The Mayo Clinic Alzheimer's Disease Research Center needs people to participate in research studies, including people with mild cognitive impairment, early dementia, Alzheimer's disease and Lewy body dementia. The Alzheimer's Disease Research Center also needs clinical trial participants who haven't been diagnosed with a memory disorder.

Learn more about clinical trials, the different types of clinical studies and deciding to volunteer for clinical studies.

Clinical Trials

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12 studies in Alzheimer's Disease Research Center

  1. DaTSCAN Imaging in Aging and Neurodegenerative Disease

    Rochester, Minn. View Summary

    DaTSCAN Imaging in Aging and Neurodegenerative Disease

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Lewy body disease (LBD) is one of the most common neurodegenerative diseases and second only to Alzheimer's disease in terms of prevalence, disability, and societal/financial burden. The phenotypic variability of LBD is striking, as it can manifest as the well-known disorder of Parkinson's disease without (PD) and with dementia (PDD), as well as DLB, MCI, REM sleep behavior disorder (RBD), pure autonomic failure (PAF), and other syndromes. One biomarker which is both highly sensitive and specific for evolving LBD in the setting of dementia is DaTscan [Ioflupane (123I)] imaging, in which loss of functional dopaminergic neuron terminals in the striatum as assessed by DaTscan reflects underlying LBD in those with dementia and particularly dementia with Lewy bodies (DLB). DaTscan is the one of the first radiopharmaceutical agents available to detect DaT distribution within the brain. DaTscan imaging involves injection of the Ioflupane radioligand followed by imaging using a standard single photon emission computed tomography (SPECT) scanner. DaTscan provides visualization of the dopamine transporter (DaT) distribution within the striata (i.e., striatal uptake, or striatal signal) by SPECT imaging in patients presenting with symptoms or signs suggestive of dopaminergic neurodegeneration. All DaTscan studies published to date have been conducted in centers outside of the US. DaTscan has not been studied in the syndrome of MCI, and minimally in corticobasal degeneration (CBD). Very little normative data exists in the aged population either. The FDA-approved indication is to assist in the evaluation of adult patients with suspected Parkinsonian syndromes (PS). In these patients, DaTscan may be used to help differentiate essential tremor from tremor due to Parkinsonian syndromes (such as idiopathic Parkinson's disease, multiple system atrophy and progressive supranuclear palsy). DaTscan will be used as an adjunct to other diagnostic evaluations. Identifying dopaminergic dysfunction is also important in other settings such as those with cognitive impairment with or without parkinsonism, and in subjects with REM sleep behavior disorder. The findings on DaTscan in subjects with these various disorders will be correlated with clinical diagnoses and other multimodal imaging studies (e.g., MRI, MRS, FDG-PET, and amyloid-PET) to enhance our understanding of neurodegenerative diseases.

    NCT ID:

    NCT01453127

    IRB Number:

    11-001999

    Who can I contact for additional information about this study?

  2. Therapeutic Effects of Intranasally-Administered Insulin in Adults With Amnestic Mild Cognitive Impairment (aMCI) or Mild Alzheimer s Disease (AD)

    Jacksonville, Fla., Rochester, Minn. View Summary

    Therapeutic Effects of Intranasally-Administered Insulin in Adults With Amnestic Mild Cognitive Impairment (aMCI) or Mild Alzheimer s Disease (AD)

    Location:

