Alzheimer DiseasePESADNCT03617497
Prevalence of Epilepsy and Sleep Wake Disorders in Alzheimer Disease
A study testing scalp EEG and polysomnography and scalp EEG with foramen ovale electrodes with polysomnography in people with Alzheimer Disease and Alzheimer Dementia, run by Universitaire Ziekenhuizen KU Leuven at 1 site in Belgium.
Trial summary
Alzheimer disease is the most common of the neurodegenerative diseases. Epilepsy and sleep wake disorders are co-morbid conditions of Alzheimer disease. The investigators propose a prospective study using long-term EEG monitoring in combination with polysomnography to determine prevalence of epilepsy and sleep wake… Read more about this study
- Who is it for?
- Ages 55 to 85 yearsHealthy volunteers can take part
- Conditions the study is for
- Alzheimer Disease, Alzheimer Dementia, Epilepsy
- What is being tested?
- scalp EEG and polysomnography and scalp EEG with foramen ovale electrodes with polysomnography
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 78 participants
- Where
- 1 siteBelgium
- Study dates
- 1 Dec 2020to 30 Sep 2024
- 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 55 to 85 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Participant must be able to understand the nature of the study and has the opportunity to have any questions answered. The participant has voluntarily signed the independent Review Board (IRB)/independent Ethics Committee (IEC) approved Informed Consent, prior to the conduct of any study procedures. If the participant is not fully competent, full informed consent must be obtained from a representative and assent must be obtained from the participant.
- Participant who meets the National Institute on Aging and the Alzheimer's Association (NIA-AA) clinical criteria for mild cognitive impairment or probable Alzheimer Disease, and have:
- Clinical Dementia Rating (CDR)-Global Score of 0.5
- A Mini-Mental State Examination (MMSE) score of 22 to 30
- Repeatable Battery for the Assessment of Neuropsychological Status-Delayed Memory Index (RBANS-DMI) score of 85 or lower
- Participant has a positive amyloid Positron Emission Tomography (PET) scan.
- Participant has a Modified Hachinski Ischemic Scale (MHIS) score of ≤ 4.
- Participant has an identified, reliable, study partner (e.g., family member), who has frequent contact with the participant and who will provide information as to the participant's cognitive and functional abilities.
Who cannot join
- Participant has evidence of any other clinically significant neurological disorder other than Alzheimer disease, including but not limited to:
- Parkinson's disease
- vascular dementia
- significant cerebrovascular abnormalities
- frontal-temporal dementia
- Huntington's disease
Show all 28Show fewer
- normal pressure hydrocephalus
- brain tumor
- progressive supranuclear palsy
- seizure disorder
- subdural hematoma
- multiple sclerosis
- history of significant head trauma followed by persistent neurologic deficits
- known structural brain abnormalities
- obstructive sleep apnea syndrome treated with continuous positive airway pressure (CPAP)
- Participant has a screening MRI scan, interpreted by a radiologist with evidence of infection, infarction (including multiple lacunas in a critical memory structure), or other focal lesions.
- Participant has a history of or currently has schizophrenia, schizoaffective disorder or bipolar disorder according to Diagnostic and Statistical Manual of Mental Disorders (DSM)-V or International Classification of Diseases (ICD)-10 criteria.
- Participant has a current diagnosis or history of drug or alcohol abuse (by DSM-V criteria) within 24 months prior to the study.
- Participant has a history or evidence of a malignancy within the 2 years prior to the study.
- Participant has a known history of Human Immunodeficiency Virus (HIV) infection.
- Participant has had surgery under general anesthesia within 3 months prior to the study.
- Receipt of an investigational product within a time period equal to 5 half-lives, if known, or within 6 weeks (for small molecules) or 6 months (for monoclonal antibodies or other biologics) prior the study.
- Participant has any history of prior receipt of active immunotherapy directed against tau or amyloid.
- Participant is taking anti-epileptic drugs or benzodiazepines.
- Participant has an abnormally low vitamin B 12 (cobalamin), abnormal thyroxine (T4) or an abnormally high thyroid stimulating hormone (TSH) that is considered clinically significant by the investigator.
