Cognitive ImpairmentADONISNCT06321588
Autoimmune Dementia: Predictors of Neuronal Synaptic Antibodies in Patients With New-ONset Cognitive Impairment
An observational study of Cognitive Impairment and Dementia, run by Azienda Usl di Bologna at 3 sites in Italy.
Trial summary
The goal of this observational study is to investigate the frequency and the possible pathogenic role of neuronal synaptic antibodies (NSAb) in patients with cognitive impairment (CI). The main questions it aims to answer are: 1. Read more about this study
- Who is it for?
- Ages 40 to 90 years
- Conditions the study is for
- Cognitive Impairment, Dementia
- How many people
- 300 participants
- Where
- 3 sitesItaly
- Study dates
- 10 May 2023to 30 Jun 2026
- Phase
- Observational
- 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 40 to 90 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: patients with a diagnosis of new-onset neurocognitive disorders (major and minor)
Who may be able to join
- both sexes
- adult (aged between 40 and 90 years)
- patients with a diagnosis of new-onset neurocognitive disorders (major and minor), as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria, with onset within the previous 24 months
Who cannot join
- presence of a history of seizures within 4 weeks from onset.
Trial locations and contacts
3 sites in 1 country. Contact the study team or a site near you to ask about taking part.
Italy3 sites, 3 recruiting
- Recruiting
IRCCS Istituto delle Scienze Neurologiche di Bologna
Bologna, Bologna, 40139
Maria Pia Giannoccaro, Dr., 0514966117, mariapia.giannoccaro@ausl.bologna.it
- Recruiting
Istituto Auxologico Italiano IRCCS
Milan, Milano, 20095
Federico Verde, Dr., +3902619112247, f.verde@auxologico.it
- Recruiting
Fondazione IRCCS Istituto Neurologico Carlo Besta
Milan, Milano, 20133
Chiara Maria Giulia De Luca, Dr., +390223942498, chiara.deluca@istituto-besta.it
About this study
Official title: Autoimmune Dementia: Predictors of Neuronal Synaptic Antibodies in Patients With New-ONset Cognitive Impairment and Their Relevance in Non-encephalitic formS: The ADONIS Study
The goal of this observational study is to investigate the frequency and the possible pathogenic role of neuronal synaptic antibodies (NSAb) in patients with cognitive impairment (CI). The main questions it aims to answer are:
- the frequency and associated features of NSAb in patients with CI and the usefulness of a clinical score in improving autoimmune dementia (AID) diagnosis;
- the clinical significance of NSAb in patients with CI not fulfilling the autoimmune encephalitis (AE) criteria and serum NSAb (NSAb-pos-CI);
- the impact of blood-brain-barrier (BBB) dysfunction on their pathogenicity.
Read the detailed description
AE can mimic dementia and, contrarily to neurodegenerative dementia syndromes, affected patients can improve with timely immunotherapies. Consensus-based diagnostic criteria for AE help to select patients for antibody testing. However, encephalitis signs can be absent, particularly in the elderly, and AE can present with slowly progressing CI mimicking classical neurodegenerative diseases, misleading the diagnostic process. Data on the prevalence of NSAb and AE in unselected patients with CI are sparse and mostly affected by retrospective design, small cohorts, and antibody assay shortcomings. There is an urgent need to define the frequency of NSAb and AE in CI patients and elucidate the associated clinical, laboratory and imaging features. Filling these gaps is the first aim of this project. This will allow the early identification and the best management of patients with AID. On the other hand, a proportion of CI patients have NSAb and do not fit the AE criteria (NSAb-pos-CI).
