SchizophreniaNCT06482918
Cognitive Remediation in Schizophrenia: Efficacy and Role of Neuroplasticity in "Top-down" and "Bottom-up" Mechanisms
A study testing Cognitive Remediation in people with Schizophrenia, run by University of Chile at 1 site in Chile.
Trial summary
Schizophrenia patients have deficits of different degrees in several cognitive domains, impacting their social functioning and quality of life. Cognitive remediation strategies are useful to treat cognitive deficits in patients with schizophrenia. Read more about this study
- Who is it for?
- Ages 18 to 59 years
- Conditions the study is for
- Schizophrenia
- What is being tested?
- Cognitive Remediation
- Type of treatment
- Pill or oral medicine, Lifestyle or therapy programme
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 160 participants
- Where
- 1 siteChile
- Study dates
- Jun 2024to 15 Mar 2026
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 59 years
- All sexes
- No healthy volunteers
- Adult
Who may be able to join
- Diagnosis of schizophrenia according to Diagnostic and Statistical Manual (DSM)-5
- Age between 18 and 59 years
- Clinically stable outpatients
- Current treatment with at least one antipsychotic medication
Who cannot join
- Significant medical or neurological comorbidity
- Substance use disorder with illegal drugs in active use
- Participation in a cognitive remediation program in the last 6 months
Trial locations and contacts
1 site in 1 country.
Chile1 site, 1 recruiting
- Recruiting
Clinica Psiquiatrica Universitaria, Hospital Clinico de la Universidad de Chile
Santiago, RM
Rodrigo R. Nieto, MD PhD, +56229788601, rnieto@uchile.cl
About this study
Official title: Cognitive Remediation in Schizophrenia Patients: Study of the Efficacy and of the Role of Neuroplasticity in Two Different Approaches Based on "Top-down" and "Bottom-up" Mechanisms
Schizophrenia patients have deficits of different degrees in several cognitive domains, impacting their social functioning and quality of life. Cognitive remediation strategies are useful to treat cognitive deficits in patients with schizophrenia. There are at least two different cognitive remediation strategies: one has a "top-down" approach, and is aimed at higher-order cognitive processes, focusing on the training of executive functions. The other one has a "bottom-up" approach, aiming to first recovering the perceptual processing alterations that may affect performance in higher-order cognitive functions. This study addresses in parallel two research questions, one of clinical interest (Are both strategies effective in improving neurocognitive performance?) and another one focused on the psychological / neurobiological mechanisms of neurocognitive remediation (Which cognitive remediation strategies are related to changes in BDNF levels?). The specific objectives are: (1) Evaluate the effectiveness of two cognitive remediation strategies. (2) Study the critical moments of neuroplasticity for each cognitive remediation strategy, observing changes in BDNF levels at the end of the intervention and 12 weeks after the intervention. (3) Identify potential clinical and/or molecular predictors (BDNF levels or val66met polymorphism) of response for each cognitive remediation strategy. For these objectives, two randomized controlled trials with two arms will be carried out in parallel, one where patients will receive cognitive remediation and another consisting of a control group (with usual treatment). The control group subjects will remain on a waiting and observation list for 10 weeks, to later enter the active arm, which will also last 10 weeks. In one of the trials the active arm will consist of cognitive remediation therapy with a "bottom-up" approach (focused on perceptual training), while in the other trial the active arm will consist of cognitive remediation with a "top-down" approach (focused on executive skills training). Neurocognitive and clinical assessments will be carried out along with the measurement of BDNF levels at four evaluation times: one at baseline, one at the end of the observation period with treatment-as-usual, another at the end of cognitive remediation, and another after a 12 week follow-up period.
Read the detailed description
Schizophrenia is a severe psychiatric illness that has a significant impact on patients, their families, and society. It presents with deficits of different degrees in all cognitive domains, including memory, processing speed, attention and executive functions, which have been consistently demonstrated by different studies across several geographical regions. This has implications for patients' social functioning and quality of life, as cognitive symptoms together constitute the most important predictors of patients' functioning in the community. Antipsychotic drugs, although effective for psychotic symptoms, have little effect on cognition, however, cognitive rehabilitation achieves at least a medium effect size to improve cognition. There are at least two different cognitive remediation strategies, depending on the cognitive processes to which the intervention is targeted. One has a "top-down" approach, and is aimed at higher-order cognitive processes, and focuses on the training of executive functions. The other has a "bottom-up" approach and aims to first recovering the perceptual processing alterations that some patients with schizophrenia have and that would affect performance in higher-order cognitive functions.
