Parkinson's Disease (PD)SYNchronPDNCT07474779
Understanding Alpha-Synuclein Spread in Parkinson's Disease Through Blood Biomarkers and Neuroimaging
A study testing brain imaging, blood draw and Skin biopsy in people with Parkinson's Disease (PD) and GBA1 Parkinson Disease, run by University of Pavia at 2 sites in Italy.
Trial summary
The project aims to investigate how abnormal accumulation of alpha synuclein and its interaction with tau influence brain function across the Parkinson's disease (PD) spectrum, with particular focus on individuals carrying GBA1 mutations. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Parkinson's Disease (PD), GBA1 Parkinson Disease, REM Sleep Behavior Disorder (iRBD)
- What is being tested?
- brain imaging, blood draw and Skin biopsy
- Type of treatment
- Surgery or procedure
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 160 participants
- Where
- 2 sitesItaly
- Study dates
- 11 May 2026to Feb 2029
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
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 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
None listed.
Who cannot join
- Diagnosis of atypical and/or secondary parkinsonism;
- Diagnosis of dementia according to DSM-5 criteria;
- Presence of other neurological disorders and/or essential tremor;
- Presence of systemic inflammatory or infectious diseases, autoimmune diseases, or malignant tumors at the time of enrollment.
- Inclusion criteria for unaffected subjects (GBA-nonPD and nonGBA-nonPD):
- Age > 18 Years;
Show all 25Show fewer
- Ability to understand and voluntarily sign informed consent and to comply with study procedures;
- No diagnosis of PD or other neurological disorders;
- Presence of a heterozygous GBA mutation for the GBA-nonPD group and absence of such mutation for control subjects (nonGBA-nonPD);
- Absence of mutations in other known genes associated with PD susceptibility.
- Exclusion criteria for unaffected subjects (GBA-nonPD and nonGBA-nonPD):
- Presence of systemic inflammatory or infectious diseases, autoimmune diseases, or malignant tumors at the time of enrollment;
- Diagnosis of atypical and/or secondary parkinsonism;
- Diagnosis of dementia according to DSM-5 criteria.
- Inclusion criteria for subjects with idiopathic REM Sleep Behavior Disorder (GBA-iRBD and nonGBA-iRBD):
- Diagnosis of idiopathic REM Sleep Behavior Disorder according to ICSD-3;
- Age > 18 Years;
- Ability to understand and voluntarily sign informed consent and to comply with study procedures;
- No diagnosis of PD or other neurological disorders;
- Presence of a heterozygous GBA mutation for the GBA-iRBD group and absence of such mutation for the nonGBA-iRBD group;
- Absence of mutations in other known genes associated with PD susceptibility.
- Exclusion criteria for subjects with idiopathic REM Sleep Behavior Disorder (GBA-iRBD and nonGBA-iRBD):
- Presence of systemic inflammatory or infectious diseases, autoimmune diseases, or malignant tumors at the time of enrollment;
- Diagnosis of atypical and/or secondary parkinsonism;
- Diagnosis of dementia according to DSM-5 criteria.
Trial locations and contacts
2 sites in 1 country. Contact the study team or a site near you to ask about taking part.
Italy2 sites
Neurological Institute Foundation Casimiro Mondino
Pavia, PV, 27100
Micol Avenali, MD, PhD, 0382380390 ext. +39, micol.avenali@mondino.it
University of Pavia
Pavia, PV, 27100
Silvia P Caminiti, PhD, 0382380390 ext. +39, silviapaola.caminiti@unipv.it
About this study
Official title: From Genes to Virtual Brain: Defining the Pathogenic Mechanisms Promoting Alfa-synuclein Seeding and Spreading in Parkinson's Disease.
The project aims to investigate how abnormal accumulation of alpha synuclein and its interaction with tau influence brain function across the Parkinson's disease (PD) spectrum, with particular focus on individuals carrying GBA1 mutations. This interventional, monocentric, cross sectional study includes patients with PD, individuals with idiopathic REM sleep behavior disorder, and participants without PD.
