Alzheimer DiseaseActiGliANCT06224920
Activity of Cerebral Networks, Amyloid and Microglia in Aging and Alzheimer's Disease
An observational study of Alzheimer Disease and Corticobasal Syndrome, run by Ludwig-Maximilians - University of Munich.
Trial summary
The temporal sequence of microglial activation, changes in functional and structural connectivity and the progression of neurocognitive deficits has not been conclusively clarified. Read more about this study
- Who is it for?
- Ages 55 to 80 years
- Conditions the study is for
- Alzheimer Disease, Corticobasal Syndrome
- What is being tested?
- magnetic resonance imaging, electroencephalography and blood and CSF biomarker
- Type of treatment
- Injection or infusion
- How many people
- 140 participants
- Where
- No sites listed yet
- Study dates
- 1 Jan 2017to 1 Jan 2024
- 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 55 to 80 years
- All sexes
- Adult, Older adult
Study population: recruitment of participants via the outpatient clinics of Department of Psychiatry and Psychotherapy, Department of Neurology and Institute of Stroke and Dementia Research (LMU hospital)
Who may be able to join
- Informed consent for the additional examinations, written declaration of consent
- Constant pharmacotherapy in a period of one week before the MRI/EEG/PET examination
Who cannot join
- Existence of legal guardianship/restricted capacity to consent
- Other severe concomitant psychiatric illnesses, e.g. schizophrenia, bipolar affective disorder
- Clinically relevant depressive symptoms (Beck Depression Inventory, BDI, score > 17/GDS > 5)
- Acute suicidal tendencies
- Drug, medication or alcohol abuse at the time of the study
- Severe traumatic brain injury (> 2nd degree TBI) in the medical history or 1st degree within the last 3 months.
Show all 14Show fewer
- Evidence of structural damage to the basal ganglia or brainstem
- Severe neurological diseases (such as disc prolapse in the last 6 months, sensory, motor or autonomic polyneuropathies)
- Severe internal diseases (such as manifest arterial hypertension, severe heart disease, pacemaker, respiratory insufficiency)
- Any electronic implants (e.g. pacemakers) or other MRI and/or PET contraindications
- Malignant diseases of any kind in the last 5 years, severe active infectious diseases, chronic and systemic skin diseases
- Bone diseases (such as Paget's disease, osteoporosis with spontaneous fractures, recent fractures)
- Other circumstances which, in the opinion of the investigator, speak against the patient's participation in this study
- Occupational or other radiation exposure >15 mSv/a
About this study
Official title: Aktivität Von Zerebralen Netzwerken, Amyloid Und Mikroglia Bei Alterung Und Alzheimer-Krankheit
The temporal sequence of microglial activation, changes in functional and structural connectivity and the progression of neurocognitive deficits has not been conclusively clarified. To date, there have been no studies of the topographical and pathogenetic relationship between microglial activation and network degeneration. The main aim of the present study is to investigate the relationships between functional, structural MRI connectivity and microglial activation at different stages of AD in a multimodal approach. Genetic predisposition and biomarkers in blood and cerebrospinal fluid will also be taken into account in order to close the explanatory gap in pathogenesis between the known molecular pathological changes and their effects at system level in an integrative approach.
Read the detailed description
The main aim of the present study is to investigate correlations between functional and structural MRI connectivity and microglial activation in PET at different stages of AD. Some previous studies have described that especially the brain regions affected by AD-related alterations show increased microglial activity. How these relationships known at the anatomical level relate to changes in functional connectivity is still largely unclear. The multimodal analysis of functional connectivity in the resting networks and the investigation of inflammatory effects using microglia PET may be able to reveal previously unknown neuropathological connections between different stages of AD. Since a direct toxicity effect of Aβ on surrounding neurons can also be assumed, the topography of fibrillar Aβ deposits is also recorded using PET. To date, there are no studies investigating changes in functional and structural connectivity with microglia-associated inflammatory changes and Aβ at different disease stages.
