Postpartum DepressionGnRHaNCT02661789
Neuropsychobiological Correlates of Sex-steroid Hormone Manipulation in Healthy Women: a Risk Model for Depression
A study testing Goserelin 3.6 mg implant in people with Postpartum Depression and Major Depressive Disorder, run by Gitte Moos Knudsen at 1 site in Denmark.
Trial summary
The project aimed at identifying neuropsychobiological signatures of pharmacological sex-steroid hormone manipulations in healthy women as a risk model for depression. The study is a double-blind, randomized, placebo-controlled study. Read more about this study
- Who is it for?
- Ages 18 to 40 years, women onlyHealthy volunteers can take part
- Conditions the study is for
- Postpartum Depression, Major Depressive Disorder, Postpartum Psychosis
- What is being tested?
- Goserelin 3.6 mg implant
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 63 participants
- Where
- 1 siteDenmark
- Study dates
- Jan 2011to Dec 2012
- 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 40 years
- Women only
- Healthy volunteers accepted
- Adult
Who may be able to join
- Healthy women
- Regular menstrual cycles (23 -35 days cycle length)
- No systemic or intrauterine steroid hormone use
Who cannot join
- Psychiatric disorder (DSM IV Axis I or WHO ICD-10 diagnostic classification).
- Prior or present neurological or other severe medical condition including substance abuse.
- No drug intake suspected to influence results
- Conditions that may increase risk by participating in the study program including ovarian cysts
- Pregnancy during the last year
- Delivery during the last 2 years
Show all 12Show fewer
- Presently wishing to obtain pregnancy
- Breast feeding
- Not fluent in Danish or severe visual or hearing impairments
- Earlier or present learning disabilities
- Claustrophobia (due to MRI scans)
- Metal implants (excludes MRI)
Trial locations and contacts
1 site in 1 country.
About this study
The project aimed at identifying neuropsychobiological signatures of pharmacological sex-steroid hormone manipulations in healthy women as a risk model for depression.
The study is a double-blind, randomized, placebo-controlled study. Investigators included 63 healthy female volunteers with regular menstrual cycles between 23 and 35 days. Participants were randomized to active Gonadotrophin-Releasing-Hormone agonist (GnRHa) (goserelin 3.6 mg implant) or placebo (saline injection) intervention, which was initiated in the mid follicular phase (i.e. cycle day 22.6 ±2.5). Sixty women completed follow-up and entered the analyses, except for a few drop outs on some domains. The following domains were addressed at baseline and at follow-up (16±3 days post intervention), (which corresponded to the early ovarian suppression phase of the biphasic hormone response to GnRHa): 1) serotonin transporter binding as imaged by 11CDASB Positron Emission Tomography (PET), 2) functional Magnetic Resonance Imaging (fMRI) emotional processing, 3) fMRI reward processing, 3) rating state fMRI (rsfMRI), 4) structural MRI, 5) Neuropsychology, 6) Psychophysiology, 7) Hypothalamus-Pituitary-Adrenal cortex (HPA)-axis dynamics, 8) Peripheral markers of immunoactive cell responses, 9) Epigenetic factors.
Psychometrics in terms of self reported mental distress and interview based ratings were monitored across the intervention period to monitor potential symptoms of mental distress and psychopathology. Also ovarian hormone responses, peripheral blood markers, and side effects scores were collected across the intervention period.
Read the detailed description
Aims and hypotheses:
Gender matters in normal brain function as well as in neuropsychiatric disorders. E.g. the vulnerability to mood and anxiety disorders is considerably greater in women. Among other factors, this possibly reflects gender differences in central serotonergic function since dysfunction of serotonergic neurotransmission is critically involved in the pathophysiology of mood and anxiety disorders, schizophrenia, and Alzheimer's disease. In particular, women going through phases in life where sex hormones decline rapidly from high levels or fluctuate, have a higher frequency of severe mood state changes and are more vulnerable to psychiatric disorders, e.g. across the pre to postpartum and menopausal transition. Interestingly, this risk is associated with increased variability of the plasma levels of the sex-hormone estradiol. Therefore, sex-hormone manipulation with a pharmacologically induced biphasic ovarian hormone response serve as a unique opportunity to study how sex-hormone fluctuations provoke mood state changes and increase vulnerability to neuropsychiatric disorders.