- Subject has any visual, auditory or other impairment that in the Investigator's opinion would preclude collection of outcome measures.
- In the opinion of the investigator, the subject has any clinically significant or uncontrolled medical or psychiatric illness, or has had an infection requiring medical intervention in the past 30 days.
- Subject has had a myocardial infarction, unstable angina, stroke, transient ischemic attack or required intervention for any of these conditions (e.g., coronary artery bypass graft, percutaneous coronary intervention via cardiac catheterization, thrombolytic therapy), within 6 months of the study.
Trial locations and contacts
1 site in 1 country.
Belgium1 site
University Hospitals Leuven, department of Neurology
Leuven, Vlaams-Brabant, 3000
About this study
Alzheimer disease is the most common of the neurodegenerative diseases. Epilepsy and sleep wake disorders are co-morbid conditions of Alzheimer disease. The investigators propose a prospective study using long-term EEG monitoring in combination with polysomnography to determine prevalence of epilepsy and sleep wake disorders in Alzheimer disease, and correlate these findings with clinical data, Alzheimer disease biomarkers and imaging studies (MRI and amyloid/tau-PET). In selected patients, the investigators will perform EEG studies with foramen ovale electrodes. The ultimate goal is to improve the outcome of patients with Alzheimer disease by early treatment of epilepsy and restoring sleep-wake disturbances.
Read the detailed description
Alzheimer disease is the most common of the neurodegenerative diseases. Epilepsy and sleep wake disorders are co-morbid conditions of Alzheimer disease, and there is evidence to suggest that the interactions are bidirectional. Neuronal activity promotes the production and secretion of amyloid β, which could actually drive pathogenesis early in the course of Alzheimer disease, and has been described in sleep wake disorders and epilepsy. Epileptic seizures in Alzheimer disease are often subtle, nocturnal and easily overlooked. We propose a prospective study using long-term EEG monitoring in combination with polysomnography to diagnose epilepsy and sleep wake disorders in Alzheimer disease, and correlate these findings with clinical data, Alzheimer disease biomarkers and imaging studies (MRI and amyloid/tau-PET). It is the hypothesis of the investigators that participants with Alzheimer disease and interictal spikes or specified sleep wake disorders (e.g., frequent nocturnal awakenings) during 48 hour scalp EEG and polysomnography are at risk for having hippocampal seizures, which are often clinically silent and not detected on scalp EEG. The investigators will invite 15 of these participants to undergo EEG studies with foramen ovale electrodes to determine the prevalence of these hippocampal seizures. The ultimate goal is to improve the outcome of patients with Alzheimer disease by early treatment of epilepsy and restoring sleep-wake disturbances.
- Conditions
- Alzheimer Disease, Alzheimer Dementia, Epilepsy, Sleep Wake Disorders
- Being tested
- scalp EEG and polysomnography, scalp EEG with foramen ovale electrodes with polysomnography
- Keywords
- Alzheimer Disease, Alzheimer dementia, Epilepsy, Sleep Wake Disorders, EEG, Polysomnography, Foramen ovale electrodes
- Medical subject headings
- Alzheimer Disease, Epilepsy, Sleep Wake Disorders
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
scalp EEG and polysomnographyDiagnostic test
48 hour 22 channel EEG with polysomnography
scalp EEG with foramen ovale electrodes with polysomnographyDiagnostic test
long-term scalp EEG with additional foramen ovale electrodes with polysomnography
| Study group | Role | What they receive |
|---|---|---|
| Healthy control participants | Active comparator | Age- and gender matched healthy participant (n=30) with no cognitive problems and normal amyloid PET scan will undergo 48 hour scalp EEG and polysomnography Receives: Diagnostic Test: scalp EEG and polysomnography |
| Alzheimer disease | Active comparator | Participants with Alzheimer disease (n=100) will undergo 48 hour scalp EEG and polysomnography Receives: Diagnostic Test: scalp EEG and polysomnography |
| Alzheimer disease with high seizure risk | Experimental | Selected participants with Alzheimer disease, with higher risk for silent hippocampal seizures after 48 hour scalp EEG and polysomnography (e.g. presence of interictal spikes or frequent nocturnal awakenings) (n=15) will undergo scalp EEG with foramen ovale electrodes with polysomnography Receives: Diagnostic Test: scalp EEG and polysomnography; Diagnostic Test: scalp EEG with foramen ovale electrodes with polysomnography |
What is being measured
The primary outcome is the main question the study is designed to answer.