These NSAb are often in the serum, and not in the Cerebrospinal Fluid (CSF), or belong to the Immunoglobulin A/M (Ig A/M) subclasses, as opposite to the AE-associated Immunoglobulin G (IgG) subclass, thus triggering questions about their clinical and therapeutic implications. As NSAb can be found at low titers in the serum of healthy controls, a hypothesis explaining their pathogenicity relies on dysfunctions of the BBB, in a context of indolent inflammation, that might allow the antibodies to reach the Central Nervous System (CNS). Alternatively, NSAb may not be directly pathogenic and could even be secondary to an ongoing neurodegenerative process. However, even in this context, known and unknown NSAb, could still contribute to the clinical phenotype, modulating the disease progression or the presence of additional clinical features (i.e. psychiatric symptoms). Understanding if these serum NSAb, along with other factors such as inflammation and BBB alterations, have a role in modifying the disease trajectory, i.e. accelerating the neurodegeneration and CI progression, is the other main goal. This project will represent a chance to clarify the role of NSAb in NSAb-pos-CI and potentially help to identify a subgroup of patients with specific phenotypes, who could benefit from immunotherapies. The identification of such patients will allow their best clinical management.
- Conditions
- Cognitive Impairment, Dementia
- Medical subject headings
- Cognitive Dysfunction, Dementia
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| retrospective cohort | patients with a diagnosis of new-onset neurocognitive disorders (major and minor) with onset within the previous 24 months | |
| prospective cohort | patients with a diagnosis of new-onset neurocognitive disorders (major and minor) with onset within the previous 24 months |
What is being measured
The primary outcome is the main question the study is designed to answer.
frequency of antibodies against neuronal antigens
NSAb frequency will be calculated by dividing the number of patients with NSAb with the total number of patients
Measured: at baseline
frequency of antibodies against neuronal antigens
NSAb frequency will be calculated by dividing the number of patients with NSAb with the total number of patients
Measured: 12 months (54 weeks)
creation of a score that predicts the presence of NSAb
Based on logistic regression models including the clinical, imaging and biomarkers data. The minimum and maximum score is to be defined on the bases of the analyses of the clinical data at 24 months milestone.An higher score is expected to be associated with the antibody presence.
Measured: 24 months (108 weeks)
Secondary outcomes (8)
changes of neurodegeneration biomarkers
comparison of blood biomarkers from baseline to one year follow up in seropositive versus seronegative patients. The blood biomarkers are: phosphorylated tau protein 181 (p-tau 181) (pg/mL), Neurofilament Light chain (NfL) (pg/mL), Glial Fibrillary Acidic Protein (GFAP) (pg/mL).
Measured: at baseline
changes of neurodegeneration biomarkers
comparison of blood biomarkers from baseline to one year follow up in seropositive versus seronegative patients. The blood biomarkers are: phosphorylated tau protein 181 (p-tau 181) (pg/mL), Neurofilament Light chain (NfL) (pg/mL), Glial Fibrillary Acidic Protein (GFAP) (pg/mL).
Measured: 1 year (54 weeks)
changes of neuroanatomy
comparison of Brain MRI from baseline to one year follow up in seropositive versus seronegative patients
Measured: at baseline
changes of neuroanatomy
comparison of Brain MRI from baseline to one year follow up in seropositive versus seronegative patients
Measured: 1 year (54 weeks)
changes of inflammatory biomarkers
comparison of inflammatory biomarkers from baseline to one year follow up in seropositive versus seronegative patients. The inflammatory biomarkers are: Interferon alpha (IFN alpha) (pg/mL), Interferon gamma (IFN gamma) (pg/mL), Interleukin-1 beta (IL-1 beta) (pg/mL), Interleukin-2 (IL-2) (pg/mL), Interleukin-4 (IL-4) (pg/mL), Interleukin-5 (IL-5) (pg/mL), Interleukin-6 (IL-6) (pg/mL), Interleukin-8 (IL-8) (pg/mL), Interleukin-17A (IL-17A) (pg/mL), Tumor necrosis factor alpha (TNF alpha) (pg/mL), Interferon gamma-induced protein 10 (IP-10) known as C-X-C motif chemokine 10(CXCL10) (pg/mL), Monocyte chemoattractant protein-1 (MCP-1) known as C-C motif chemokine ligand 2 (CCL2) (pg/mL).