In this project investigators aimed at investigating whether sex-hormone manipulation affects: 1. Molecular imaging markers of serotonergic neurotransmission in vivo, 2. Brain structure, architecture and functional connectivity, 3. Stress and inflammatory responses, and 4. Cognitive functions, emotional processing, and information filtering, of importance in the pathophysiology of neuropsychiatric disorders.
Mentally healthy female volunteers were assessed at baseline (i.e cycle day 6.6 ±2.2) and at follow-up (i.e 16.2 ±2.6 days post intervention) in the early ovarian suppression phase af a Gonadotrophin-Releasing-Hormone agonist response in a placebo-controlled, double-blinded design (cohort size aim: N=30x2).
Research in neurobiological correlates of vulnerability related to sex-hormone changes is pivotal to improve the etiological understanding of brain disorders with gender differences in their incidence and/or nature. Such research may contribute to ameliorate fertility treatment, to improve treatment of mood disorders and schizophrenia, and, ideally, shed light on possible preventive strategies in vulnerable phases of women's lives such as the pre- to post-partum and menopausal transition period.
Hypotheses:
Investigators hypothesised that sex-hormone manipulation is associated with the following: 1. Compromised serotonergic neurotransmission, 2. Changes in functional and structural connectivity and lower hippocampal brain volumes and/or markers of decreased neurogenesis, 3. Increased stress reactivity and inflammatory responses, and 4. Changes in neurocognitive functioning and negative bias in emotional processing and information filtering. Investigators further hypothesised that these changes occur in a manner dependent on the magnitude of the estradiol drop from baseline and dependent on symptoms of depressed and anxious mood.
General study design:
The study is a prospective, double-blinded, placebo-controlled, combined within-subject and between-group design of neuropsychobiological changes in response to hormonal down-regulation. The investigation program will be performed at baseline in the mid-follicular phase, at day 5-8 of the menstrual cycle, and in the down-regulated state, 14-19 days after GnRHa intervention.
Participants. Investigators aimed at including 60 healthy female volunteers, in the age range 18-40 years. Group 1 (N=30) will receive sex-hormone manipulation with GnRHa, and group 2 (N=30) will receive placebo (saline injection). The inclusion will be stratified according to a polymorphism in the serotonin transporter promoter region (5-HTLPR).
The investigation program includes functional brain imaging of the serotonin transporter with [11C]DASB PET (6) and fMRI, structural brain imaging, blood measurements of sex-hormone levels, inflammatory and epigenetic biomarkers, characterization of the cortisol awakening response, and psychophysiological measures of information processing, and monitoring of symptoms of mental distress and psychopathology across the intervention period. An initial screening program will secure inclusion of healthy controls only and determine trait parameters such as genotypes, IQ and personality measures.
The study was registered at and approved by the Danish Ethical Committee before participant inclusion under the protocol identification number: H-2-2010-108. All participants gave written informed consent.
- Conditions
- Postpartum Depression, Major Depressive Disorder, Postpartum Psychosis, Menopause, Neurodegeneration, Schizophrenia
- Being tested
- Goserelin 3.6 mg implant, Placebo
- Keywords
- Mental health, Brain Imaging, Steroid hormones, Serotonin, PET, MRI, fMRI, human, gender, risk model
- Medical subject headings
- Depression, Postpartum, Depressive Disorder, Major, Nerve Degeneration, Schizophrenia, Psychological Well-Being, Coitus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Goserelin 3.6 mg implantDrug
Also called Zoladex
Pharmacologically induced biphasic sex-steroid hormone fluctuation
PlaceboDrug
Also called Saline
Injection of saline
| Study group | Role | What they receive |
|---|---|---|
| GnRHa | Active comparator | Goserelin 3.6 mg implant Receives: Drug: Goserelin 3.6 mg implant |
| Placebo | Placebo comparator | Injection of saline Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes from baseline in symptoms of depression
Hamilton 17 item score
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in serotonin transporter binding in volumes of interest (VOIs)
PET scan assessed serotonin transporter binding changes
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in fMRI response to emotional faces
fMRI response changes to emotional faces in emotion processing network including amygdala reactivity
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in fMRI response to gambling paradigm
fMRI response changes to reward (monetary win) paradigm in reward processing network
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in rsfMRI changes in functional connectivity
rsfMRI changes in functional connectivity in response to intervention
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in affective cognition (VAMT-24 test)
Neuropsychological (VAMT-24 test) outcomes on affective cognition
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in reaction time
Changes in reaction time
Measured: Baseline to follow-up 16±3 days after intervention
Serial mood fluctuations (SD of total mood disturbance (TMD) score of daily POMS across intervention period)
Mood fluctuations measured by serial collection of daily POMS
Measured: Intervention start to follow-up 16±3 days after intervention
Changes from baseline in hippocampal volume
Hippocampal volumes from structural MRI
Measured: Baseline to follow-up 16±3 days after intervention
Changes in pre-pulse-inhibition (PPI) from baseline
Change in amplitude of the startle response to pulse after pre-pulse warning as measured by EMG in the orbicularis oculi muscle (subtraction of averages across a series of 10 repititions at baseline and at follow-up 16±3 days).