This study addresses in parallel two research questions, one of clinical interest, and another focused on the psychological / neurobiological mechanisms of neurocognitive remediation: What neurocognitive remediation strategy, executive skills training ("top-down" approach) or training perceptual approach ("bottom-up" approach), is it effective in improving neurocognitive performance? Which neurocognitive remediation strategies are related to changes in BDNF levels? At what point of the recovery process are these changes observed? The hypothesis is that the "bottom-up" strategy presents observable results at the end of the intervention, whereas the "top-down" strategy results in an observable effect on neurocognitive performance and functioning in the community in a delayed manner, 12 weeks after the intervention. We expect that both strategies will be associated with an increase in BDNF levels compared to the situation prior to the intervention, but that this will occur at the time when the clinical effect is observed. The specific objectives are: (1) Evaluate the effectiveness of two cognitive remediation strategies, one focused on executive skills training (top-down approach) and another on perceptual training (bottom-up approach). (2) Study the critical moments of neuroplasticity for each cognitive remediation strategy, observing changes in BDNF levels at the end of the intervention and 12 weeks after the intervention. (3) Identify potential clinical and/or molecular predictors (BDNF levels or val66met polymorphism) of the response to treatment from the neurocognitive point of view for each cognitive remediation strategy.
In order to achieve this, two randomized controlled trials with two arms will be carried out in parallel, one where patients will receive cognitive remediation and another consisting of a control group (with usual treatment). The control group subjects will remain on a waiting and observation list for 10 weeks, to later enter the active arm, which will also last 10 weeks. In one of the trials the active arm will consist of cognitive remediation therapy with a "bottom-up" approach (focused on perceptual training), while in the other trial the active arm will consist of cognitive remediation with a "top-down" approach (focused on executive skills training). Neurocognitive and clinical assessments will be carried out along with the measurement of BDNF levels at four measurement times: one at baseline, one at the end of the observation period with treatment-as-usual, another at the end of cognitive remediation, and another after a 12 weeks follow-up period.
- Conditions
- Schizophrenia
- Being tested
- Cognitive Remediation
- Keywords
- Cognitive Remediation, Cognitive Training, Cognition, Brain-Derived Neurotrophic Factor
- Medical subject headings
- Schizophrenia
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Cognitive RemediationBehavioural
Computer-assisted top-down or bottom-up cognitive remediation using tablets
| Study group | Role | What they receive |
|---|---|---|
| Top-Down Cognitive Remediation | Experimental | Executive functions training Receives: Behavioral: Cognitive Remediation |
| Bottom-Up Cognitive Remediation | Experimental | Perceptual training Receives: Behavioral: Cognitive Remediation |
| Treatment-As-Usual | No intervention | Treatment as usual |
What is being measured
The primary outcome is the main question the study is designed to answer.
MCCB Global Cognition
Global Cognition Composite T Score in Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB)
Measured: After 10 weeks of cognitive remediation and at 12 week follow-up assessment
BDNF levels in peripheral blood
Brain-Derived Neurotrophic Factor levels in peripheral blood measured with ELISA
Measured: After 10 weeks of cognitive remediation and at 12 weeks follow-up assessment
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted1 Jul 2024
- Study startJun 2024 (estimated)
- Primary completion15 Mar 2026 (estimated)
- Study completion15 Mar 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for SchizophreniaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind
- Who is masked
- Participant, Outcomes assessor
- Enrolment
- 160 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Chile
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, RODRIGO NIETO, University of Chile
- Investigators
- Rodrigo R. Nieto, MD PhD, Principal investigator, University of Chile
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06482918
- Sponsor's protocol ID
- Fondecyt 11231216
- Status last verified
- Jun 2024
- First submitted
- 19 Jun 2024
- Last updated
- 1 Jul 2024
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Owen MJ, Sawa A, Mortensen PB. Schizophrenia. Lancet. 2016 Jul 2;388(10039):86-97. doi: 10.1016/S0140-6736(15)01121-6. Epub 2016 Jan 15.