Measured: at baseline
changes of inflammatory biomarkers
comparison of inflammatory biomarkers from baseline to one year follow up in seropositive versus seronegative patients. The inflammatory biomarkers are: Interferon alpha (IFN alpha) (pg/mL), Interferon gamma (IFN gamma) (pg/mL), Interleukin-1 beta (IL-1 beta) (pg/mL), Interleukin-2 (IL-2) (pg/mL), Interleukin-4 (IL-4) (pg/mL), Interleukin-5 (IL-5) (pg/mL), Interleukin-6 (IL-6) (pg/mL), Interleukin-8 (IL-8) (pg/mL), Interleukin-17A (IL-17A) (pg/mL), Tumor necrosis factor alpha (TNF alpha) (pg/mL), Interferon gamma-induced protein 10 (IP-10) known as C-X-C motif chemokine 10(CXCL10) (pg/mL), Monocyte chemoattractant protein-1 (MCP-1) known as C-C motif chemokine ligand 2 (CCL2) (pg/mL).
Measured: 1 year (54 weeks)
changes of brain blood barrier biomarkers
comparison of brain blood barrier biomarkers from baseline to one year follow up in seropositive versus seronegative patients. The biomarkers are: S100 calcium-binding protein B (S-100b) (pg/mL), Glial Fibrillary Acidic Protein (GFAP) (pg/mL).
Measured: at baseline
changes of brain blood barrier biomarkers
comparison of brain blood barrier biomarkers from baseline to one year follow up in seropositive versus seronegative patients. The biomarkers are: S100 calcium-binding protein B (S-100b) (pg/mL), Glial Fibrillary Acidic Protein (GFAP) (pg/mL).
Measured: 1 year (54 weeks)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Mar 2024
- Study start10 May 2023
- Primary completion30 Jun 2026 (estimated)
- Study completion30 Jun 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (12)Papers the sponsor has linked to this study.
- Other trials for Cognitive ImpairmentStudies 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
- Other
- Enrolment
- 300 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Azienda Usl di Bologna
- Sponsor type
- Other government
- Responsible party
- Sponsor
- Investigators
- Maria Pia Giannoccaro, Dr., Principal investigator, IRCCS Istituto delle Scienze Neurologiche di Bologna
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06321588
- Sponsor's protocol ID
- GR-2021-12373134
- Acronym
- ADONIS
- Status last verified
- Jul 2025
- First submitted
- 14 Mar 2024
- Last updated
- 11 Feb 2026
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Bartels F, Stronisch T, Farmer K, Rentzsch K, Kiecker F, Finke C. Neuronal autoantibodies associated with cognitive impairment in melanoma patients. Ann Oncol. 2019 May 1;30(5):823-829. doi: 10.1093/annonc/mdz083.
PubMed 30840061Brunkhorst R, Pfeilschifter W, Foerch C. Astroglial proteins as diagnostic markers of acute intracerebral hemorrhage-pathophysiological background and clinical findings. Transl Stroke Res. 2010 Dec;1(4):246-51. doi: 10.1007/s12975-010-0040-6. Epub 2010 Aug 28.
PubMed 24323552Castillo-Gomez E, Oliveira B, Tapken D, Bertrand S, Klein-Schmidt C, Pan H, Zafeiriou P, Steiner J, Jurek B, Trippe R, Pruss H, Zimmermann WH, Bertrand D, Ehrenreich H, Hollmann M. All naturally occurring autoantibodies against the NMDA receptor subunit NR1 have pathogenic potential irrespective of epitope and immunoglobulin class. Mol Psychiatry. 2017 Dec;22(12):1776-1784. doi: 10.1038/mp.2016.125. Epub 2016 Aug 9.