Measured: Baseline to follow-up 16±3 days after intervention
Changes in a set of markers of immunoactivity across study period
Cytokines, hsCRP and gene transcript profile markers of
Measured: Baseline, intervention time, flare-up phase and follow-up
Changes in epigenetic markers of estrogen sensitivity
Epigenetic (methylation) markers
Measured: Baseline to follow-up 16±3 days after intervention
Changes in HPA-axis dynamics (the cortisol awakening response)
The cortical awakening response
Measured: Baseline to follow-up 16±3 days after intervention
Changes in sensorimotor gating (P50 suppression) from baseline
Changes in sensorimotor gating (P50 suppression) from baseline
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in hippocampal microstructure
Hippocampal microstructure from MRI
Measured: Baseline to follow-up 16±3 days after intervention
Secondary outcomes (7)
Changes from baseline in fMRI responses to emotional memory paradigm
Changes in brain activation to fMRI emotional memory paradigm - delayed recall forgetting of word prior to emotional disturbance
Measured: Baseline to follow-up 16±3 days after intervention
Changes from baseline in Cohens perceived stress score
Changes Cohens perceived stress score
Measured: Baseline to follow-up 16±3 days after intervention
Changes in Pittsburg Sleep Quality Inventory (PSQI)
Sleep quality self reported weekly across intervention period
Measured: Baseline and 1 time per week until follow-up at 16 ±3 days
Side effects scores (project specific 15 items questionnaire)
Total side effect score across and after intervention period
Measured: 7, 12 and 30 days post intervention
Changes in SCL-R (Symptom check-list revised)
Changes in symptoms of psychopathology across intervention period
Measured: Baseline and 1 time per week from intervention to follow up at 16±3 days post intervention
Major Depression Inventory (MDI)
Changes in self-reported symptoms of depression across intervention period
Measured: Baseline and 1 time per week from intervention to follow up at 16±3 days post intervention
Changes in profile of mood states (POMS TMD score)
Changes in self-reported symptoms of mental distress across intervention period
Measured: Baseline and 1 time per week from intervention to follow up at 16±3 days post intervention
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted22 Jan 2016 (estimated)
- Study startJan 2011
- Primary completionDec 2012
- Study completionDec 2012
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (2)Papers the sponsor has linked to this study.
- Other trials for Postpartum DepressionStudies 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
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 63 participants (actual)
Sponsor and investigators
- Lead sponsor
- Gitte Moos Knudsen
- Sponsor type
- University, hospital or other
- Collaborators
- Center for Integrated Molecular Brain Imaging, Copenhagen, Denmak, Copenhagen University Hospital, Rigshospitalet, Glostrup University Hospital, Copenhagen, Danish Multiple Sclerosis Center Rigshospitalet
- Responsible party
- Sponsor-investigator, Gitte Moos Knudsen, Copenhagen University Hospital, Rigshospitalet
- Investigators
- Vibe G Frokjaer, MD, Phd, Principal investigator, Neurobiology Research Unit
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02661789
- Sponsor's protocol ID
- GnRHa
- Other IDs
- H-2-2010-108
- Acronym
- GnRHa
- Status last verified
- Jan 2016
- First submitted
- 13 Jan 2016
- Last updated
- 22 Jan 2016
- Results posted
- No
- Data monitoring committee
- Yes
- Individual data sharing
- Yes: Via database of Center for Integrated Molecular Brain Imaging (Knudsen et al 2016, NeuroImage) data will be available for neuroscience research community contingent on approval by scientific board
Publications
Mehta D, Rex-Haffner M, Sondergaard HB, Pinborg A, Binder EB, Frokjaer VG. Genome-wide gene expression in a pharmacological hormonal transition model and its relation to depressive symptoms. Acta Psychiatr Scand. 2019 Jul;140(1):77-84. doi: 10.1111/acps.13038. Epub 2019 May 24.