Epilepsy
presence of epileptic activity
Measured: during EEG recording
Sleep wake disorder
presence of sleep wake disorders
Measured: during polysomnographic recording
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted6 Aug 2018
- Study start1 Dec 2020
- Primary completion30 Sep 2024 (estimated)
- Study completion30 Sep 2024 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (44)Papers the sponsor has linked to this study.
- Other trials for Alzheimer DiseaseStudies of the same condition, open and under way.
- More trials run by Universitaire Ziekenhuizen KU LeuvenThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Diagnosis
- Allocation
- Non-randomised
- Intervention model
- Factorial
- Model description
- The investigators will perform 48-hour ambulatory scalp-EEG and polysomnography in 100 participants with Alzheimer disease and 30 age-and gender-matched healthy participants. The investigators will determine the prevalence of 1.) epileptic discharges and epileptic seizures, 2.) sleep wake disorders and 3.) the interaction of epilepsy and sleep wake disorders in these two groups. A subgroup of 15 of these 100 participants with Alzheimer disease, with interictal epileptic spikes or sleep wake disorders (e.g., frequent nocturnal awakenings) will be invited to undergo an invasive EEG study with foramen ovale electrodes to determine the prevalence of hippocampal seizures, which are usually clinically silent and not detected with scalp EEG.
- Masking
- None (open label)
- Enrolment
- 78 participants (actual)
Sponsor and investigators
- Lead sponsor
- Universitaire Ziekenhuizen KU Leuven
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Prof Dr W Van Paesschen, Universitaire Ziekenhuizen KU Leuven
- Investigators
- Wim Van Paesschen, MD PhD, Principal investigator, UZ and KU Leuven
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03617497
- Sponsor's protocol ID
- S61745
- Acronym
- PESAD
- Status last verified
- Oct 2023
- First submitted
- 24 Jul 2018
- Last updated
- 13 Oct 2023
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Ju YE, Lucey BP, Holtzman DM. Sleep and Alzheimer disease pathology--a bidirectional relationship. Nat Rev Neurol. 2014 Feb;10(2):115-9. doi: 10.1038/nrneurol.2013.269. Epub 2013 Dec 24.
PubMed 24366271Musiek ES, Holtzman DM. Mechanisms linking circadian clocks, sleep, and neurodegeneration. Science. 2016 Nov 25;354(6315):1004-1008. doi: 10.1126/science.aah4968.
PubMed 27885006Ooms S, Overeem S, Besse K, Rikkert MO, Verbeek M, Claassen JA. Effect of 1 night of total sleep deprivation on cerebrospinal fluid beta-amyloid 42 in healthy middle-aged men: a randomized clinical trial. JAMA Neurol. 2014 Aug;71(8):971-7. doi: 10.1001/jamaneurol.2014.1173.
PubMed 24887018Noebels J. A perfect storm: Converging paths of epilepsy and Alzheimer's dementia intersect in the hippocampal formation. Epilepsia. 2011 Jan;52 Suppl 1(Suppl 1):39-46. doi: 10.1111/j.1528-1167.2010.02909.x.
PubMed 21214538Horvath A, Szucs A, Barcs G, Noebels JL, Kamondi A. Epileptic Seizures in Alzheimer Disease: A Review. Alzheimer Dis Assoc Disord. 2016 Apr-Jun;30(2):186-92. doi: 10.1097/WAD.0000000000000134.
PubMed 26756385Lam AD, Deck G, Goldman A, Eskandar EN, Noebels J, Cole AJ. Silent hippocampal seizures and spikes identified by foramen ovale electrodes in Alzheimer's disease. Nat Med. 2017 Jun;23(6):678-680. doi: 10.1038/nm.4330. Epub 2017 May 1.