All enrolled subjects will undergo clinical and neuropsychological assessments, blood based biomarker analyses related to neurodegeneration, synaptic and mitochondrial function, and multimodal brain MRI to evaluate brain structure, white matter integrity, and functional connectivity.
Read more
The study aims to:
- characterize the relationship between alpha synuclein/tau pathology and synaptic mitochondrial dysfunction;
- identify biomarker and connectivity signatures across disease stages and genetic backgrounds;
- integrate preclinical, clinical, biological, and imaging data to support the development of mechanistic models of alpha synuclein propagation.
In parallel, preclinical studies in GBA PD mouse models and wild type mice will be used to investigate how changes in PD-related pathology (alpha-synuclein and tau) relates to behavior, brain imaging alterations and mitochondrial, axonal and synaptic damage. Animal model will also aid the validation of a new PET tracer that targets alpha synuclein (i.e., [¹⁸F]Syntacasyn).
Together, human and preclinical studies are designed to provide a translational framework integrating molecular changes with brain network alterations and clinical heterogeneity in PD.
Read the detailed description
Parkinson's disease (PD) is characterized by pathological aggregation and propagation of alpha synuclein, leading to synaptic and mitochondrial dysfunction. Heterozygous mutations in the GBA1 gene represent the strongest genetic risk factor for PD and are associated with earlier onset, faster progression, and increased burden of misfolded alpha synuclein. Experimental evidence suggests that alpha synuclein toxicity may be amplified by its interaction with tau, promoting synergistic neurodegenerative mechanisms; however, in vivo human data on these processes remain limited.
This study aims to define, through a personalized and multimodal approach, how alpha synuclein accumulation and its interaction with tau influence synaptic and mitochondrial dysfunction and brain connectivity across the PD spectrum, from periclinal stages to established disease, with particular focus on the impact of GBA1 mutations. The study includes patients with PD, individuals with idiopathic REM sleep behavior disorder (iRBD), and subjects without PD, both carriers and non carriers of GBA1 mutations.
All participants will undergo comprehensive clinical and neuropsychological assessments to characterize motor, non motor, and cognitive manifestations across disease stages. Blood samples will be collected to define a fluid biomarker profile, including alpha synuclein, tau, markers of synaptic integrity, mitochondrial function, and neurodegeneration. In addition, all participants will undergo multimodal brain MRI, including structural, diffusion weighted, and resting state functional sequences, to evaluate brain structure, white matter integrity, and functional connectivity.
In a subset of participants, a skin biopsy will be performed to generate patient specific induced pluripotent stem cell (hiPSC) derived dopaminergic neurons. These cellular models will be used to investigate neuronal and synaptic function in relation to individual biomarker profiles and genetic background. In parallel, preclinical studies will be conducted in GBA-PD mouse models and wild type mice injected with saline, alpha synuclein or combined alpha synuclein/tau fibrils. Mice will undergo behavioral, in vivo MRI and PET imaging and post mortem assessment of synaptic, axonal and mitochondrial pathology. In addition, a novel alpha synuclein PET tracer, [¹⁸F]Syntacasyn, will undergo preclinical validation.
Multimodal human and animal data will be integrated using advanced statistical and computational approaches to identify vulnerable network hubs and generate subject specific "virtual brain" models of alpha synuclein pathology propagation.
The study is designed to provide a translational framework linking molecular pathology, brain network dysfunction and clinical heterogeneity in PD, supporting biomarker development and precision medicine strategies across the prodromal and clinical spectrum, with particular focus on genetically defined populations such as GBA1 mutation carriers.