PubMed 27502473Constantinescu R, Krysl D, Bergquist F, Andren K, Malmestrom C, Asztely F, Axelsson M, Menachem EB, Blennow K, Rosengren L, Zetterberg H. Cerebrospinal fluid markers of neuronal and glial cell damage to monitor disease activity and predict long-term outcome in patients with autoimmune encephalitis. Eur J Neurol. 2016 Apr;23(4):796-806. doi: 10.1111/ene.12942. Epub 2016 Jan 29.
PubMed 26822123Dubey D, Kothapalli N, McKeon A, Flanagan EP, Lennon VA, Klein CJ, Britton JW, So E, Boeve BF, Tillema JM, Sadjadi R, Pittock SJ. Predictors of neural-specific autoantibodies and immunotherapy response in patients with cognitive dysfunction. J Neuroimmunol. 2018 Oct 15;323:62-72. doi: 10.1016/j.jneuroim.2018.07.009. Epub 2018 Jul 25.
PubMed 30196836Dubois B, Villain N, Frisoni GB, Rabinovici GD, Sabbagh M, Cappa S, Bejanin A, Bombois S, Epelbaum S, Teichmann M, Habert MO, Nordberg A, Blennow K, Galasko D, Stern Y, Rowe CC, Salloway S, Schneider LS, Cummings JL, Feldman HH. Clinical diagnosis of Alzheimer's disease: recommendations of the International Working Group. Lancet Neurol. 2021 Jun;20(6):484-496. doi: 10.1016/S1474-4422(21)00066-1. Epub 2021 Apr 29.
PubMed 33933186Flanagan EP, McKeon A, Lennon VA, Boeve BF, Trenerry MR, Tan KM, Drubach DA, Josephs KA, Britton JW, Mandrekar JN, Lowe V, Parisi JE, Pittock SJ. Autoimmune dementia: clinical course and predictors of immunotherapy response. Mayo Clin Proc. 2010 Oct;85(10):881-97. doi: 10.4065/mcp.2010.0326.
PubMed 20884824Giannoccaro MP, Cossins J, Sorland K, Fluge O, Vincent A. Searching for Serum Antibodies to Neuronal Proteins in Patients With Myalgic Encephalopathy/Chronic Fatigue Syndrome. Clin Ther. 2019 May;41(5):836-847. doi: 10.1016/j.clinthera.2019.04.001. Epub 2019 May 1.
PubMed 31053295Gibson LL, McKeever A, Cullen AE, Nicholson TR, Aarsland D, Zandi MS, Pollak TA. Neuronal surface autoantibodies in dementia: a systematic review and meta-analysis. J Neurol. 2021 Aug;268(8):2769-2779. doi: 10.1007/s00415-020-09825-0. Epub 2020 Apr 18.
PubMed 32306172Pollak TA, Vincent A, Iyegbe C, Coutinho E, Jacobson L, Rujescu D, Stone J, Jezequel J, Rogemond V, Jamain S, Groc L, David A, Egerton A, Kahn RS, Honnorat J, Dazzan P, Leboyer M, McGuire P. Relationship Between Serum NMDA Receptor Antibodies and Response to Antipsychotic Treatment in First-Episode Psychosis. Biol Psychiatry. 2021 Jul 1;90(1):9-15. doi: 10.1016/j.biopsych.2020.11.014. Epub 2020 Nov 24.
PubMed 33536130Wagner J, Witt JA, Helmstaedter C, Malter MP, Weber B, Elger CE. Automated volumetry of the mesiotemporal structures in antibody-associated limbic encephalitis. J Neurol Neurosurg Psychiatry. 2015 Jul;86(7):735-42. doi: 10.1136/jnnp-2014-307875. Epub 2014 Sep 2.
PubMed 25185210Yeshokumar AK, Gordon-Lipkin E, Arenivas A, Cohen J, Venkatesan A, Saylor D, Probasco JC. Neurobehavioral outcomes in autoimmune encephalitis. J Neuroimmunol. 2017 Nov 15;312:8-14. doi: 10.1016/j.jneuroim.2017.08.010. Epub 2017 Aug 31.