PubMed 28459436Vossel KA, Beagle AJ, Rabinovici GD, Shu H, Lee SE, Naasan G, Hegde M, Cornes SB, Henry ML, Nelson AB, Seeley WW, Geschwind MD, Gorno-Tempini ML, Shih T, Kirsch HE, Garcia PA, Miller BL, Mucke L. Seizures and epileptiform activity in the early stages of Alzheimer disease. JAMA Neurol. 2013 Sep 1;70(9):1158-66. doi: 10.1001/jamaneurol.2013.136.
PubMed 23835471Vossel KA, Ranasinghe KG, Beagle AJ, Mizuiri D, Honma SM, Dowling AF, Darwish SM, Van Berlo V, Barnes DE, Mantle M, Karydas AM, Coppola G, Roberson ED, Miller BL, Garcia PA, Kirsch HE, Mucke L, Nagarajan SS. Incidence and impact of subclinical epileptiform activity in Alzheimer's disease. Ann Neurol. 2016 Dec;80(6):858-870. doi: 10.1002/ana.24794. Epub 2016 Nov 7.
PubMed 27696483Vossel KA, Tartaglia MC, Nygaard HB, Zeman AZ, Miller BL. Epileptic activity in Alzheimer's disease: causes and clinical relevance. Lancet Neurol. 2017 Apr;16(4):311-322. doi: 10.1016/S1474-4422(17)30044-3.
PubMed 28327340Lam AD, Zepeda R, Cole AJ, Cash SS. Widespread changes in network activity allow non-invasive detection of mesial temporal lobe seizures. Brain. 2016 Oct;139(Pt 10):2679-2693. doi: 10.1093/brain/aww198. Epub 2016 Jul 29.
PubMed 27474219Rabinowicz AL, Starkstein SE, Leiguarda RC, Coleman AE. Transient epileptic amnesia in dementia: a treatable unrecognized cause of episodic amnestic wandering. Alzheimer Dis Assoc Disord. 2000 Oct-Dec;14(4):231-3. doi: 10.1097/00002093-200010000-00008.
PubMed 11186602Zarea A, Charbonnier C, Rovelet-Lecrux A, Nicolas G, Rousseau S, Borden A, Pariente J, Le Ber I, Pasquier F, Formaglio M, Martinaud O, Rollin-Sillaire A, Sarazin M, Croisile B, Boutoleau-Bretonniere C, Ceccaldi M, Gabelle A, Chamard L, Blanc F, Sellal F, Paquet C, Campion D, Hannequin D, Wallon D; PHRC GMAJ Collaborators. Seizures in dominantly inherited Alzheimer disease. Neurology. 2016 Aug 30;87(9):912-9. doi: 10.1212/WNL.0000000000003048. Epub 2016 Jul 27.
PubMed 27466472Tai XY, Koepp M, Duncan JS, Fox N, Thompson P, Baxendale S, Liu JY, Reeves C, Michalak Z, Thom M. Hyperphosphorylated tau in patients with refractory epilepsy correlates with cognitive decline: a study of temporal lobe resections. Brain. 2016 Sep;139(Pt 9):2441-55. doi: 10.1093/brain/aww187. Epub 2016 Aug 7.
PubMed 27497924Horvath A, Szucs A, Barcs G, Kamondi A. Sleep EEG Detects Epileptiform Activity in Alzheimer's Disease with High Sensitivity. J Alzheimers Dis. 2017;56(3):1175-1183. doi: 10.3233/JAD-160994.
PubMed 28128769Bakker A, Krauss GL, Albert MS, Speck CL, Jones LR, Stark CE, Yassa MA, Bassett SS, Shelton AL, Gallagher M. Reduction of hippocampal hyperactivity improves cognition in amnestic mild cognitive impairment. Neuron. 2012 May 10;74(3):467-74. doi: 10.1016/j.neuron.2012.03.023.