- Being tested
- brain imaging, blood draw, Skin biopsy
- Keywords
- GBA1 carriers, Brain Connectivity, Virtual Brain, Extracellular vesicles, Mitochondrial Dysfunction, Mice Models, Translational Science
- Medical subject headings
- Parkinson Disease, REM Sleep Behavior Disorder, Mitochondrial Diseases
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
brain imagingDiagnostic test
Participants will undergo a single brain MRI acquisition, including structural, diffusion-weighted, and resting-state functional MRI.
blood drawProcedure or surgery
Collection of a venous blood sample for biochemical analyses
Skin biopsyProcedure or surgery
A small punch skin biopsy (about 3-4 mm) will be performed under local anesthesia on a small sample of enrolled participants (n=10)
| Study group | Role | What they receive |
|---|---|---|
| GBA-PD | Experimental | Diagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy Receives: Diagnostic Test: brain imaging; Procedure: blood draw; Procedure: Skin biopsy |
| nonGBA-PD | Experimental | Diagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy Receives: Diagnostic Test: brain imaging; Procedure: blood draw; Procedure: Skin biopsy |
| nonGBA-iRBD | Experimental | Diagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy Receives: Diagnostic Test: brain imaging; Procedure: blood draw; Procedure: Skin biopsy |
| GBA-iRBD | Experimental | Diagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy Receives: Diagnostic Test: brain imaging; Procedure: blood draw; Procedure: Skin biopsy |
| GBA-nonPD | Experimental | Diagnostic Test: brain imaging Procedure/Surgery: blood draw Receives: Diagnostic Test: brain imaging; Procedure: blood draw |
| Healthy controls | Experimental | Diagnostic Test: brain imaging Procedure/Surgery: blood draw Receives: Diagnostic Test: brain imaging; Procedure: blood draw |
What is being measured
The primary outcome is the main question the study is designed to answer.
Concentration of alpha-synuclein levels in plasma
Quantification of levels of Total alpha-synuclein and 129P-alpha-synuclein (pg/ml) in neuronal-derived extracellular vesicles using ultrasensitive immunoassays (NULISA).
Measured: Baseline visit
Concentration of tau levels in plasma
Quantification of total-tau and p-tau18 (pg/ml) in neuronal-derived extracellular vesicles using ultrasensitive immunoassays (NULISA).
Measured: Baseline visit
Investigation of glucocerebrosidase activity in Peripheral Blood Mononuclear Cells
Glucocereborsidase activity will be estimated in Peripheral Blood Mononuclear Cells usign a flourimetry assay
Measured: Baseline visit
Secondary outcomes (6)
Assessment of mitochondrial damage in plasma
Quantification of circulating cell-free mitochondrial DNA (cf-mtDNA) in plasma, including total concentration and deletion fraction.
Measured: Baseline visit
Plasma synaptic protein concentration
Quantification of SNAP25, STX1A, and VAMP2 in neuronal-derived extracellular vesiclesusing ultrasensitive immunoassay (NULISA)
Measured: Baseline visit
Brain network connectivity in Parkinson's disease
We will exctract structural and functional connectivity information form MRI, resting-state functional MRI and diffusion weighted MRI. Connectivity metrics will include global and nodal efficiency, participation coefficient and indexes of withe matter tract integrity.
Measured: Baseline visit
In vitro neuronal responses in hiPSC-derived dopaminergic neurons
In vitro neuronal responses will be assessed in dopaminergic neurons derived from human induced pluripotent stem cells (hiPSC), following exposure to alpha-synuclein and alpha-synuclein+tau.
Measured: Baseline visit
Estimation of synaptic damage in Neuronal extracellular vesicle
Neurogranin concentration (pg/ml) will be quantified in neuronal-derived extracellular vesicles
Measured: Baseline visit
Concentration of neurofilament light chain
Neurofilament light chain concentration (pg/ml) will be quantified in plasma using Ella™.
Measured: Baseline visit
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Mar 2026
- Study start11 May 2026 (estimated)
- Primary completionDec 2028 (estimated)
- Study completionFeb 2029 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (6)Papers the sponsor has linked to this study.
- Other trials for Parkinson's Disease (PD)Studies 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
- Non-randomised
- Intervention model
- Parallel groups
- Model description
- Participants are enrolled into distinct groups based on clinical status and genetic background. Participants undergo the following procedures: neurological and neuropsychological assessment, collection of biological samples, and brain MRI. Group allocation is determined by predefined inclusion/exclusion criteria.