PubMed 28889962
Study at a glance
From the registry record, last updated by the sponsor on 11 Feb 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Autoimmune Dementia: Predictors of Neuronal Synaptic Antibodies in Patients With New-ONset Cognitive Impairment and Their Relevance in Non-encephalitic formS: The ADONIS Study
- ClinicalTrials.gov ID
- NCT06321588
- Acronym / sponsor ID
- ADONIS / GR-2021-12373134
- Conditions
- Cognitive Impairment, Dementia
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 300 participants (estimated)
- Lead sponsor
- Azienda Usl di BolognaOther government
- Study start
- 10 May 2023 (actual)
- Primary completion
- 30 Jun 2026 (estimated)
- Study completion
- 30 Jun 2026 (estimated)
- First posted
- 20 Mar 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The goal of this observational study is to investigate the frequency and the possible pathogenic role of neuronal synaptic antibodies (NSAb) in patients with cognitive impairment (CI). The main questions it aims to answer are:
- the frequency and associated features of NSAb in patients with CI and the usefulness of a clinical score in improving autoimmune dementia (AID) diagnosis;
- the clinical significance of NSAb in patients with CI not fulfilling the autoimmune encephalitis (AE) criteria and serum NSAb (NSAb-pos-CI);
- the impact of blood-brain-barrier (BBB) dysfunction on their pathogenicity.
Detailed description
AE can mimic dementia and, contrarily to neurodegenerative dementia syndromes, affected patients can improve with timely immunotherapies. Consensus-based diagnostic criteria for AE help to select patients for antibody testing. However, encephalitis signs can be absent, particularly in the elderly, and AE can present with slowly progressing CI mimicking classical neurodegenerative diseases, misleading the diagnostic process. Data on the prevalence of NSAb and AE in unselected patients with CI are sparse and mostly affected by retrospective design, small cohorts, and antibody assay shortcomings. There is an urgent need to define the frequency of NSAb and AE in CI patients and elucidate the associated clinical, laboratory and imaging features. Filling these gaps is the first aim of this project. This will allow the early identification and the best management of patients with AID. On the other hand, a proportion of CI patients have NSAb and do not fit the AE criteria (NSAb-pos-CI).
These NSAb are often in the serum, and not in the Cerebrospinal Fluid (CSF), or belong to the Immunoglobulin A/M (Ig A/M) subclasses, as opposite to the AE-associated Immunoglobulin G (IgG) subclass, thus triggering questions about their clinical and therapeutic implications. As NSAb can be found at low titers in the serum of healthy controls, a hypothesis explaining their pathogenicity relies on dysfunctions of the BBB, in a context of indolent inflammation, that might allow the antibodies to reach the Central Nervous System (CNS). Alternatively, NSAb may not be directly pathogenic and could even be secondary to an ongoing neurodegenerative process. However, even in this context, known and unknown NSAb, could still contribute to the clinical phenotype, modulating the disease progression or the presence of additional clinical features (i.e. psychiatric symptoms). Understanding if these serum NSAb, along with other factors such as inflammation and BBB alterations, have a role in modifying the disease trajectory, i.e. accelerating the neurodegeneration and CI progression, is the other main goal. This project will represent a chance to clarify the role of NSAb in NSAb-pos-CI and potentially help to identify a subgroup of patients with specific phenotypes, who could benefit from immunotherapies. The identification of such patients will allow their best clinical management.
