Mood DisordersNCT06306209
Inflammatory Control of Antidepressant Efficacy: a Pharmaco-epigenetic Approach
An observational study of Mood Disorders and Major Depressive Disorder, run by IRCCS San Raffaele at 1 site in Italy.
Trial summary
Major depressive disorder (MDD) is a chronic, recurring and potentially life-threatening illness that affects up to 10% of the population across the globe.It posits that the increase in serotonin levels induced by Selective Serotonin Reuptake Inhibitors (SSRIs) does not affect mood per se, but enhances brain… Read more about this study
- Who is it for?
- Ages 18 to 65 years
- Conditions the study is for
- Mood Disorders, Major Depressive Disorder
- What is being tested?
- Treatment as usual (TAU), i.e., pharmacotherapy plus clinical management
- How many people
- 80 participants
- Where
- 1 siteItaly
- Study dates
- 18 May 2021to 14 Jan 2025
- Phase
- Observational
- 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 65 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients are always informed on currently ongoing and upcoming (clinical) duties during their regular outpatient clinic visits and at the first interview during hospitalization
Who may be able to join
- A depressive episode according to Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria in the course of MDD with:
- HDRS score > 17 Age 18-65 years; In treatment with SSRIs Signed informed consent, able to understand, speak and write the national language
Who cannot join
- History of bipolar disorder, schizophrenia, schizoaffective disorder, psychosis not otherwise specified; anorexia or bulimia nervosa;
- Taking following medications: antipsychotics, anticonvulsants, mood stabilizers; stimulants
- Active infection requiring antibiotics therapy;
- Immunosuppressed patient
- Other chronic diseases
- Signs of active infection requiring treatment
Show all 13Show fewer
- Use of anti-inflammatory medication on a regular basis for a chronic inflammatory/autoimmune Disorder.
- Forbidden treatment: corticosteroids, Non Steroidal Anti-inflammatory Drugs, immunosuppressant IV-Ig based treatment
- Ongoing fever, infection treated by antibiotics or uncontrolled diabetes type I or II;
- Existing cancer or history of cancer in the last 5 years (except skin epidermoid cancer or in-situ cervix cancer);
- Known HIV infection or clinically manifest Acquired Immune Deficiency Syndrome (AIDS),
- Parkinson's or Alzheimer's disease, or any other serious condition likely to interfere e with the conduct of the trial;
- Abuse of drugs or alcohol in the past 6 months
Trial locations and contacts
1 site in 1 country.
Italy1 site, 1 recruiting
- Recruiting
IRCCS Ospedale San Raffaele
Milan, Mi, 20132
Sara sp Poletti, phd, +390226433156, poletti.sara@hsr.it
About this study
Major depressive disorder (MDD) is a chronic, recurring and potentially life-threatening illness that affects up to 10% of the population across the globe.It posits that the increase in serotonin levels induced by Selective Serotonin Reuptake Inhibitors (SSRIs) does not affect mood per se, but enhances brain plasticity and thus amplifies the influence of the environment on the individual. Thus, SSRI treatment has not a univocal effect but, in a favorable environment, it would lead to a reduction of symptoms while in a stressful environment might lead to a worse prognosis.Such innovative view opens new perspectives on how to improve SSRI efficacy by controlling the environment. However, often it is not possible to act on the quality of the living environment because of constraints due to patient's personal history and unchangeable life circumstances. In these cases, the pharmacological modulation of the factors underlying the link between living environment and SSRI efficacy represents a novel and desirable strategy to improve treatment outcome even in patients living in adverse conditions, which are very common in depressed patients. Inflammatory levels are markedly affected by the socioeconomic status and thus by the quality of the living environment. The hypothesis of the present project is that inflammation mediates the influence of the environment on SSRI outcome.Therefore, the control of inflammatory levels is a promising strategy to improve treatment efficacy and overcome the limited SSRI efficacy, especially when administered in patients living in adverse conditions. A further hypothesis is that the influence of the environment on inflammation, in turn affecting SSRI efficacy, occurs through epigenetic modifications. Therefore, the project aims at developing a pharmaco-epigenetic approach as effective treatment for MDD. In addition, through neuroimaging investigations, it will provide important information about functional and structural brain modifications associated to SSRI efficacy in patients.