- evaluation of the correlation of microglial activation determined in PET with the degeneration of functional networks depending on the stage of the disease.
- Is microglial activation or Aβ deposition the cause of changes in functional networks?
- What is the overlap between microglia- and Aβ-induced network degeneration (modulation of synaptic pruning vs. neurotoxic effect of ß-amyloid)
- How reliable is functional connectivity as a biomarker for AD stratification at different disease stages?
- What is the temporal and topographical spread of AD pathologies along the hub regions of the resting networks and can a pattern of spread indicative of a specific molecular mechanism be identified?
- Does the extent (quantitative and regional) of microglial activation correlate with existing amyloid and tau deposits, as well as network changes? How does microglial activation change in relation to the progression of tau deposits?
- correlation of inflammatory changes in a multimodal comparison with changes in structural connectivity, metabolic alterations, biomarker abnormalities and changes at the neurotransmitter level.
- Is there an image morphologic correlate of soluble TREM2 receptor concentration in cerebrospinal fluid at different disease stages?
- What role does oxidative stress (glutathione changes) play in the pathogenesis of AD and is there a connection to other disease-related changes at the multimodal level?
- are there certain correlations between genetic factors (especially carriers vs. non-carriers of apolipoprotein E, APOE, risk allele ε4 as the strongest genetic risk factor of sporadic AD) and structural or functional connectivity changes depending on the disease stage that can be derived from the multimodal data analysis? a. What is the temporal relationship between microglial activation and Aβ deposits or functional and structural network alterations?
- Conditions
- Alzheimer Disease, Corticobasal Syndrome
- Being tested
- magnetic resonance imaging, electroencephalography, blood and CSF biomarker, positron emission tomography, neuropsychological test
- Keywords
- Alzheimer´s disease, corticobasal degeneration, microglial activation, neuroinflammation, amyloid, tau protein
- Medical subject headings
- Alzheimer Disease, Corticobasal Degeneration, Neuroinflammatory Diseases, Frontotemporal Dementia
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
magnetic resonance imagingDiagnostic test
MRI data acquisition was performed on a 3 Tesla MRI scanner with parallel transmission and reception technology (Skyra Magnetom, Siemens Healthcare, Erlangen, Germany). Imaging is performed with a maximum gradient strength of 45mT/m and a maximum slew rate of 200 T/m/s and a 64-element head coil.
electroencephalographyOther
Also called eeg
A 20-channel resting EEG (Brain Products, Gilching, Germany) is recorded as part of routine clinical diagnostics in the Department of Psychiatry and Psychotherapy at the LMU to rule out focal neurophysiological pathologies. Within the scope of the present study, an extended examination will be carried out, which includes a 64-channel EEG, including a passive visual paradigm. After completion of the clinical evaluation, the neurophysiological changes in resting activity will be scientifically analyzed in comparison to the MRI and PET data.
blood and CSF biomarkerDiagnostic test
Aβ1-42 and 1-40, total tau protein and phosphorylated tau protein 181 (p-Tau), apolipoprotein E (APOE), soluble TREM2 protein, neurofilament light chain and glial fibrillary protein (GFAP) will be determined.
positron emission tomographyDiagnostic test
Also called PET
According to an established and standardized protocol, PET scans are performed with the TSPO receptor ligand [18F]-GE-180, [18F]flutemetamol for assessment of fibrillar Aβ 162 accumulation and the Tau ligand [18F]-PI-2620. In brief, [18F]GE-180 TSPO PET images (mean dose: 177 ± 17 MBq) with an emission window of 60-80 min after injection will be acquired to measure the activation of glial cells. [18F]Flutemetamol Aβ PET images (average dose: 182 ± 11 MBq) are acquired with an emission window of 90-110 min after injection to assess fibrillar Aβ accumulation. Dynamic [18F]PI-2620 tau PET (average dose: 186 ± 14 MBq) with an emission window of 0-60 minutes after injection are performed for quantification of tau aggregation. Static images of the late phase (20-40 min) are reconstructed. These images are used for further processing and analysis.