Study design
- Observational model
- Cohort
- Time perspective
- Other
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| retrospective cohort | – | –patients with a diagnosis of new-onset neurocognitive disorders (major and minor) with onset within the previous 24 months |
| prospective cohort | – | –patients with a diagnosis of new-onset neurocognitive disorders (major and minor) with onset within the previous 24 months |
Who may qualify
- Ages
- 40 to 90 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- patients with a diagnosis of new-onset neurocognitive disorders (major and minor)
Key inclusion criteria (3 listed)
- both sexes
- adult (aged between 40 and 90 years)
- patients with a diagnosis of new-onset neurocognitive disorders (major and minor), as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria, with onset within the previous 24 months
Key exclusion criteria (1 listed)
- presence of a history of seizures within 4 weeks from onset.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
frequency of antibodies against neuronal antigens
Time frame: at baseline
NSAb frequency will be calculated by dividing the number of patients with NSAb with the total number of patients
frequency of antibodies against neuronal antigens
Time frame: 12 months (54 weeks)
NSAb frequency will be calculated by dividing the number of patients with NSAb with the total number of patients
creation of a score that predicts the presence of NSAb
Time frame: 24 months (108 weeks)
Based on logistic regression models including the clinical, imaging and biomarkers data. The minimum and maximum score is to be defined on the bases of the analyses of the clinical data at 24 months milestone.An higher score is expected to be associated with the antibody presence.
8 secondary outcomes
changes of neurodegeneration biomarkers
Time frame: at baseline
changes of neurodegeneration biomarkers
Time frame: 1 year (54 weeks)
changes of neuroanatomy
Time frame: at baseline
changes of neuroanatomy
Time frame: 1 year (54 weeks)
changes of inflammatory biomarkers
Time frame: at baseline
changes of inflammatory biomarkers
Time frame: 1 year (54 weeks)
changes of brain blood barrier biomarkers
Time frame: at baseline
changes of brain blood barrier biomarkers
Time frame: 1 year (54 weeks)
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 11 Feb 2026.
- Results publication: PubMed 30840061Bartels F, Stronisch T, Farmer K, Rentzsch K, Kiecker F, Finke C. Neuronal autoantibodies associated with cognitive impairment in melanoma patients. Ann Oncol. 2019 May 1;30(5):823-829. doi: 10.1093/annonc/mdz083.
- Results publication: PubMed 24323552Brunkhorst R, Pfeilschifter W, Foerch C. Astroglial proteins as diagnostic markers of acute intracerebral hemorrhage-pathophysiological background and clinical findings. Transl Stroke Res. 2010 Dec;1(4):246-51. doi: 10.1007/s12975-010-0040-6. Epub 2010 Aug 28.
- Results publication: PubMed 27502473Castillo-Gomez E, Oliveira B, Tapken D, Bertrand S, Klein-Schmidt C, Pan H, Zafeiriou P, Steiner J, Jurek B, Trippe R, Pruss H, Zimmermann WH, Bertrand D, Ehrenreich H, Hollmann M. All naturally occurring autoantibodies against the NMDA receptor subunit NR1 have pathogenic potential irrespective of epitope and immunoglobulin class. Mol Psychiatry. 2017 Dec;22(12):1776-1784. doi: 10.1038/mp.2016.125. Epub 2016 Aug 9.
- Results publication: PubMed 26822123Constantinescu R, Krysl D, Bergquist F, Andren K, Malmestrom C, Asztely F, Axelsson M, Menachem EB, Blennow K, Rosengren L, Zetterberg H. Cerebrospinal fluid markers of neuronal and glial cell damage to monitor disease activity and predict long-term outcome in patients with autoimmune encephalitis. Eur J Neurol. 2016 Apr;23(4):796-806. doi: 10.1111/ene.12942. Epub 2016 Jan 29.
- Results publication: PubMed 30196836Dubey D, Kothapalli N, McKeon A, Flanagan EP, Lennon VA, Klein CJ, Britton JW, So E, Boeve BF, Tillema JM, Sadjadi R, Pittock SJ. Predictors of neural-specific autoantibodies and immunotherapy response in patients with cognitive dysfunction. J Neuroimmunol. 2018 Oct 15;323:62-72. doi: 10.1016/j.jneuroim.2018.07.009. Epub 2018 Jul 25.