Both males and females will be considered because MDD is twice as common in women than men, suggesting that different mechanisms may underlie the psychopathology in the two sexes.
- Conditions
- Mood Disorders, Major Depressive Disorder
- Being tested
- Treatment as usual (TAU), i.e., pharmacotherapy plus clinical management
- Medical subject headings
- Mood Disorders, Depressive Disorder, Major
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Treatment as usual (TAU), i.e., pharmacotherapy plus clinical managementOther
All participants enrolled in the study will receive Treatment as usual (TAU), i.e., pharmacotherapy plus clinical management. Clinicians will be free to choose antidepressant medication, doses and drug combinations, including augmentations strategies and non-pharmacological treatments, which will follow standard clinical treatment guidelines for MDD.
| Study group | Role | What they receive |
|---|---|---|
| MDD | 80 patients with a depressive episode in course of major depression (MDD) and treated with SSRI's will be studied. The study does not include the evaluation of pharmacological treatments. The treatments will be administered in the judgment of the attending physician, independently of the experimental protocol. Receives: Other: Treatment as usual (TAU), i.e., pharmacotherapy plus clinical management |
What is being measured
The primary outcome is the main question the study is designed to answer.
The potential role of inflammation as the causal link between the quality of the environment and SSRI efficacy
we will measure the levels of peripheral inflammatory markers and implement mediation/moderation model to investigate if inflammatory markers mediate/moderate the association between the environment (number of stressful events) and SSRIs efficacy (response to treatment: 50% reduction at the hamilton depression rating scale (HDRS) - scores min 0 max 52, higher score higher severity).
Measured: Blood samples will be collected at baseline time and after 3 months in correspondence with routine blood sampling performed at the patients arrival in the hospital.
interaction between early stress and recent stress on the response to treatment and the role of inflammation
we will investigate whether patients exposed to early stress (Risk Families Questionnaire (RFQ) score min 13, max 65, higher scores higher exposure to early life events;Childhood Trauma Questionnaire (CTQ) score min 28, max 140, higher score higher childhood trauma) have higher levels of inflammatory markers and are more vulnerable to recent stress (number of events) and if this interaction affects the response to treatment (50% reduction at HDRS)
Measured: at baseline, at 3 months follow up
identification of neurobiological predictors of response to treatment
MRI scans will be performed at baseline and 3 month followup (Functional MRI). Changes in gray matter volumes which predict response to treatment (50% reduction at HDRS)will be identified
Measured: at baseline, at 3 months follow up
identification of neurobiological predictors of response to treatment
MRI scans will be performed at baseline and 3 month followup (Diffusion Tensor Imaging (DTI);) Changes in white matter microstructure (fractional anisotropy) which predict response to treatment (50% reduction at HDRS)will be identified
Measured: at baseline, at 3 months follow up
identification of neurobiological predictors of response to treatment
Changes in peripheral inflammatory markers and transcriptomic between baseline and follow-up able to predict response to treatment (50% reduction at HDRS) will be identified
Measured: at baseline, at 3 months follow up, at 6 months follow up
Secondary outcomes (1)
epigenetic changes in cytokine regulating genes which could mediate the effect of stress on response to treatment.
mediation/moderation models will be implemented to identify epigenetic changes (RNA sequencing) that mediate/moderate the association between recent stress (number of events) and response to treatment (50% reduction at HDRS)
Measured: Blood samples will be collected at baseline time and after 3 months in correspondence with routine blood sampling performed at the patients arrival in the hospital.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted12 Mar 2024
- Study start18 May 2021
- Primary completion30 Nov 2024 (estimated)
- Study completion14 Jan 2025 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (22)Papers the sponsor has linked to this study.
- Other trials for Mood DisordersStudies of the same condition, open and under way.
- More trials run by IRCCS San RaffaeleThe sponsor's other registered studies.