- Masking
- None (open label)
- Enrolment
- 160 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Pavia
- Sponsor type
- University, hospital or other
- Collaborators
- Pavia IRCCS Mondino di Pavia
- Responsible party
- Principal investigator, Silvia Paola Caminiti, University of Pavia
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07474779
- Sponsor's protocol ID
- FIS-2023-00979
- Acronym
- SYNchronPD
- Status last verified
- Mar 2026
- First submitted
- 6 Mar 2026
- Last updated
- 1 May 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Baden P, Perez MJ, Raji H, Bertoli F, Kalb S, Illescas M, Spanos F, Giuliano C, Calogero AM, Oldrati M, Hebestreit H, Cappelletti G, Brockmann K, Gasser T, Schapira AHV, Ugalde C, Deleidi M. Glucocerebrosidase is imported into mitochondria and preserves complex I integrity and energy metabolism. Nat Commun. 2023 Apr 6;14(1):1930. doi: 10.1038/s41467-023-37454-4.
PubMed 37024507Neumann J, Bras J, Deas E, O'Sullivan SS, Parkkinen L, Lachmann RH, Li A, Holton J, Guerreiro R, Paudel R, Segarane B, Singleton A, Lees A, Hardy J, Houlden H, Revesz T, Wood NW. Glucocerebrosidase mutations in clinical and pathologically proven Parkinson's disease. Brain. 2009 Jul;132(Pt 7):1783-94. doi: 10.1093/brain/awp044. Epub 2009 Mar 13.
PubMed 19286695Vogel JW, Corriveau-Lecavalier N, Franzmeier N, Pereira JB, Brown JA, Maass A, Botha H, Seeley WW, Bassett DS, Jones DT, Ewers M. Connectome-based modelling of neurodegenerative diseases: towards precision medicine and mechanistic insight. Nat Rev Neurosci. 2023 Oct;24(10):620-639. doi: 10.1038/s41583-023-00731-8. Epub 2023 Aug 24.
PubMed 37620599Pan L, Li C, Meng L, Tian Y, He M, Yuan X, Zhang G, Zhang Z, Xiong J, Chen G, Zhang Z. Tau accelerates alpha-synuclein aggregation and spreading in Parkinson's disease. Brain. 2022 Oct 21;145(10):3454-3471. doi: 10.1093/brain/awac171.
PubMed 35552614Guo M, Wang J, Zhao Y, Feng Y, Han S, Dong Q, Cui M, Tieu K. Microglial exosomes facilitate alpha-synuclein transmission in Parkinson's disease. Brain. 2020 May 1;143(5):1476-1497. doi: 10.1093/brain/awaa090.
PubMed 32355963Recasens A, Dehay B. Alpha-synuclein spreading in Parkinson's disease. Front Neuroanat. 2014 Dec 18;8:159. doi: 10.3389/fnana.2014.00159. eCollection 2014.
PubMed 25565982
Study at a glance
From the registry record, last updated by the sponsor on 1 May 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- From Genes to Virtual Brain: Defining the Pathogenic Mechanisms Promoting Alfa-synuclein Seeding and Spreading in Parkinson's Disease.
- ClinicalTrials.gov ID
- NCT07474779
- Acronym / sponsor ID
- SYNchronPD / FIS-2023-00979
- Keywords
- GBA1 carriers, Brain Connectivity, Virtual Brain, Extracellular vesicles, Mitochondrial Dysfunction, Mice Models, Translational Science
- Study type
- Interventional
- Recruitment status
- Not yet recruiting
- Enrolment
- 160 participants (estimated)
- Lead sponsor
- University of PaviaUniversity, hospital or other
- Collaborators
- Pavia IRCCS Mondino di Pavia
- Study start
- 11 May 2026 (estimated)
- Primary completion
- Dec 2028 (estimated)
- Study completion
- Feb 2029 (estimated)
- First posted
- 16 Mar 2026 (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 project aims to investigate how abnormal accumulation of alpha synuclein and its interaction with tau influence brain function across the Parkinson's disease (PD) spectrum, with particular focus on individuals carrying GBA1 mutations. This interventional, monocentric, cross sectional study includes patients with PD, individuals with idiopathic REM sleep behavior disorder, and participants without PD.