- Results publication: PubMed 33933186Dubois B, Villain N, Frisoni GB, Rabinovici GD, Sabbagh M, Cappa S, Bejanin A, Bombois S, Epelbaum S, Teichmann M, Habert MO, Nordberg A, Blennow K, Galasko D, Stern Y, Rowe CC, Salloway S, Schneider LS, Cummings JL, Feldman HH. Clinical diagnosis of Alzheimer's disease: recommendations of the International Working Group. Lancet Neurol. 2021 Jun;20(6):484-496. doi: 10.1016/S1474-4422(21)00066-1. Epub 2021 Apr 29.
- Results publication: PubMed 20884824Flanagan EP, McKeon A, Lennon VA, Boeve BF, Trenerry MR, Tan KM, Drubach DA, Josephs KA, Britton JW, Mandrekar JN, Lowe V, Parisi JE, Pittock SJ. Autoimmune dementia: clinical course and predictors of immunotherapy response. Mayo Clin Proc. 2010 Oct;85(10):881-97. doi: 10.4065/mcp.2010.0326.
- Results publication: PubMed 31053295Giannoccaro MP, Cossins J, Sorland K, Fluge O, Vincent A. Searching for Serum Antibodies to Neuronal Proteins in Patients With Myalgic Encephalopathy/Chronic Fatigue Syndrome. Clin Ther. 2019 May;41(5):836-847. doi: 10.1016/j.clinthera.2019.04.001. Epub 2019 May 1.
- Results publication: PubMed 32306172Gibson LL, McKeever A, Cullen AE, Nicholson TR, Aarsland D, Zandi MS, Pollak TA. Neuronal surface autoantibodies in dementia: a systematic review and meta-analysis. J Neurol. 2021 Aug;268(8):2769-2779. doi: 10.1007/s00415-020-09825-0. Epub 2020 Apr 18.
- Results publication: PubMed 33536130Pollak TA, Vincent A, Iyegbe C, Coutinho E, Jacobson L, Rujescu D, Stone J, Jezequel J, Rogemond V, Jamain S, Groc L, David A, Egerton A, Kahn RS, Honnorat J, Dazzan P, Leboyer M, McGuire P. Relationship Between Serum NMDA Receptor Antibodies and Response to Antipsychotic Treatment in First-Episode Psychosis. Biol Psychiatry. 2021 Jul 1;90(1):9-15. doi: 10.1016/j.biopsych.2020.11.014. Epub 2020 Nov 24.
- Results publication: PubMed 25185210Wagner J, Witt JA, Helmstaedter C, Malter MP, Weber B, Elger CE. Automated volumetry of the mesiotemporal structures in antibody-associated limbic encephalitis. J Neurol Neurosurg Psychiatry. 2015 Jul;86(7):735-42. doi: 10.1136/jnnp-2014-307875. Epub 2014 Sep 2.
- Results publication: PubMed 28889962Yeshokumar AK, Gordon-Lipkin E, Arenivas A, Cohen J, Venkatesan A, Saylor D, Probasco JC. Neurobehavioral outcomes in autoimmune encephalitis. J Neuroimmunol. 2017 Nov 15;312:8-14. doi: 10.1016/j.jneuroim.2017.08.010. Epub 2017 Aug 31.
- 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.
Maria Pia Giannoccaro, Dr. principal investigator
IRCCS Istituto delle Scienze Neurologiche di Bologna
3 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Cognitive Impairment and Dementia, run by Azienda Usl di Bologna at 3 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 3 inclusion and 1 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: looking for participants now, as of the sponsor's last update on 11 Feb 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 3 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 Maria Pia Giannoccaro, Dr. (+390514966112, mariapia.giannoccaro@ausl.bologna.it), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
frequency of antibodies against neuronal antigens (time frame: at baseline). 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 NCT06321588, which also lists 12 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 11 Feb 2026.