PubMed 26777917Kahn RS, Sommer IE, Murray RM, Meyer-Lindenberg A, Weinberger DR, Cannon TD, O'Donovan M, Correll CU, Kane JM, van Os J, Insel TR. Schizophrenia. Nat Rev Dis Primers. 2015 Nov 12;1:15067. doi: 10.1038/nrdp.2015.67.
PubMed 27189524Schaefer J, Giangrande E, Weinberger DR, Dickinson D. The global cognitive impairment in schizophrenia: consistent over decades and around the world. Schizophr Res. 2013 Oct;150(1):42-50. doi: 10.1016/j.schres.2013.07.009. Epub 2013 Aug 2.
PubMed 23911259Green MF. What are the functional consequences of neurocognitive deficits in schizophrenia? Am J Psychiatry. 1996 Mar;153(3):321-30. doi: 10.1176/ajp.153.3.321.
PubMed 8610818Kuo SS, Almasy L, Gur RC, Prasad K, Roalf DR, Gur RE, Nimgaonkar VL, Pogue-Geile MF. Cognition and community functioning in schizophrenia: The nature of the relationship. J Abnorm Psychol. 2018 Feb;127(2):216-227. doi: 10.1037/abn0000326.
PubMed 29528675Keefe RS, Bilder RM, Davis SM, Harvey PD, Palmer BW, Gold JM, Meltzer HY, Green MF, Capuano G, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, Davis CE, Hsiao JK, Lieberman JA; CATIE Investigators; Neurocognitive Working Group. Neurocognitive effects of antipsychotic medications in patients with chronic schizophrenia in the CATIE Trial. Arch Gen Psychiatry. 2007 Jun;64(6):633-47. doi: 10.1001/archpsyc.64.6.633.
PubMed 17548746Hori H, Noguchi H, Hashimoto R, Nakabayashi T, Omori M, Takahashi S, Tsukue R, Anami K, Hirabayashi N, Harada S, Saitoh O, Iwase M, Kajimoto O, Takeda M, Okabe S, Kunugi H. Antipsychotic medication and cognitive function in schizophrenia. Schizophr Res. 2006 Sep;86(1-3):138-46. doi: 10.1016/j.schres.2006.05.004. Epub 2006 Jun 21.
PubMed 16793238Moncrieff J, Cohen D, Mason JP. The subjective experience of taking antipsychotic medication: a content analysis of Internet data. Acta Psychiatr Scand. 2009 Aug;120(2):102-11. doi: 10.1111/j.1600-0447.2009.01356.x. Epub 2009 Feb 15.
PubMed 19222405McCleery A, Nuechterlein KH. Cognitive impairment in psychotic illness: prevalence, profile of impairment, developmental course, and treatment considerations . Dialogues Clin Neurosci. 2019 Sep;21(3):239-248. doi: 10.31887/DCNS.2019.21.3/amccleery.
PubMed 31749648Marder SR, Fenton W. Measurement and Treatment Research to Improve Cognition in Schizophrenia: NIMH MATRICS initiative to support the development of agents for improving cognition in schizophrenia. Schizophr Res. 2004 Dec 15;72(1):5-9. doi: 10.1016/j.schres.2004.09.010.
PubMed 15531402Green MF, Nuechterlein KH. The MATRICS initiative: developing a consensus cognitive battery for clinical trials. Schizophr Res. 2004 Dec 15;72(1):1-3. doi: 10.1016/j.schres.2004.09.006. No abstract available.
PubMed 15531401Best MW, Milanovic M, Iftene F, Bowie CR. A Randomized Controlled Trial of Executive Functioning Training Compared With Perceptual Training for Schizophrenia Spectrum Disorders: Effects on Neurophysiology, Neurocognition, and Functioning. Am J Psychiatry. 2019 Apr 1;176(4):297-306. doi: 10.1176/appi.ajp.2018.18070849. Epub 2019 Mar 8.