PubMed 22578498
Study at a glance
From the registry record, last updated by the sponsor on 13 Oct 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Prevalence of Epilepsy and Sleep Wake Disorders in Alzheimer Disease
- ClinicalTrials.gov ID
- NCT03617497
- Acronym / sponsor ID
- PESAD / S61745
- Conditions
- Alzheimer Disease, Alzheimer Dementia, Epilepsy, Sleep Wake Disorders
- Keywords
- Alzheimer Disease, Alzheimer dementia, Epilepsy, Sleep Wake Disorders, EEG, Polysomnography, Foramen ovale electrodes
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 78 participants (actual)
- Lead sponsor
- Universitaire Ziekenhuizen KU LeuvenUniversity, hospital or other
- Study start
- 1 Dec 2020 (actual)
- Primary completion
- 30 Sep 2024 (estimated)
- Study completion
- 30 Sep 2024 (estimated)
- First posted
- 6 Aug 2018 (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.
Alzheimer disease is the most common of the neurodegenerative diseases. Epilepsy and sleep wake disorders are co-morbid conditions of Alzheimer disease. The investigators propose a prospective study using long-term EEG monitoring in combination with polysomnography to determine prevalence of epilepsy and sleep wake disorders in Alzheimer disease, and correlate these findings with clinical data, Alzheimer disease biomarkers and imaging studies (MRI and amyloid/tau-PET). In selected patients, the investigators will perform EEG studies with foramen ovale electrodes. The ultimate goal is to improve the outcome of patients with Alzheimer disease by early treatment of epilepsy and restoring sleep-wake disturbances.
Detailed description
Alzheimer disease is the most common of the neurodegenerative diseases. Epilepsy and sleep wake disorders are co-morbid conditions of Alzheimer disease, and there is evidence to suggest that the interactions are bidirectional. Neuronal activity promotes the production and secretion of amyloid β, which could actually drive pathogenesis early in the course of Alzheimer disease, and has been described in sleep wake disorders and epilepsy. Epileptic seizures in Alzheimer disease are often subtle, nocturnal and easily overlooked. We propose a prospective study using long-term EEG monitoring in combination with polysomnography to diagnose epilepsy and sleep wake disorders in Alzheimer disease, and correlate these findings with clinical data, Alzheimer disease biomarkers and imaging studies (MRI and amyloid/tau-PET). It is the hypothesis of the investigators that participants with Alzheimer disease and interictal spikes or specified sleep wake disorders (e.g., frequent nocturnal awakenings) during 48 hour scalp EEG and polysomnography are at risk for having hippocampal seizures, which are often clinically silent and not detected on scalp EEG. The investigators will invite 15 of these participants to undergo EEG studies with foramen ovale electrodes to determine the prevalence of these hippocampal seizures. The ultimate goal is to improve the outcome of patients with Alzheimer disease by early treatment of epilepsy and restoring sleep-wake disturbances.
Study design
- Primary purpose
- Diagnosis
- Allocation
- Non-randomised
- Intervention model
- Factorial
- Masking
- None (open label)
- Number of arms
- 3
- Model description
- The investigators will perform 48-hour ambulatory scalp-EEG and polysomnography in 100 participants with Alzheimer disease and 30 age-and gender-matched healthy participants. The investigators will determine the prevalence of 1.) epileptic discharges and epileptic seizures, 2.) sleep wake disorders and 3.) the interaction of epilepsy and sleep wake disorders in these two groups. A subgroup of 15 of these 100 participants with Alzheimer disease, with interictal epileptic spikes or sleep wake disorders (e.g., frequent nocturnal awakenings) will be invited to undergo an invasive EEG study with foramen ovale electrodes to determine the prevalence of hippocampal seizures, which are usually clinically silent and not detected with scalp EEG.