- 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 80 participants (estimated)
Sponsor and investigators
- Lead sponsor
- IRCCS San Raffaele
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Sara Poletti, IRCCS Ospedale San Raffaele
- Investigators
- sara Poletti, PhD, Principal investigator, IRCCS Ospedale San Raffaele
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06306209
- Sponsor's protocol ID
- DeFLAME
- Status last verified
- Mar 2024
- First submitted
- 27 Feb 2024
- Last updated
- 12 Mar 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L, Norquist G, Howland RH, Lebowitz B, McGrath PJ, Shores-Wilson K, Biggs MM, Balasubramani GK, Fava M; STAR*D Study Team. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006 Jan;163(1):28-40. doi: 10.1176/appi.ajp.163.1.28.
PubMed 16390886Branchi I. The double edged sword of neural plasticity: increasing serotonin levels leads to both greater vulnerability to depression and improved capacity to recover. Psychoneuroendocrinology. 2011 Apr;36(3):339-51. doi: 10.1016/j.psyneuen.2010.08.011. Epub 2010 Sep 26.
PubMed 20875703Maya Vetencourt JF, Sale A, Viegi A, Baroncelli L, De Pasquale R, O'Leary OF, Castren E, Maffei L. The antidepressant fluoxetine restores plasticity in the adult visual cortex. Science. 2008 Apr 18;320(5874):385-8. doi: 10.1126/science.1150516.
PubMed 18420937Belsky J, Jonassaint C, Pluess M, Stanton M, Brummett B, Williams R. Vulnerability genes or plasticity genes? Mol Psychiatry. 2009 Aug;14(8):746-54. doi: 10.1038/mp.2009.44. Epub 2009 May 19.
PubMed 19455150Alboni S, van Dijk RM, Poggini S, Milior G, Perrotta M, Drenth T, Brunello N, Wolfer DP, Limatola C, Amrein I, Cirulli F, Maggi L, Branchi I. Fluoxetine effects on molecular, cellular and behavioral endophenotypes of depression are driven by the living environment. Mol Psychiatry. 2017 Apr;22(4):552-561. doi: 10.1038/mp.2015.142. Epub 2015 Sep 15.
PubMed 26645631Branchi I, Santarelli S, Capoccia S, Poggini S, D'Andrea I, Cirulli F, Alleva E. Antidepressant treatment outcome depends on the quality of the living environment: a pre-clinical investigation in mice. PLoS One. 2013 Apr 30;8(4):e62226. doi: 10.1371/journal.pone.0062226. Print 2013.
PubMed 23653679Chiarotti F, Viglione A, Giuliani A, Branchi I. Citalopram amplifies the influence of living conditions on mood in depressed patients enrolled in the STAR*D study. Transl Psychiatry. 2017 Mar 21;7(3):e1066. doi: 10.1038/tp.2017.35.
PubMed 28323288Cohen A, Houck PR, Szanto K, Dew MA, Gilman SE, Reynolds CF 3rd. Social inequalities in response to antidepressant treatment in older adults. Arch Gen Psychiatry. 2006 Jan;63(1):50-6. doi: 10.1001/archpsyc.63.1.50.
PubMed 16389196Iosifescu DV, Clementi-Craven N, Fraguas R, Papakostas GI, Petersen T, Alpert JE, Nierenberg AA, Fava M. Cardiovascular risk factors may moderate pharmacological treatment effects in major depressive disorder. Psychosom Med. 2005 Sep-Oct;67(5):703-6. doi: 10.1097/01.psy.0000170338.75346.d0.
PubMed 16204427Alley DE, Seeman TE, Ki Kim J, Karlamangla A, Hu P, Crimmins EM. Socioeconomic status and C-reactive protein levels in the US population: NHANES IV. Brain Behav Immun. 2006 Sep;20(5):498-504. doi: 10.1016/j.bbi.2005.10.003. Epub 2005 Dec 2.
PubMed 16330181Miller AH, Maletic V, Raison CL. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biol Psychiatry. 2009 May 1;65(9):732-41. doi: 10.1016/j.biopsych.2008.11.029. Epub 2009 Jan 15.