neuropsychological testDiagnostic test
Trained psychologists at the Memory Clinic of the LMU Hospital administered the CDR, CERAD-NB and Mini-Mental State Examination (MMSE). The CERAD-NB battery was used to generate a total score for the six subscales: semantic fluency (animals/60 s), modified Boston naming test, lexical items, construction practice, lexical items retrieval, and lexical items discrimination, with higher scores indicating better performance.
| Study group | Role | What they receive |
|---|---|---|
| Alzheimer´s disease spectrum | MCI-AD patients Evidence of minor cognitive impairment with essentially preserved everyday competence and evidence of reduced Aβ42 concentration in the cerebrospinal fluid. Score in the CERAD word list 1.5 SD below the normal range.
Patients with AD-dementia Evidence of pronounced cognitive impairment and relevant impairment of everyday life and evidence of reduced Aβ42 concentration in the cerebrospinal fluid (diagnostic criteria (NIA-AA fulfilled)). Receives: Diagnostic Test: magnetic resonance imaging; Other: electroencephalography; Diagnostic Test: blood and CSF biomarker; Diagnostic Test: positron emission tomography; Diagnostic Test: neuropsychological test | |
| corticobasal syndrome due to probable 4 repeat taupathy | Evidence of the typical clinical picture of an atypical Parkinson's syndrome with onset of symptoms > 1 year. No evidence of reduced Aβ42 concentration in the cerebrospinal fluid. Fulfillment of the revised Armstrong criteria for probable CBS or the Movement Disorder's Society criteria for suggestive/possible PSP-CBS. Receives: Diagnostic Test: magnetic resonance imaging; Other: electroencephalography; Diagnostic Test: blood and CSF biomarker; Diagnostic Test: positron emission tomography; Diagnostic Test: neuropsychological test | |
| subjective congnitive decline | Subjective memory impairment, with age-appropriate unremarkable neurocognitive test battery (CERAD) and no evidence of reduced Aβ42 concentration or increased total tau or phospho-tau concentration in the cerebrospinal fluid. Subjective cognitive deterioration over a period of 6 months to 5 years. Receives: Diagnostic Test: magnetic resonance imaging; Other: electroencephalography; Diagnostic Test: blood and CSF biomarker; Diagnostic Test: positron emission tomography; Diagnostic Test: neuropsychological test |
What is being measured
The primary outcome is the main question the study is designed to answer.
association of cerebral connectivity with microglia activation patterns
association between functional/structural connectivity and TSPO SUVR
Measured: until 06/2024
Individual regional associations between Aβ-, tau- and neurodegeneration with microglial activation
association of regional amyloid and tau with microglial activation (measured by TSPO-PET)
Measured: until 06/2024
validation of blood-based biomarkers in the differentiation of AD, SCI and CBS cases
comparison of AD-related biomarkers (pTau181, Abeta1-42/1-40), plasma apolipoprotein E and inflammatory biomarkers (GFAP, NfL)
Measured: until 06/2024
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Jan 2024
- Study start1 Jan 2017
- Primary completion1 Jan 2024
- Study completion1 Jan 2024
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for Alzheimer DiseaseStudies 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
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 140 participants (actual)
Sponsor and investigators
- Lead sponsor
- Ludwig-Maximilians - University of Munich
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Robert Perneczky, Ludwig-Maximilians - University of Munich
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06224920
- Sponsor's protocol ID
- 17-755 and 17-569
- Acronym
- ActiGliA
- Status last verified
- Jul 2025
- First submitted
- 16 Jan 2024
- Last updated
- 4 Jul 2025
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Ochsner M, Brendel M, Franzmeier N, Trappmann L, Zaganjori M, Ersoezlue E, Kurz C, Haeckert J, Utecht J, Schirge PM, Papazov B, Pogarell O, Janowitz D, Buerger K, Ewers M, Palleis C, Weidinger E, Biechele G, Schuster S, Finze A, Eckenweber F, Rupprecht R, Rominger A, Goldhardt O, Grimmer T, Keeser D, Stoecklein S, Dietrich O, Bartenstein P, Levin J, Hoglinger G, Perneczky R, Rauchmann BS. Microglial dynamics associate with the spatial pattern of tau deposition in early Alzheimer's disease. Alzheimers Res Ther. 2026 Oct 12;18(1):232. doi: 10.1186/s13195-026-02230-1.