All enrolled subjects will undergo clinical and neuropsychological assessments, blood based biomarker analyses related to neurodegeneration, synaptic and mitochondrial function, and multimodal brain MRI to evaluate brain structure, white matter integrity, and functional connectivity.
The study aims to:
- characterize the relationship between alpha synuclein/tau pathology and synaptic mitochondrial dysfunction;
- identify biomarker and connectivity signatures across disease stages and genetic backgrounds;
- integrate preclinical, clinical, biological, and imaging data to support the development of mechanistic models of alpha synuclein propagation.
In parallel, preclinical studies in GBA PD mouse models and wild type mice will be used to investigate how changes in PD-related pathology (alpha-synuclein and tau) relates to behavior, brain imaging alterations and mitochondrial, axonal and synaptic damage. Animal model will also aid the validation of a new PET tracer that targets alpha synuclein (i.e., [¹⁸F]Syntacasyn).
Together, human and preclinical studies are designed to provide a translational framework integrating molecular changes with brain network alterations and clinical heterogeneity in PD.
Detailed description
Parkinson's disease (PD) is characterized by pathological aggregation and propagation of alpha synuclein, leading to synaptic and mitochondrial dysfunction. Heterozygous mutations in the GBA1 gene represent the strongest genetic risk factor for PD and are associated with earlier onset, faster progression, and increased burden of misfolded alpha synuclein. Experimental evidence suggests that alpha synuclein toxicity may be amplified by its interaction with tau, promoting synergistic neurodegenerative mechanisms; however, in vivo human data on these processes remain limited.
This study aims to define, through a personalized and multimodal approach, how alpha synuclein accumulation and its interaction with tau influence synaptic and mitochondrial dysfunction and brain connectivity across the PD spectrum, from periclinal stages to established disease, with particular focus on the impact of GBA1 mutations. The study includes patients with PD, individuals with idiopathic REM sleep behavior disorder (iRBD), and subjects without PD, both carriers and non carriers of GBA1 mutations.
All participants will undergo comprehensive clinical and neuropsychological assessments to characterize motor, non motor, and cognitive manifestations across disease stages. Blood samples will be collected to define a fluid biomarker profile, including alpha synuclein, tau, markers of synaptic integrity, mitochondrial function, and neurodegeneration. In addition, all participants will undergo multimodal brain MRI, including structural, diffusion weighted, and resting state functional sequences, to evaluate brain structure, white matter integrity, and functional connectivity.
In a subset of participants, a skin biopsy will be performed to generate patient specific induced pluripotent stem cell (hiPSC) derived dopaminergic neurons. These cellular models will be used to investigate neuronal and synaptic function in relation to individual biomarker profiles and genetic background. In parallel, preclinical studies will be conducted in GBA-PD mouse models and wild type mice injected with saline, alpha synuclein or combined alpha synuclein/tau fibrils. Mice will undergo behavioral, in vivo MRI and PET imaging and post mortem assessment of synaptic, axonal and mitochondrial pathology. In addition, a novel alpha synuclein PET tracer, [¹⁸F]Syntacasyn, will undergo preclinical validation.
Multimodal human and animal data will be integrated using advanced statistical and computational approaches to identify vulnerable network hubs and generate subject specific "virtual brain" models of alpha synuclein pathology propagation.
The study is designed to provide a translational framework linking molecular pathology, brain network dysfunction and clinical heterogeneity in PD, supporting biomarker development and precision medicine strategies across the prodromal and clinical spectrum, with particular focus on genetically defined populations such as GBA1 mutation carriers.