PubMed 31099405Fisher PM, Larsen CB, Beliveau V, Henningsson S, Pinborg A, Holst KK, Jensen PS, Svarer C, Siebner HR, Knudsen GM, Frokjaer VG. Pharmacologically Induced Sex Hormone Fluctuation Effects on Resting-State Functional Connectivity in a Risk Model for Depression: A Randomized Trial. Neuropsychopharmacology. 2017 Jan;42(2):446-453. doi: 10.1038/npp.2016.208. Epub 2016 Sep 21.
PubMed 27649641
Study at a glance
From the registry record, last updated by the sponsor on 22 Jan 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Neuropsychobiological Correlates of Sex-steroid Hormone Manipulation in Healthy Women: a Risk Model for Depression
- ClinicalTrials.gov ID
- NCT02661789
- Acronym / sponsor ID
- GnRHa / GnRHa
- Conditions
- Postpartum Depression, Major Depressive Disorder, Postpartum Psychosis, Menopause, Neurodegeneration, Schizophrenia
- Keywords
- Mental health, Brain Imaging, Steroid hormones, Serotonin, PET, MRI, fMRI, human
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 63 participants (actual)
- Lead sponsor
- Gitte Moos KnudsenUniversity, hospital or other
- Collaborators
- Center for Integrated Molecular Brain Imaging, Copenhagen, Denmak, Copenhagen University Hospital, Rigshospitalet, Glostrup University Hospital, Copenhagen, Danish Multiple Sclerosis Center Rigshospitalet
- Study start
- Jan 2011
- Primary completion
- Dec 2012 (actual)
- Study completion
- Dec 2012 (actual)
- First posted
- 22 Jan 2016 (estimated)
- 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.
The project aimed at identifying neuropsychobiological signatures of pharmacological sex-steroid hormone manipulations in healthy women as a risk model for depression.
The study is a double-blind, randomized, placebo-controlled study. Investigators included 63 healthy female volunteers with regular menstrual cycles between 23 and 35 days. Participants were randomized to active Gonadotrophin-Releasing-Hormone agonist (GnRHa) (goserelin 3.6 mg implant) or placebo (saline injection) intervention, which was initiated in the mid follicular phase (i.e. cycle day 22.6 ±2.5). Sixty women completed follow-up and entered the analyses, except for a few drop outs on some domains. The following domains were addressed at baseline and at follow-up (16±3 days post intervention), (which corresponded to the early ovarian suppression phase of the biphasic hormone response to GnRHa): 1) serotonin transporter binding as imaged by 11CDASB Positron Emission Tomography (PET), 2) functional Magnetic Resonance Imaging (fMRI) emotional processing, 3) fMRI reward processing, 3) rating state fMRI (rsfMRI), 4) structural MRI, 5) Neuropsychology, 6) Psychophysiology, 7) Hypothalamus-Pituitary-Adrenal cortex (HPA)-axis dynamics, 8) Peripheral markers of immunoactive cell responses, 9) Epigenetic factors.
Psychometrics in terms of self reported mental distress and interview based ratings were monitored across the intervention period to monitor potential symptoms of mental distress and psychopathology. Also ovarian hormone responses, peripheral blood markers, and side effects scores were collected across the intervention period.
Detailed description
Aims and hypotheses:
Gender matters in normal brain function as well as in neuropsychiatric disorders. E.g. the vulnerability to mood and anxiety disorders is considerably greater in women. Among other factors, this possibly reflects gender differences in central serotonergic function since dysfunction of serotonergic neurotransmission is critically involved in the pathophysiology of mood and anxiety disorders, schizophrenia, and Alzheimer's disease. In particular, women going through phases in life where sex hormones decline rapidly from high levels or fluctuate, have a higher frequency of severe mood state changes and are more vulnerable to psychiatric disorders, e.g. across the pre to postpartum and menopausal transition. Interestingly, this risk is associated with increased variability of the plasma levels of the sex-hormone estradiol. Therefore, sex-hormone manipulation with a pharmacologically induced biphasic ovarian hormone response serve as a unique opportunity to study how sex-hormone fluctuations provoke mood state changes and increase vulnerability to neuropsychiatric disorders.
In this project investigators aimed at investigating whether sex-hormone manipulation affects: 1. Molecular imaging markers of serotonergic neurotransmission in vivo, 2. Brain structure, architecture and functional connectivity, 3. Stress and inflammatory responses, and 4. Cognitive functions, emotional processing, and information filtering, of importance in the pathophysiology of neuropsychiatric disorders.