PubMed 42875788
Study at a glance
From the registry record, last updated by the sponsor on 4 Jul 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Aktivität Von Zerebralen Netzwerken, Amyloid Und Mikroglia Bei Alterung Und Alzheimer-Krankheit
- ClinicalTrials.gov ID
- NCT06224920
- Acronym / sponsor ID
- ActiGliA / 17-755 and 17-569
- Conditions
- Alzheimer Disease, Corticobasal Syndrome
- Keywords
- Alzheimer´s disease, corticobasal degeneration, microglial activation, neuroinflammation, amyloid, tau protein
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 140 participants (actual)
- Lead sponsor
- Ludwig-Maximilians - University of MunichUniversity, hospital or other
- Study start
- 1 Jan 2017 (actual)
- Primary completion
- 1 Jan 2024 (actual)
- Study completion
- 1 Jan 2024 (actual)
- First posted
- 25 Jan 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.
The temporal sequence of microglial activation, changes in functional and structural connectivity and the progression of neurocognitive deficits has not been conclusively clarified. To date, there have been no studies of the topographical and pathogenetic relationship between microglial activation and network degeneration. The main aim of the present study is to investigate the relationships between functional, structural MRI connectivity and microglial activation at different stages of AD in a multimodal approach. Genetic predisposition and biomarkers in blood and cerebrospinal fluid will also be taken into account in order to close the explanatory gap in pathogenesis between the known molecular pathological changes and their effects at system level in an integrative approach.
Detailed description
The main aim of the present study is to investigate correlations between functional and structural MRI connectivity and microglial activation in PET at different stages of AD. Some previous studies have described that especially the brain regions affected by AD-related alterations show increased microglial activity. How these relationships known at the anatomical level relate to changes in functional connectivity is still largely unclear. The multimodal analysis of functional connectivity in the resting networks and the investigation of inflammatory effects using microglia PET may be able to reveal previously unknown neuropathological connections between different stages of AD. Since a direct toxicity effect of Aβ on surrounding neurons can also be assumed, the topography of fibrillar Aβ deposits is also recorded using PET. To date, there are no studies investigating changes in functional and structural connectivity with microglia-associated inflammatory changes and Aβ at different disease stages.
- evaluation of the correlation of microglial activation determined in PET with the degeneration of functional networks depending on the stage of the disease.
- Is microglial activation or Aβ deposition the cause of changes in functional networks?
- What is the overlap between microglia- and Aβ-induced network degeneration (modulation of synaptic pruning vs. neurotoxic effect of ß-amyloid)
- How reliable is functional connectivity as a biomarker for AD stratification at different disease stages?
- What is the temporal and topographical spread of AD pathologies along the hub regions of the resting networks and can a pattern of spread indicative of a specific molecular mechanism be identified?
- Does the extent (quantitative and regional) of microglial activation correlate with existing amyloid and tau deposits, as well as network changes? How does microglial activation change in relation to the progression of tau deposits?
- correlation of inflammatory changes in a multimodal comparison with changes in structural connectivity, metabolic alterations, biomarker abnormalities and changes at the neurotransmitter level.
- Is there an image morphologic correlate of soluble TREM2 receptor concentration in cerebrospinal fluid at different disease stages?
- What role does oxidative stress (glutathione changes) play in the pathogenesis of AD and is there a connection to other disease-related changes at the multimodal level?
- are there certain correlations between genetic factors (especially carriers vs. non-carriers of apolipoprotein E, APOE, risk allele ε4 as the strongest genetic risk factor of sporadic AD) and structural or functional connectivity changes depending on the disease stage that can be derived from the multimodal data analysis? a. What is the temporal relationship between microglial activation and Aβ deposits or functional and structural network alterations?