| Arm | Type | Receives |
|---|---|---|
| Healthy control participants | Active comparator | Diagnostic Test: scalp EEG and polysomnographyAge- and gender matched healthy participant (n=30) with no cognitive problems and normal amyloid PET scan will undergo 48 hour scalp EEG and polysomnography |
| Alzheimer disease | Active comparator | Diagnostic Test: scalp EEG and polysomnographyParticipants with Alzheimer disease (n=100) will undergo 48 hour scalp EEG and polysomnography |
| Alzheimer disease with high seizure risk | Experimental | Diagnostic Test: scalp EEG and polysomnography, Diagnostic Test: scalp EEG with foramen ovale electrodes with polysomnographySelected participants with Alzheimer disease, with higher risk for silent hippocampal seizures after 48 hour scalp EEG and polysomnography (e.g. presence of interictal spikes or frequent nocturnal awakenings) (n=15) will undergo scalp EEG with foramen ovale electrodes with polysomnography |
Who may qualify
- Ages
- 55 to 85 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (8 listed)
- Participant must be able to understand the nature of the study and has the opportunity to have any questions answered. The participant has voluntarily signed the independent Review Board (IRB)/independent Ethics Committee (IEC) approved Informed Consent, prior to the conduct of any study procedures. If the participant is not fully competent, full informed consent must be obtained from a representative and assent must be obtained from the participant.
- Participant who meets the National Institute on Aging and the Alzheimer's Association (NIA-AA) clinical criteria for mild cognitive impairment or probable Alzheimer Disease, and have:
- Participant has a positive amyloid Positron Emission Tomography (PET) scan.
- Participant has a Modified Hachinski Ischemic Scale (MHIS) score of ≤ 4.
- Participant has an identified, reliable, study partner (e.g., family member), who has frequent contact with the participant and who will provide information as to the participant's cognitive and functional abilities.
Key exclusion criteria (28 listed)
- Participant has evidence of any other clinically significant neurological disorder other than Alzheimer disease, including but not limited to:
- Participant has a screening MRI scan, interpreted by a radiologist with evidence of infection, infarction (including multiple lacunas in a critical memory structure), or other focal lesions.
- Participant has a history of or currently has schizophrenia, schizoaffective disorder or bipolar disorder according to Diagnostic and Statistical Manual of Mental Disorders (DSM)-V or International Classification of Diseases (ICD)-10 criteria.
- Participant has a current diagnosis or history of drug or alcohol abuse (by DSM-V criteria) within 24 months prior to the study.
- Participant has a history or evidence of a malignancy within the 2 years prior to 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 |
|---|---|---|
| scalp EEG and polysomnography48 hour 22 channel EEG with polysomnography | Diagnostic test | Alzheimer disease, Alzheimer disease with high seizure risk, Healthy control participants |
| scalp EEG with foramen ovale electrodes with polysomnographylong-term scalp EEG with additional foramen ovale electrodes with polysomnography | Diagnostic test | Alzheimer disease with high seizure risk |
Primary outcome
Epilepsy
Time frame: during EEG recording
presence of epileptic activity
Sleep wake disorder
Time frame: during polysomnographic recording
presence of sleep wake disorders
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Oct 2023.
- Background: PubMed 24366271Ju YE, Lucey BP, Holtzman DM. Sleep and Alzheimer disease pathology--a bidirectional relationship. Nat Rev Neurol. 2014 Feb;10(2):115-9. doi: 10.1038/nrneurol.2013.269. Epub 2013 Dec 24.
- Background: PubMed 27885006Musiek ES, Holtzman DM. Mechanisms linking circadian clocks, sleep, and neurodegeneration. Science. 2016 Nov 25;354(6315):1004-1008. doi: 10.1126/science.aah4968.
- Background: PubMed 24887018Ooms S, Overeem S, Besse K, Rikkert MO, Verbeek M, Claassen JA. Effect of 1 night of total sleep deprivation on cerebrospinal fluid beta-amyloid 42 in healthy middle-aged men: a randomized clinical trial. JAMA Neurol. 2014 Aug;71(8):971-7. doi: 10.1001/jamaneurol.2014.1173.
- Background: PubMed 21214538Noebels J. A perfect storm: Converging paths of epilepsy and Alzheimer's dementia intersect in the hippocampal formation. Epilepsia. 2011 Jan;52 Suppl 1(Suppl 1):39-46. doi: 10.1111/j.1528-1167.2010.02909.x.