Mentally healthy female volunteers were assessed at baseline (i.e cycle day 6.6 ±2.2) and at follow-up (i.e 16.2 ±2.6 days post intervention) in the early ovarian suppression phase af a Gonadotrophin-Releasing-Hormone agonist response in a placebo-controlled, double-blinded design (cohort size aim: N=30x2).
Research in neurobiological correlates of vulnerability related to sex-hormone changes is pivotal to improve the etiological understanding of brain disorders with gender differences in their incidence and/or nature. Such research may contribute to ameliorate fertility treatment, to improve treatment of mood disorders and schizophrenia, and, ideally, shed light on possible preventive strategies in vulnerable phases of women's lives such as the pre- to post-partum and menopausal transition period.
Hypotheses:
Investigators hypothesised that sex-hormone manipulation is associated with the following: 1. Compromised serotonergic neurotransmission, 2. Changes in functional and structural connectivity and lower hippocampal brain volumes and/or markers of decreased neurogenesis, 3. Increased stress reactivity and inflammatory responses, and 4. Changes in neurocognitive functioning and negative bias in emotional processing and information filtering. Investigators further hypothesised that these changes occur in a manner dependent on the magnitude of the estradiol drop from baseline and dependent on symptoms of depressed and anxious mood.
General study design:
The study is a prospective, double-blinded, placebo-controlled, combined within-subject and between-group design of neuropsychobiological changes in response to hormonal down-regulation. The investigation program will be performed at baseline in the mid-follicular phase, at day 5-8 of the menstrual cycle, and in the down-regulated state, 14-19 days after GnRHa intervention.
Participants. Investigators aimed at including 60 healthy female volunteers, in the age range 18-40 years. Group 1 (N=30) will receive sex-hormone manipulation with GnRHa, and group 2 (N=30) will receive placebo (saline injection). The inclusion will be stratified according to a polymorphism in the serotonin transporter promoter region (5-HTLPR).
The investigation program includes functional brain imaging of the serotonin transporter with [11C]DASB PET (6) and fMRI, structural brain imaging, blood measurements of sex-hormone levels, inflammatory and epigenetic biomarkers, characterization of the cortisol awakening response, and psychophysiological measures of information processing, and monitoring of symptoms of mental distress and psychopathology across the intervention period. An initial screening program will secure inclusion of healthy controls only and determine trait parameters such as genotypes, IQ and personality measures.
The study was registered at and approved by the Danish Ethical Committee before participant inclusion under the protocol identification number: H-2-2010-108. All participants gave written informed consent.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| GnRHa | Active comparator | Drug: Goserelin 3.6 mg implantGoserelin 3.6 mg implant |
| Placebo | Placebo comparator | Drug: PlaceboInjection of saline |
Who may qualify
- Ages
- 18 to 40 years
- Sex
- Female only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (3 listed)
- Healthy women
- Regular menstrual cycles (23 -35 days cycle length)
- No systemic or intrauterine steroid hormone use
Key exclusion criteria (12 listed)
- Psychiatric disorder (DSM IV Axis I or WHO ICD-10 diagnostic classification).
- Prior or present neurological or other severe medical condition including substance abuse.
- No drug intake suspected to influence results
- Conditions that may increase risk by participating in the study program including ovarian cysts
- Pregnancy during the last year
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 |
|---|---|---|
| Goserelin 3.6 mg implantAlso: ZoladexPharmacologically induced biphasic sex-steroid hormone fluctuation | Drug | GnRHa |
| PlaceboAlso: SalineInjection of saline | Drug | Placebo |
Primary outcome
Changes from baseline in symptoms of depression
Time frame: Baseline to follow-up 16±3 days after intervention
Hamilton 17 item score
Changes from baseline in serotonin transporter binding in volumes of interest (VOIs)
Time frame: Baseline to follow-up 16±3 days after intervention
PET scan assessed serotonin transporter binding changes
Changes from baseline in fMRI response to emotional faces
Time frame: Baseline to follow-up 16±3 days after intervention
fMRI response changes to emotional faces in emotion processing network including amygdala reactivity
Changes from baseline in fMRI response to gambling paradigm
Time frame: Baseline to follow-up 16±3 days after intervention
fMRI response changes to reward (monetary win) paradigm in reward processing network
Changes from baseline in rsfMRI changes in functional connectivity
Time frame: Baseline to follow-up 16±3 days after intervention
rsfMRI changes in functional connectivity in response to intervention
Changes from baseline in affective cognition (VAMT-24 test)
Time frame: Baseline to follow-up 16±3 days after intervention
Neuropsychological (VAMT-24 test) outcomes on affective cognition
Changes from baseline in reaction time
Time frame: Baseline to follow-up 16±3 days after intervention
Changes in reaction time
Serial mood fluctuations (SD of total mood disturbance (TMD) score of daily POMS across intervention period)
Time frame: Intervention start to follow-up 16±3 days after intervention
Mood fluctuations measured by serial collection of daily POMS
Changes from baseline in hippocampal volume
Time frame: Baseline to follow-up 16±3 days after intervention
Hippocampal volumes from structural MRI
Changes in pre-pulse-inhibition (PPI) from baseline
Time frame: Baseline to follow-up 16±3 days after intervention
Change in amplitude of the startle response to pulse after pre-pulse warning as measured by EMG in the orbicularis oculi muscle (subtraction of averages across a series of 10 repititions at baseline and at follow-up 16±3 days).