PubMed 19150053Miller AH, Raison CL. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nat Rev Immunol. 2016 Jan;16(1):22-34. doi: 10.1038/nri.2015.5.
PubMed 26711676Raison CL, Rutherford RE, Woolwine BJ, Shuo C, Schettler P, Drake DF, Haroon E, Miller AH. A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers. JAMA Psychiatry. 2013 Jan;70(1):31-41. doi: 10.1001/2013.jamapsychiatry.4.
PubMed 22945416Harrison NA, Brydon L, Walker C, Gray MA, Steptoe A, Critchley HD. Inflammation causes mood changes through alterations in subgenual cingulate activity and mesolimbic connectivity. Biol Psychiatry. 2009 Sep 1;66(5):407-14. doi: 10.1016/j.biopsych.2009.03.015. Epub 2009 May 7.
PubMed 19423079Hepgul N, Cattaneo A, Agarwal K, Baraldi S, Borsini A, Bufalino C, Forton DM, Mondelli V, Nikkheslat N, Lopizzo N, Riva MA, Russell A, Hotopf M, Pariante CM. Transcriptomics in Interferon-alpha-Treated Patients Identifies Inflammation-, Neuroplasticity- and Oxidative Stress-Related Signatures as Predictors and Correlates of Depression. Neuropsychopharmacology. 2016 Sep;41(10):2502-11. doi: 10.1038/npp.2016.50. Epub 2016 Apr 12.
PubMed 27067128
Study at a glance
From the registry record, last updated by the sponsor on 12 Mar 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Inflammatory Control of Antidepressant Efficacy: a Pharmaco-epigenetic Approach
- ClinicalTrials.gov ID
- NCT06306209
- Acronym / sponsor ID
- DeFLAME
- Conditions
- Mood Disorders, Major Depressive Disorder
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 80 participants (estimated)
- Lead sponsor
- IRCCS San RaffaeleUniversity, hospital or other
- Study start
- 18 May 2021 (actual)
- Primary completion
- 30 Nov 2024 (estimated)
- Study completion
- 14 Jan 2025 (estimated)
- First posted
- 12 Mar 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.
Major depressive disorder (MDD) is a chronic, recurring and potentially life-threatening illness that affects up to 10% of the population across the globe.It posits that the increase in serotonin levels induced by Selective Serotonin Reuptake Inhibitors (SSRIs) does not affect mood per se, but enhances brain plasticity and thus amplifies the influence of the environment on the individual. Thus, SSRI treatment has not a univocal effect but, in a favorable environment, it would lead to a reduction of symptoms while in a stressful environment might lead to a worse prognosis.Such innovative view opens new perspectives on how to improve SSRI efficacy by controlling the environment. However, often it is not possible to act on the quality of the living environment because of constraints due to patient's personal history and unchangeable life circumstances. In these cases, the pharmacological modulation of the factors underlying the link between living environment and SSRI efficacy represents a novel and desirable strategy to improve treatment outcome even in patients living in adverse conditions, which are very common in depressed patients. Inflammatory levels are markedly affected by the socioeconomic status and thus by the quality of the living environment. The hypothesis of the present project is that inflammation mediates the influence of the environment on SSRI outcome.Therefore, the control of inflammatory levels is a promising strategy to improve treatment efficacy and overcome the limited SSRI efficacy, especially when administered in patients living in adverse conditions. A further hypothesis is that the influence of the environment on inflammation, in turn affecting SSRI efficacy, occurs through epigenetic modifications. Therefore, the project aims at developing a pharmaco-epigenetic approach as effective treatment for MDD. In addition, through neuroimaging investigations, it will provide important information about functional and structural brain modifications associated to SSRI efficacy in patients.