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Alzheimer´s disease spectrum | – | Diagnostic Test: magnetic resonance imaging, Other: electroencephalography, Diagnostic Test: blood and CSF biomarker, Diagnostic Test: positron emission tomography, Diagnostic Test: neuropsychological testMCI-AD patients Evidence of minor cognitive impairment with essentially preserved everyday competence and evidence of reduced Aβ42 concentration in the cerebrospinal fluid. Score in the CERAD word list 1.5 SD below the normal range. Patients with AD-dementia Evidence of pronounced cognitive impairment and relevant impairment of everyday life and evidence of reduced Aβ42 concentration in the cerebrospinal fluid (diagnostic criteria (NIA-AA fulfilled)). |
| corticobasal syndrome due to probable 4 repeat taupathy | – | Diagnostic Test: magnetic resonance imaging, Other: electroencephalography, Diagnostic Test: blood and CSF biomarker, Diagnostic Test: positron emission tomography, Diagnostic Test: neuropsychological testEvidence of the typical clinical picture of an atypical Parkinson's syndrome with onset of symptoms > 1 year. No evidence of reduced Aβ42 concentration in the cerebrospinal fluid. Fulfillment of the revised Armstrong criteria for probable CBS or the Movement Disorder's Society criteria for suggestive/possible PSP-CBS. |
| subjective congnitive decline | – | Diagnostic Test: magnetic resonance imaging, Other: electroencephalography, Diagnostic Test: blood and CSF biomarker, Diagnostic Test: positron emission tomography, Diagnostic Test: neuropsychological testSubjective memory impairment, with age-appropriate unremarkable neurocognitive test battery (CERAD) and no evidence of reduced Aβ42 concentration or increased total tau or phospho-tau concentration in the cerebrospinal fluid. Subjective cognitive deterioration over a period of 6 months to 5 years. |
Who may qualify
- Ages
- 55 to 80 years
- Sex
- All
- Age groups
- Adult, Older adult
- Study population
- recruitment of participants via the outpatient clinics of Department of Psychiatry and Psychotherapy, Department of Neurology and Institute of Stroke and Dementia Research (LMU hospital)
Key inclusion criteria (2 listed)
- Informed consent for the additional examinations, written declaration of consent
- Constant pharmacotherapy in a period of one week before the MRI/EEG/PET examination
Key exclusion criteria (14 listed)
- Existence of legal guardianship/restricted capacity to consent
- Other severe concomitant psychiatric illnesses, e.g. schizophrenia, bipolar affective disorder
- Clinically relevant depressive symptoms (Beck Depression Inventory, BDI, score > 17/GDS > 5)
- Acute suicidal tendencies
- Drug, medication or alcohol abuse at the time of the study
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 |
|---|---|---|
| magnetic resonance imagingMRI data acquisition was performed on a 3 Tesla MRI scanner with parallel transmission and reception technology (Skyra Magnetom, Siemens Healthcare, Erlangen, Germany). Imaging is performed with a maximum gradient strength of 45mT/m and a maximum slew rate of 200 T/m/s and a 64-element head coil. | Diagnostic test | Alzheimer´s disease spectrum, corticobasal syndrome due to probable 4 repeat taupathy, subjective congnitive decline |
| electroencephalographyAlso: eegA 20-channel resting EEG (Brain Products, Gilching, Germany) is recorded as part of routine clinical diagnostics in the Department of Psychiatry and Psychotherapy at the LMU to rule out focal neurophysiological pathologies. Within the scope of the present study, an extended examination will be carried out, which includes a 64-channel EEG, including a passive visual paradigm. After completion of the clinical evaluation, the neurophysiological changes in resting activity will be scientifically analyzed in comparison to the MRI and PET data. | Other | Alzheimer´s disease spectrum, corticobasal syndrome due to probable 4 repeat taupathy, subjective congnitive decline |
| blood and CSF biomarkerAβ1-42 and 1-40, total tau protein and phosphorylated tau protein 181 (p-Tau), apolipoprotein E (APOE), soluble TREM2 protein, neurofilament light chain and glial fibrillary protein (GFAP) will be determined. | Diagnostic test | Alzheimer´s disease spectrum, corticobasal syndrome due to probable 4 repeat taupathy, subjective congnitive decline |