Changes in a set of markers of immunoactivity across study period
Time frame: Baseline, intervention time, flare-up phase and follow-up
Cytokines, hsCRP and gene transcript profile markers of
Changes in epigenetic markers of estrogen sensitivity
Time frame: Baseline to follow-up 16±3 days after intervention
Epigenetic (methylation) markers
Changes in HPA-axis dynamics (the cortisol awakening response)
Time frame: Baseline to follow-up 16±3 days after intervention
The cortical awakening response
Changes in sensorimotor gating (P50 suppression) from baseline
Time frame: Baseline to follow-up 16±3 days after intervention
Changes in sensorimotor gating (P50 suppression) from baseline
Changes from baseline in hippocampal microstructure
Time frame: Baseline to follow-up 16±3 days after intervention
Hippocampal microstructure from MRI
7 secondary outcomes
Changes from baseline in fMRI responses to emotional memory paradigm
Time frame: Baseline to follow-up 16±3 days after intervention
Changes from baseline in Cohens perceived stress score
Time frame: Baseline to follow-up 16±3 days after intervention
Changes in Pittsburg Sleep Quality Inventory (PSQI)
Time frame: Baseline and 1 time per week until follow-up at 16 ±3 days
Side effects scores (project specific 15 items questionnaire)
Time frame: 7, 12 and 30 days post intervention
Changes in SCL-R (Symptom check-list revised)
Time frame: Baseline and 1 time per week from intervention to follow up at 16±3 days post intervention
Major Depression Inventory (MDI)
Time frame: Baseline and 1 time per week from intervention to follow up at 16±3 days post intervention
Changes in profile of mood states (POMS TMD score)
Time frame: Baseline and 1 time per week from intervention to follow up at 16±3 days post intervention
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 22 Jan 2016.
- Derived from this study: PubMed 31099405Mehta D, Rex-Haffner M, Sondergaard HB, Pinborg A, Binder EB, Frokjaer VG. Genome-wide gene expression in a pharmacological hormonal transition model and its relation to depressive symptoms. Acta Psychiatr Scand. 2019 Jul;140(1):77-84. doi: 10.1111/acps.13038. Epub 2019 May 24.
- Derived from this study: PubMed 27649641Fisher PM, Larsen CB, Beliveau V, Henningsson S, Pinborg A, Holst KK, Jensen PS, Svarer C, Siebner HR, Knudsen GM, Frokjaer VG. Pharmacologically Induced Sex Hormone Fluctuation Effects on Resting-State Functional Connectivity in a Risk Model for Depression: A Randomized Trial. Neuropsychopharmacology. 2017 Jan;42(2):446-453. doi: 10.1038/npp.2016.208. Epub 2016 Sep 21.
- Individual participant dataSharing planned: Yes. Via database of Center for Integrated Molecular Brain Imaging (Knudsen et al 2016, NeuroImage) data will be available for neuroscience research community contingent on approval by scientific board
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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.
Vibe G Frokjaer, MD, Phd principal investigator
Neurobiology Research Unit
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Goserelin 3.6 mg implant in people with Postpartum Depression and Major Depressive Disorder, run by Gitte Moos Knudsen at 1 site in Denmark.
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 3 inclusion and 12 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: finished, as of the sponsor's last update on 22 Jan 2016. 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 Denmark. 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. Some participants in this study may receive a placebo. 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?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Changes from baseline in symptoms of depression (time frame: Baseline to follow-up 16±3 days after intervention). The study lists 15 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 NCT02661789, which also lists 2 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 22 Jan 2016.