PubMed 30845819McGurk SR, Twamley EW, Sitzer DI, McHugo GJ, Mueser KT. A meta-analysis of cognitive remediation in schizophrenia. Am J Psychiatry. 2007 Dec;164(12):1791-802. doi: 10.1176/appi.ajp.2007.07060906.
PubMed 18056233Wykes T, Huddy V, Cellard C, McGurk SR, Czobor P. A meta-analysis of cognitive remediation for schizophrenia: methodology and effect sizes. Am J Psychiatry. 2011 May;168(5):472-85. doi: 10.1176/appi.ajp.2010.10060855. Epub 2011 Mar 15.
PubMed 21406461Lejeune JA, Northrop A, Kurtz MM. A Meta-analysis of Cognitive Remediation for Schizophrenia: Efficacy and the Role of Participant and Treatment Factors. Schizophr Bull. 2021 Jul 8;47(4):997-1006. doi: 10.1093/schbul/sbab022.
PubMed 33772310
Study at a glance
From the registry record, last updated by the sponsor on 1 Jul 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Cognitive Remediation in Schizophrenia Patients: Study of the Efficacy and of the Role of Neuroplasticity in Two Different Approaches Based on "Top-down" and "Bottom-up" Mechanisms
- ClinicalTrials.gov ID
- NCT06482918
- Acronym / sponsor ID
- Fondecyt 11231216
- Conditions
- Schizophrenia
- Keywords
- Cognitive Remediation, Cognitive Training, Cognition, Brain-Derived Neurotrophic Factor
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 160 participants (estimated)
- Lead sponsor
- University of ChileUniversity, hospital or other
- Study start
- Jun 2024 (estimated)
- Primary completion
- 15 Mar 2026 (estimated)
- Study completion
- 15 Mar 2026 (estimated)
- First posted
- 1 Jul 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Schizophrenia patients have deficits of different degrees in several cognitive domains, impacting their social functioning and quality of life. Cognitive remediation strategies are useful to treat cognitive deficits in patients with schizophrenia. There are at least two different cognitive remediation strategies: one has a "top-down" approach, and is aimed at higher-order cognitive processes, focusing on the training of executive functions. The other one has a "bottom-up" approach, aiming to first recovering the perceptual processing alterations that may affect performance in higher-order cognitive functions. This study addresses in parallel two research questions, one of clinical interest (Are both strategies effective in improving neurocognitive performance?) and another one focused on the psychological / neurobiological mechanisms of neurocognitive remediation (Which cognitive remediation strategies are related to changes in BDNF levels?). The specific objectives are: (1) Evaluate the effectiveness of two cognitive remediation strategies. (2) Study the critical moments of neuroplasticity for each cognitive remediation strategy, observing changes in BDNF levels at the end of the intervention and 12 weeks after the intervention. (3) Identify potential clinical and/or molecular predictors (BDNF levels or val66met polymorphism) of response for each cognitive remediation strategy. For these objectives, two randomized controlled trials with two arms will be carried out in parallel, one where patients will receive cognitive remediation and another consisting of a control group (with usual treatment). The control group subjects will remain on a waiting and observation list for 10 weeks, to later enter the active arm, which will also last 10 weeks. In one of the trials the active arm will consist of cognitive remediation therapy with a "bottom-up" approach (focused on perceptual training), while in the other trial the active arm will consist of cognitive remediation with a "top-down" approach (focused on executive skills training). Neurocognitive and clinical assessments will be carried out along with the measurement of BDNF levels at four evaluation times: one at baseline, one at the end of the observation period with treatment-as-usual, another at the end of cognitive remediation, and another after a 12 week follow-up period.
Detailed description
Schizophrenia is a severe psychiatric illness that has a significant impact on patients, their families, and society. It presents with deficits of different degrees in all cognitive domains, including memory, processing speed, attention and executive functions, which have been consistently demonstrated by different studies across several geographical regions. This has implications for patients' social functioning and quality of life, as cognitive symptoms together constitute the most important predictors of patients' functioning in the community. Antipsychotic drugs, although effective for psychotic symptoms, have little effect on cognition, however, cognitive rehabilitation achieves at least a medium effect size to improve cognition. There are at least two different cognitive remediation strategies, depending on the cognitive processes to which the intervention is targeted. One has a "top-down" approach, and is aimed at higher-order cognitive processes, and focuses on the training of executive functions. The other has a "bottom-up" approach and aims to first recovering the perceptual processing alterations that some patients with schizophrenia have and that would affect performance in higher-order cognitive functions.