Both males and females will be considered because MDD is twice as common in women than men, suggesting that different mechanisms may underlie the psychopathology in the two sexes.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| MDD | – | Other: Treatment as usual (TAU), i.e., pharmacotherapy plus clinical management80 patients with a depressive episode in course of major depression (MDD) and treated with SSRI's will be studied. The study does not include the evaluation of pharmacological treatments. The treatments will be administered in the judgment of the attending physician, independently of the experimental protocol. |
Who may qualify
- Ages
- 18 to 65 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients are always informed on currently ongoing and upcoming (clinical) duties during their regular outpatient clinic visits and at the first interview during hospitalization
Key inclusion criteria (2 listed)
- A depressive episode according to Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria in the course of MDD with:
- HDRS score > 17 Age 18-65 years; In treatment with SSRIs Signed informed consent, able to understand, speak and write the national language
Key exclusion criteria (13 listed)
- History of bipolar disorder, schizophrenia, schizoaffective disorder, psychosis not otherwise specified; anorexia or bulimia nervosa;
- Taking following medications: antipsychotics, anticonvulsants, mood stabilizers; stimulants
- Active infection requiring antibiotics therapy;
- Immunosuppressed patient
- Other chronic diseases
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 |
|---|---|---|
| Treatment as usual (TAU), i.e., pharmacotherapy plus clinical managementAll participants enrolled in the study will receive Treatment as usual (TAU), i.e., pharmacotherapy plus clinical management. Clinicians will be free to choose antidepressant medication, doses and drug combinations, including augmentations strategies and non-pharmacological treatments, which will follow standard clinical treatment guidelines for MDD. | Other | MDD |
Primary outcome
The potential role of inflammation as the causal link between the quality of the environment and SSRI efficacy
Time frame: Blood samples will be collected at baseline time and after 3 months in correspondence with routine blood sampling performed at the patients arrival in the hospital.
we will measure the levels of peripheral inflammatory markers and implement mediation/moderation model to investigate if inflammatory markers mediate/moderate the association between the environment (number of stressful events) and SSRIs efficacy (response to treatment: 50% reduction at the hamilton depression rating scale (HDRS) - scores min 0 max 52, higher score higher severity).
interaction between early stress and recent stress on the response to treatment and the role of inflammation
Time frame: at baseline, at 3 months follow up
we will investigate whether patients exposed to early stress (Risk Families Questionnaire (RFQ) score min 13, max 65, higher scores higher exposure to early life events;Childhood Trauma Questionnaire (CTQ) score min 28, max 140, higher score higher childhood trauma) have higher levels of inflammatory markers and are more vulnerable to recent stress (number of events) and if this interaction affects the response to treatment (50% reduction at HDRS)
identification of neurobiological predictors of response to treatment
Time frame: at baseline, at 3 months follow up
MRI scans will be performed at baseline and 3 month followup (Functional MRI). Changes in gray matter volumes which predict response to treatment (50% reduction at HDRS)will be identified
identification of neurobiological predictors of response to treatment
Time frame: at baseline, at 3 months follow up
MRI scans will be performed at baseline and 3 month followup (Diffusion Tensor Imaging (DTI);) Changes in white matter microstructure (fractional anisotropy) which predict response to treatment (50% reduction at HDRS)will be identified
identification of neurobiological predictors of response to treatment
Time frame: at baseline, at 3 months follow up, at 6 months follow up
Changes in peripheral inflammatory markers and transcriptomic between baseline and follow-up able to predict response to treatment (50% reduction at HDRS) will be identified
1 secondary outcome
epigenetic changes in cytokine regulating genes which could mediate the effect of stress on response to treatment.
Time frame: Blood samples will be collected at baseline time and after 3 months in correspondence with routine blood sampling performed at the patients arrival in the hospital.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Mar 2024.
- Background: PubMed 16390886Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L, Norquist G, Howland RH, Lebowitz B, McGrath PJ, Shores-Wilson K, Biggs MM, Balasubramani GK, Fava M; STAR*D Study Team. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006 Jan;163(1):28-40. doi: 10.1176/appi.ajp.163.1.28.
- Background: PubMed 20875703Branchi I. The double edged sword of neural plasticity: increasing serotonin levels leads to both greater vulnerability to depression and improved capacity to recover. Psychoneuroendocrinology. 2011 Apr;36(3):339-51. doi: 10.1016/j.psyneuen.2010.08.011. Epub 2010 Sep 26.