Study design
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 6
- Model description
- Participants are enrolled into distinct groups based on clinical status and genetic background. Participants undergo the following procedures: neurological and neuropsychological assessment, collection of biological samples, and brain MRI. Group allocation is determined by predefined inclusion/exclusion criteria.
| Arm | Type | Receives |
|---|---|---|
| GBA-PD | Experimental | Diagnostic Test: brain imaging, Procedure: blood draw, Procedure: Skin biopsyDiagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy |
| nonGBA-PD | Experimental | Diagnostic Test: brain imaging, Procedure: blood draw, Procedure: Skin biopsyDiagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy |
| nonGBA-iRBD | Experimental | Diagnostic Test: brain imaging, Procedure: blood draw, Procedure: Skin biopsyDiagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy |
| GBA-iRBD | Experimental | Diagnostic Test: brain imaging, Procedure: blood draw, Procedure: Skin biopsyDiagnostic Test: brain imaging Procedure/Surgery: blood draw, skin biopsy |
| GBA-nonPD | Experimental | Diagnostic Test: brain imaging, Procedure: blood drawDiagnostic Test: brain imaging Procedure/Surgery: blood draw |
| Healthy controls | Experimental | Diagnostic Test: brain imaging, Procedure: blood drawDiagnostic Test: brain imaging Procedure/Surgery: blood draw |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (0 listed)
Key exclusion criteria (25 listed)
- Diagnosis of atypical and/or secondary parkinsonism;
- Diagnosis of dementia according to DSM-5 criteria;
- Presence of other neurological disorders and/or essential tremor;
- Presence of systemic inflammatory or infectious diseases, autoimmune diseases, or malignant tumors at the time of enrollment.
- Age > 18 Years;
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 |
|---|---|---|
| brain imagingParticipants will undergo a single brain MRI acquisition, including structural, diffusion-weighted, and resting-state functional MRI. | Diagnostic test | GBA-PD, GBA-iRBD, GBA-nonPD, Healthy controls, nonGBA-PD, nonGBA-iRBD |
| blood drawCollection of a venous blood sample for biochemical analyses | Procedure or surgery | GBA-PD, GBA-iRBD, GBA-nonPD, Healthy controls, nonGBA-PD, nonGBA-iRBD |
| Skin biopsyA small punch skin biopsy (about 3-4 mm) will be performed under local anesthesia on a small sample of enrolled participants (n=10) | Procedure or surgery | GBA-PD, GBA-iRBD, nonGBA-PD, nonGBA-iRBD |
Primary outcome
Concentration of alpha-synuclein levels in plasma
Time frame: Baseline visit
Quantification of levels of Total alpha-synuclein and 129P-alpha-synuclein (pg/ml) in neuronal-derived extracellular vesicles using ultrasensitive immunoassays (NULISA).
Concentration of tau levels in plasma
Time frame: Baseline visit
Quantification of total-tau and p-tau18 (pg/ml) in neuronal-derived extracellular vesicles using ultrasensitive immunoassays (NULISA).
Investigation of glucocerebrosidase activity in Peripheral Blood Mononuclear Cells
Time frame: Baseline visit
Glucocereborsidase activity will be estimated in Peripheral Blood Mononuclear Cells usign a flourimetry assay
6 secondary outcomes
Assessment of mitochondrial damage in plasma
Time frame: Baseline visit
Plasma synaptic protein concentration
Time frame: Baseline visit
Brain network connectivity in Parkinson's disease
Time frame: Baseline visit
In vitro neuronal responses in hiPSC-derived dopaminergic neurons
Time frame: Baseline visit
Estimation of synaptic damage in Neuronal extracellular vesicle
Time frame: Baseline visit
Concentration of neurofilament light chain
Time frame: Baseline visit
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 1 May 2026.