This study addresses in parallel two research questions, one of clinical interest, and another focused on the psychological / neurobiological mechanisms of neurocognitive remediation: What neurocognitive remediation strategy, executive skills training ("top-down" approach) or training perceptual approach ("bottom-up" approach), is it effective in improving neurocognitive performance? Which neurocognitive remediation strategies are related to changes in BDNF levels? At what point of the recovery process are these changes observed? The hypothesis is that the "bottom-up" strategy presents observable results at the end of the intervention, whereas the "top-down" strategy results in an observable effect on neurocognitive performance and functioning in the community in a delayed manner, 12 weeks after the intervention. We expect that both strategies will be associated with an increase in BDNF levels compared to the situation prior to the intervention, but that this will occur at the time when the clinical effect is observed. The specific objectives are: (1) Evaluate the effectiveness of two cognitive remediation strategies, one focused on executive skills training (top-down approach) and another on perceptual training (bottom-up approach). (2) Study the critical moments of neuroplasticity for each cognitive remediation strategy, observing changes in BDNF levels at the end of the intervention and 12 weeks after the intervention. (3) Identify potential clinical and/or molecular predictors (BDNF levels or val66met polymorphism) of the response to treatment from the neurocognitive point of view for each cognitive remediation strategy.
In order to achieve this, two randomized controlled trials with two arms will be carried out in parallel, one where patients will receive cognitive remediation and another consisting of a control group (with usual treatment). The control group subjects will remain on a waiting and observation list for 10 weeks, to later enter the active arm, which will also last 10 weeks. In one of the trials the active arm will consist of cognitive remediation therapy with a "bottom-up" approach (focused on perceptual training), while in the other trial the active arm will consist of cognitive remediation with a "top-down" approach (focused on executive skills training). Neurocognitive and clinical assessments will be carried out along with the measurement of BDNF levels at four measurement times: one at baseline, one at the end of the observation period with treatment-as-usual, another at the end of cognitive remediation, and another after a 12 weeks follow-up period.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Double blind (participant, outcomes assessor)
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Top-Down Cognitive Remediation | Experimental | Behavioral: Cognitive RemediationExecutive functions training |
| Bottom-Up Cognitive Remediation | Experimental | Behavioral: Cognitive RemediationPerceptual training |
| Treatment-As-Usual | No intervention | –Treatment as usual |
Who may qualify
- Ages
- 18 to 59 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult
Key inclusion criteria (4 listed)
- Diagnosis of schizophrenia according to Diagnostic and Statistical Manual (DSM)-5
- Age between 18 and 59 years
- Clinically stable outpatients
- Current treatment with at least one antipsychotic medication
Key exclusion criteria (3 listed)
- Significant medical or neurological comorbidity
- Substance use disorder with illegal drugs in active use
- Participation in a cognitive remediation program in the last 6 months
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Cognitive RemediationComputer-assisted top-down or bottom-up cognitive remediation using tablets | Behavioural | Bottom-Up Cognitive Remediation, Top-Down Cognitive Remediation |
Primary outcome
MCCB Global Cognition
Time frame: After 10 weeks of cognitive remediation and at 12 week follow-up assessment
Global Cognition Composite T Score in Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB)
BDNF levels in peripheral blood
Time frame: After 10 weeks of cognitive remediation and at 12 weeks follow-up assessment
Brain-Derived Neurotrophic Factor levels in peripheral blood measured with ELISA
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 1 Jul 2024.
- Background: PubMed 26777917Owen MJ, Sawa A, Mortensen PB. Schizophrenia. Lancet. 2016 Jul 2;388(10039):86-97. doi: 10.1016/S0140-6736(15)01121-6. Epub 2016 Jan 15.
- Background: PubMed 27189524Kahn RS, Sommer IE, Murray RM, Meyer-Lindenberg A, Weinberger DR, Cannon TD, O'Donovan M, Correll CU, Kane JM, van Os J, Insel TR. Schizophrenia. Nat Rev Dis Primers. 2015 Nov 12;1:15067. doi: 10.1038/nrdp.2015.67.