- Background: PubMed 18420937Maya Vetencourt JF, Sale A, Viegi A, Baroncelli L, De Pasquale R, O'Leary OF, Castren E, Maffei L. The antidepressant fluoxetine restores plasticity in the adult visual cortex. Science. 2008 Apr 18;320(5874):385-8. doi: 10.1126/science.1150516.
- Background: PubMed 19455150Belsky J, Jonassaint C, Pluess M, Stanton M, Brummett B, Williams R. Vulnerability genes or plasticity genes? Mol Psychiatry. 2009 Aug;14(8):746-54. doi: 10.1038/mp.2009.44. Epub 2009 May 19.
- Background: PubMed 26645631Alboni S, van Dijk RM, Poggini S, Milior G, Perrotta M, Drenth T, Brunello N, Wolfer DP, Limatola C, Amrein I, Cirulli F, Maggi L, Branchi I. Fluoxetine effects on molecular, cellular and behavioral endophenotypes of depression are driven by the living environment. Mol Psychiatry. 2017 Apr;22(4):552-561. doi: 10.1038/mp.2015.142. Epub 2015 Sep 15.
- Background: PubMed 23653679Branchi I, Santarelli S, Capoccia S, Poggini S, D'Andrea I, Cirulli F, Alleva E. Antidepressant treatment outcome depends on the quality of the living environment: a pre-clinical investigation in mice. PLoS One. 2013 Apr 30;8(4):e62226. doi: 10.1371/journal.pone.0062226. Print 2013.
- Background: PubMed 28323288Chiarotti F, Viglione A, Giuliani A, Branchi I. Citalopram amplifies the influence of living conditions on mood in depressed patients enrolled in the STAR*D study. Transl Psychiatry. 2017 Mar 21;7(3):e1066. doi: 10.1038/tp.2017.35.
- Background: PubMed 16389196Cohen A, Houck PR, Szanto K, Dew MA, Gilman SE, Reynolds CF 3rd. Social inequalities in response to antidepressant treatment in older adults. Arch Gen Psychiatry. 2006 Jan;63(1):50-6. doi: 10.1001/archpsyc.63.1.50.
- Background: PubMed 16204427Iosifescu DV, Clementi-Craven N, Fraguas R, Papakostas GI, Petersen T, Alpert JE, Nierenberg AA, Fava M. Cardiovascular risk factors may moderate pharmacological treatment effects in major depressive disorder. Psychosom Med. 2005 Sep-Oct;67(5):703-6. doi: 10.1097/01.psy.0000170338.75346.d0.
- Background: PubMed 16330181Alley DE, Seeman TE, Ki Kim J, Karlamangla A, Hu P, Crimmins EM. Socioeconomic status and C-reactive protein levels in the US population: NHANES IV. Brain Behav Immun. 2006 Sep;20(5):498-504. doi: 10.1016/j.bbi.2005.10.003. Epub 2005 Dec 2.
- Background: PubMed 19150053Miller AH, Maletic V, Raison CL. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biol Psychiatry. 2009 May 1;65(9):732-41. doi: 10.1016/j.biopsych.2008.11.029. Epub 2009 Jan 15.
- Background: PubMed 26711676Miller AH, Raison CL. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nat Rev Immunol. 2016 Jan;16(1):22-34. doi: 10.1038/nri.2015.5.
- Individual participant dataSharing planned: No
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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.
sara Poletti, PhD principal investigator
IRCCS Ospedale San Raffaele
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Mood Disorders and Major Depressive Disorder, run by IRCCS San Raffaele at 1 site in Italy.
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 2 inclusion and 13 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 12 Mar 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 Italy. 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 Sara Poletti, phd (+390226433156, poletti.sara@hsr.it), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
The potential role of inflammation as the causal link between the quality of the environment and SSRI efficacy (time frame: Blood samples will be collected at baseline time and after 3 months in correspondence with routine blood sampling performed at the patients arrival in the hospital.). The study lists 5 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 NCT06306209, which also lists 22 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 12 Mar 2024.