- Background: PubMed 37024507Baden P, Perez MJ, Raji H, Bertoli F, Kalb S, Illescas M, Spanos F, Giuliano C, Calogero AM, Oldrati M, Hebestreit H, Cappelletti G, Brockmann K, Gasser T, Schapira AHV, Ugalde C, Deleidi M. Glucocerebrosidase is imported into mitochondria and preserves complex I integrity and energy metabolism. Nat Commun. 2023 Apr 6;14(1):1930. doi: 10.1038/s41467-023-37454-4.
- Background: PubMed 19286695Neumann J, Bras J, Deas E, O'Sullivan SS, Parkkinen L, Lachmann RH, Li A, Holton J, Guerreiro R, Paudel R, Segarane B, Singleton A, Lees A, Hardy J, Houlden H, Revesz T, Wood NW. Glucocerebrosidase mutations in clinical and pathologically proven Parkinson's disease. Brain. 2009 Jul;132(Pt 7):1783-94. doi: 10.1093/brain/awp044. Epub 2009 Mar 13.
- Background: PubMed 37620599Vogel JW, Corriveau-Lecavalier N, Franzmeier N, Pereira JB, Brown JA, Maass A, Botha H, Seeley WW, Bassett DS, Jones DT, Ewers M. Connectome-based modelling of neurodegenerative diseases: towards precision medicine and mechanistic insight. Nat Rev Neurosci. 2023 Oct;24(10):620-639. doi: 10.1038/s41583-023-00731-8. Epub 2023 Aug 24.
- Background: PubMed 35552614Pan L, Li C, Meng L, Tian Y, He M, Yuan X, Zhang G, Zhang Z, Xiong J, Chen G, Zhang Z. Tau accelerates alpha-synuclein aggregation and spreading in Parkinson's disease. Brain. 2022 Oct 21;145(10):3454-3471. doi: 10.1093/brain/awac171.
- Background: PubMed 32355963Guo M, Wang J, Zhao Y, Feng Y, Han S, Dong Q, Cui M, Tieu K. Microglial exosomes facilitate alpha-synuclein transmission in Parkinson's disease. Brain. 2020 May 1;143(5):1476-1497. doi: 10.1093/brain/awaa090.
- Background: PubMed 25565982Recasens A, Dehay B. Alpha-synuclein spreading in Parkinson's disease. Front Neuroanat. 2014 Dec 18;8:159. doi: 10.3389/fnana.2014.00159. eCollection 2014.
- Individual participant dataSharing planned: No
Related trials for Parkinson's Disease (PD)
Active, not recruitingPhase 1/2
Clinical Safety and Efficacy of Umbilical Cord Mesenchymal Stromal Cells-derived Exosomes in Patients With Parkinson's Disease
Parkinson Disease (PD)
Active, not recruitingObservational study
Adaptive DBS to Offset STN Dysregulation During Exercise in PD
Parkinson Disease
Not yet recruiting
Evaluating the Effect of the Zeen Mobility Device on Clinical Practicality, Safety, and Impact (Via Assessments of Walking, Standing Tolerance, Balance, Endurance, Effort, and Participation in Daily Tasks) in an Outpatient Rehabilitation Setting for Individuals With Mobility Impairments.
Stroke, Parkinson's Disease (PD)
RecruitingObservational study
Striatal and Extra-Striatal Cholinergic Terminal Density in LRRK2-PD Mutation
Parkinson Disease
Not yet recruiting
Unilateral and Staged Bilateral Pallidothalamic Tractotomy Using Exablate MRgFUS in Advanced Parkinson's Disease.
Parkinson Disease
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.
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing brain imaging, blood draw and Skin biopsy in people with Parkinson's Disease (PD) and GBA1 Parkinson Disease, run by University of Pavia at 2 sites 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 0 inclusion and 25 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: opening soon, as of the sponsor's last update on 1 May 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites 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?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Silvia P Caminiti, PhD (0382380390 ext. 39, silviapaola.caminiti@unipv.it), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Concentration of alpha-synuclein levels in plasma (time frame: Baseline visit). 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 NCT07474779, which also lists 6 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 1 May 2026.