- Background: PubMed 26756385Horvath A, Szucs A, Barcs G, Noebels JL, Kamondi A. Epileptic Seizures in Alzheimer Disease: A Review. Alzheimer Dis Assoc Disord. 2016 Apr-Jun;30(2):186-92. doi: 10.1097/WAD.0000000000000134.
- Background: PubMed 28459436Lam AD, Deck G, Goldman A, Eskandar EN, Noebels J, Cole AJ. Silent hippocampal seizures and spikes identified by foramen ovale electrodes in Alzheimer's disease. Nat Med. 2017 Jun;23(6):678-680. doi: 10.1038/nm.4330. Epub 2017 May 1.
- Background: PubMed 23835471Vossel KA, Beagle AJ, Rabinovici GD, Shu H, Lee SE, Naasan G, Hegde M, Cornes SB, Henry ML, Nelson AB, Seeley WW, Geschwind MD, Gorno-Tempini ML, Shih T, Kirsch HE, Garcia PA, Miller BL, Mucke L. Seizures and epileptiform activity in the early stages of Alzheimer disease. JAMA Neurol. 2013 Sep 1;70(9):1158-66. doi: 10.1001/jamaneurol.2013.136.
- Background: PubMed 27696483Vossel KA, Ranasinghe KG, Beagle AJ, Mizuiri D, Honma SM, Dowling AF, Darwish SM, Van Berlo V, Barnes DE, Mantle M, Karydas AM, Coppola G, Roberson ED, Miller BL, Garcia PA, Kirsch HE, Mucke L, Nagarajan SS. Incidence and impact of subclinical epileptiform activity in Alzheimer's disease. Ann Neurol. 2016 Dec;80(6):858-870. doi: 10.1002/ana.24794. Epub 2016 Nov 7.
- Background: PubMed 28327340Vossel KA, Tartaglia MC, Nygaard HB, Zeman AZ, Miller BL. Epileptic activity in Alzheimer's disease: causes and clinical relevance. Lancet Neurol. 2017 Apr;16(4):311-322. doi: 10.1016/S1474-4422(17)30044-3.
- Background: PubMed 27474219Lam AD, Zepeda R, Cole AJ, Cash SS. Widespread changes in network activity allow non-invasive detection of mesial temporal lobe seizures. Brain. 2016 Oct;139(Pt 10):2679-2693. doi: 10.1093/brain/aww198. Epub 2016 Jul 29.
- Background: PubMed 11186602Rabinowicz AL, Starkstein SE, Leiguarda RC, Coleman AE. Transient epileptic amnesia in dementia: a treatable unrecognized cause of episodic amnestic wandering. Alzheimer Dis Assoc Disord. 2000 Oct-Dec;14(4):231-3. doi: 10.1097/00002093-200010000-00008.
- Background: PubMed 27466472Zarea A, Charbonnier C, Rovelet-Lecrux A, Nicolas G, Rousseau S, Borden A, Pariente J, Le Ber I, Pasquier F, Formaglio M, Martinaud O, Rollin-Sillaire A, Sarazin M, Croisile B, Boutoleau-Bretonniere C, Ceccaldi M, Gabelle A, Chamard L, Blanc F, Sellal F, Paquet C, Campion D, Hannequin D, Wallon D; PHRC GMAJ Collaborators. Seizures in dominantly inherited Alzheimer disease. Neurology. 2016 Aug 30;87(9):912-9. doi: 10.1212/WNL.0000000000003048. Epub 2016 Jul 27.
- Mission Lucidity: Decoding DementiaLink provided by the sponsor.
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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.
Wim Van Paesschen, MD PhD principal investigator
UZ and KU Leuven
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing scalp EEG and polysomnography and scalp EEG with foramen ovale electrodes with polysomnography in people with Alzheimer Disease and Alzheimer Dementia, run by Universitaire Ziekenhuizen KU Leuven at 1 site in Belgium.
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 8 inclusion and 28 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 13 Oct 2023. 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 Belgium. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
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?
Epilepsy (time frame: during EEG recording). The study lists 2 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 NCT03617497, which also lists 44 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 13 Oct 2023.