- Background: PubMed 23911259Schaefer J, Giangrande E, Weinberger DR, Dickinson D. The global cognitive impairment in schizophrenia: consistent over decades and around the world. Schizophr Res. 2013 Oct;150(1):42-50. doi: 10.1016/j.schres.2013.07.009. Epub 2013 Aug 2.
- Background: PubMed 8610818Green MF. What are the functional consequences of neurocognitive deficits in schizophrenia? Am J Psychiatry. 1996 Mar;153(3):321-30. doi: 10.1176/ajp.153.3.321.
- Background: PubMed 29528675Kuo SS, Almasy L, Gur RC, Prasad K, Roalf DR, Gur RE, Nimgaonkar VL, Pogue-Geile MF. Cognition and community functioning in schizophrenia: The nature of the relationship. J Abnorm Psychol. 2018 Feb;127(2):216-227. doi: 10.1037/abn0000326.
- Background: PubMed 17548746Keefe RS, Bilder RM, Davis SM, Harvey PD, Palmer BW, Gold JM, Meltzer HY, Green MF, Capuano G, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, Davis CE, Hsiao JK, Lieberman JA; CATIE Investigators; Neurocognitive Working Group. Neurocognitive effects of antipsychotic medications in patients with chronic schizophrenia in the CATIE Trial. Arch Gen Psychiatry. 2007 Jun;64(6):633-47. doi: 10.1001/archpsyc.64.6.633.
- Background: PubMed 16793238Hori H, Noguchi H, Hashimoto R, Nakabayashi T, Omori M, Takahashi S, Tsukue R, Anami K, Hirabayashi N, Harada S, Saitoh O, Iwase M, Kajimoto O, Takeda M, Okabe S, Kunugi H. Antipsychotic medication and cognitive function in schizophrenia. Schizophr Res. 2006 Sep;86(1-3):138-46. doi: 10.1016/j.schres.2006.05.004. Epub 2006 Jun 21.
- Background: PubMed 19222405Moncrieff J, Cohen D, Mason JP. The subjective experience of taking antipsychotic medication: a content analysis of Internet data. Acta Psychiatr Scand. 2009 Aug;120(2):102-11. doi: 10.1111/j.1600-0447.2009.01356.x. Epub 2009 Feb 15.
- Background: PubMed 31749648McCleery A, Nuechterlein KH. Cognitive impairment in psychotic illness: prevalence, profile of impairment, developmental course, and treatment considerations . Dialogues Clin Neurosci. 2019 Sep;21(3):239-248. doi: 10.31887/DCNS.2019.21.3/amccleery.
- Background: PubMed 15531402Marder SR, Fenton W. Measurement and Treatment Research to Improve Cognition in Schizophrenia: NIMH MATRICS initiative to support the development of agents for improving cognition in schizophrenia. Schizophr Res. 2004 Dec 15;72(1):5-9. doi: 10.1016/j.schres.2004.09.010.
- Background: PubMed 15531401Green MF, Nuechterlein KH. The MATRICS initiative: developing a consensus cognitive battery for clinical trials. Schizophr Res. 2004 Dec 15;72(1):1-3. doi: 10.1016/j.schres.2004.09.006. No abstract available.
- Background: PubMed 30845819Best MW, Milanovic M, Iftene F, Bowie CR. A Randomized Controlled Trial of Executive Functioning Training Compared With Perceptual Training for Schizophrenia Spectrum Disorders: Effects on Neurophysiology, Neurocognition, and Functioning. Am J Psychiatry. 2019 Apr 1;176(4):297-306. doi: 10.1176/appi.ajp.2018.18070849. Epub 2019 Mar 8.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Rodrigo R. Nieto, MD PhD principal investigator
University of Chile
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Cognitive Remediation in people with Schizophrenia, run by University of Chile at 1 site in Chile.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 1 Jul 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Chile. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Rodrigo R. Nieto, MD PhD (+56229788601, rnieto@uchile.cl), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
MCCB Global Cognition (time frame: After 10 weeks of cognitive remediation and at 12 week follow-up assessment). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06482918, which also lists 19 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 1 Jul 2024.