| positron emission tomographyAlso: PETAccording to an established and standardized protocol, PET scans are performed with the TSPO receptor ligand [18F]-GE-180, [18F]flutemetamol for assessment of fibrillar Aβ 162 accumulation and the Tau ligand [18F]-PI-2620. In brief, [18F]GE-180 TSPO PET images (mean dose: 177 ± 17 MBq) with an emission window of 60-80 min after injection will be acquired to measure the activation of glial cells. [18F]Flutemetamol Aβ PET images (average dose: 182 ± 11 MBq) are acquired with an emission window of 90-110 min after injection to assess fibrillar Aβ accumulation. Dynamic [18F]PI-2620 tau PET (average dose: 186 ± 14 MBq) with an emission window of 0-60 minutes after injection are performed for quantification of tau aggregation. Static images of the late phase (20-40 min) are reconstructed. These images are used for further processing and analysis. | Diagnostic test | Alzheimer´s disease spectrum, corticobasal syndrome due to probable 4 repeat taupathy, subjective congnitive decline |
| neuropsychological testTrained psychologists at the Memory Clinic of the LMU Hospital administered the CDR, CERAD-NB and Mini-Mental State Examination (MMSE). The CERAD-NB battery was used to generate a total score for the six subscales: semantic fluency (animals/60 s), modified Boston naming test, lexical items, construction practice, lexical items retrieval, and lexical items discrimination, with higher scores indicating better performance. | Diagnostic test | Alzheimer´s disease spectrum, corticobasal syndrome due to probable 4 repeat taupathy, subjective congnitive decline |
Primary outcome
association of cerebral connectivity with microglia activation patterns
Time frame: until 06/2024
association between functional/structural connectivity and TSPO SUVR
Individual regional associations between Aβ-, tau- and neurodegeneration with microglial activation
Time frame: until 06/2024
association of regional amyloid and tau with microglial activation (measured by TSPO-PET)
validation of blood-based biomarkers in the differentiation of AD, SCI and CBS cases
Time frame: until 06/2024
comparison of AD-related biomarkers (pTau181, Abeta1-42/1-40), plasma apolipoprotein E and inflammatory biomarkers (GFAP, NfL)
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 4 Jul 2025.
- Derived from this study: PubMed 42875788Ochsner M, Brendel M, Franzmeier N, Trappmann L, Zaganjori M, Ersoezlue E, Kurz C, Haeckert J, Utecht J, Schirge PM, Papazov B, Pogarell O, Janowitz D, Buerger K, Ewers M, Palleis C, Weidinger E, Biechele G, Schuster S, Finze A, Eckenweber F, Rupprecht R, Rominger A, Goldhardt O, Grimmer T, Keeser D, Stoecklein S, Dietrich O, Bartenstein P, Levin J, Hoglinger G, Perneczky R, Rauchmann BS. Microglial dynamics associate with the spatial pattern of tau deposition in early Alzheimer's disease. Alzheimers Res Ther. 2026 Oct 12;18(1):232. doi: 10.1186/s13195-026-02230-1.
- Individual participant dataSharing planned: Undecided
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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.
The record lists no contact. Use the official record to reach the sponsor.
Questions about this trial
What is this clinical trial studying?
An observational study of Alzheimer Disease and Corticobasal Syndrome, run by Ludwig-Maximilians - University of Munich.
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 14 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 4 Jul 2025. Status can change between updates, so confirm with the study contact before making plans.
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?
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?
association of cerebral connectivity with microglia activation patterns (time frame: until 06/2024). The study lists 3 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 NCT06224920, which also lists 1 linked publication.
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 4 Jul 2025; AzTrials last refreshed its copy on 7 Nov 2026.