
  31. Strauss GP, Chapman HC, Keller WR, Koenig JI, Gold JM, Carpenter WT, & Buchanan RW (2019). Endogenous oxytocin levels are associated with impaired social cognition and neurocognition in schizophrenia. Journal of Psychiatric Research, 112, 38–43. 10.1016/j.jpsychires.2019.02.017 [DOI] [PubMed] [Google Scholar]
  32. Wilk CM, Gold JM, Bartko JJ, Dickerson F, Fenton WS, Knable M, … & Buchanan RW (2002). Test-retest stability of the Repeatable Battery for the Assessment of Neuropsychological Status in schizophrenia. American Journal of Psychiatry, 159(5), 838–844. 10.1176/appi.ajp.159.5.838 [DOI] [PubMed] [Google Scholar]

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