    Jacksonville, Fla., Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    An urgent need exists to find effective treatments for Alzheimer's disease (AD) that can arrest or reverse the disease at its earliest stages. The emotional and financial burden of AD to patients, family members, and society is enormous, and is predicted to grow exponentially as the median population age increases. Current FDA-approved therapies are modestly effective at best. This study will examine a novel therapeutic approach using intranasal insulin (INI) that has shown promise in short-term clinical trials. If successful, information gained from the study has the potential to move INI forward rapidly as a therapy for AD. The study will also provide evidence for the mechanisms through which INI may produce benefits by examining key cerebral spinal fluid (CSF) biomarkers and hippocampal/entorhinal atrophy. These results will have considerable clinical and scientific significance, and provide therapeutically-relevant knowledge about insulin's effects on AD pathophysiology. Growing evidence has shown that insulin carries out multiple functions in the brain, and that insulin dysregulation may contribute to AD pathogenesis. This study will examine the effects of intranasally-administered insulin on cognition, entorhinal cortex and hippocampal atrophy, and cerebrospinal fluid (CSF) biomarkers in amnestic mild cognitive impairment (aMCI) or mild AD. It is hypothesized that after 12 months of treatment with INI compared to placebo, subjects will improve performance on a global measure of cognition, on a memory composite and on daily function. In addition to the examination of CSF biomarkers and hippocampal and entorhinal atrophy, the study aims to examine whether baseline AD biomarker profile, gender, or Apolipoprotein epsilon 4 (APOE-ε4) allele carriage predict treatment response. In this study, 240 people with aMCI or AD will be given either INI or placebo for 12 months, following an open-label period of 6 months where all participants will be given active drug. The study uses insulin as a therapeutic agent and intranasal administration focusing on nose to brain transport as a mode of delivery.

    NCT ID:

    NCT01767909

    Who can I contact for additional information about this study?

  3. Effect of Aging and Aerobic Exercise Training on Brain Glucose Metabolism

    Rochester, Minn. View Summary

    Effect of Aging and Aerobic Exercise Training on Brain Glucose Metabolism

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Aging is associated with a loss of brain function and conditions such as dementia and Alzheimer's disease. It is likely that decreased brain metabolism is contributing to the progression of age related degenerative diseases. Aerobic exercise training can increase brain volumes and is associated with decreased risk for degenerative brain conditions. However, little is know about the changes that occur to brain metabolism with aerobic training and aging.

    NCT ID:

    NCT01738568

    IRB Number:

    12-003357

    Who can I contact for additional information about this study?

    Rochester: Robinson, PhD 507-255-9610
                        


  4. Dominantly Inherited Alzheimer Network (DIAN)

    Jacksonville, Fla. View Summary

    Dominantly Inherited Alzheimer Network (DIAN)

    Location:

    Jacksonville, Fla.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Dominantly inherited Alzheimer's disease (AD) represents less than 1% of all cases of AD and is an important model for study because the responsible mutations have known biochemical consequences that are believed to underlie the pathological basis of the disorder. Three major hypotheses will be tested: - First, that there is a period of preclinical (presymptomatic) AD in individuals who are destined to develop early-onset dementia (gene carriers) that can be detected by changes in biological fluids and in neuroimaging correlates in comparison with individuals who will not develop early-onset dementia (non-carriers). - Second, because all identified causative mutations for AD affect the normal processing of amyloid precursor protein (APP) and increase brain levels of amyloid-beta 42 (Aβ42), the sequence of preclinical changes initially will involve Aβ42 (production and clearance; reduced levels in cerebrospinal fluid [CSF]), followed by evidence for cerebral deposition of Aβ42 (amyloid imaging), followed by cerebral metabolic activity (functional imaging), and finally by regional atrophy (structural imaging). - Finally, that the phenotype of symptomatic early-onset familial AD, including its clinical course, is similar to that of late-onset "sporadic" AD. The following specific aims will be used to test these hypotheses: 1. Establish an international, multicenter registry of individuals (mutation carriers and non-carriers; pre-symptomatic and symptomatic) who are biological adult children of a parent with a known causative mutation for AD in the APP, PSEN1, or PSEN2 genes in which the individuals are evaluated in a uniform manner at entry and longitudinally thereafter with standardized instruments. 2. In pre-symptomatic individuals, compare mutation carriers and non-carriers to determine the order in which changes in clinical, cognitive, neuroimaging, and biomarker indicators of AD occur prior to the occurrence of dementia. 3. In symptomatic individuals, compare the clinical and neuropathological phenotypes of autosomal dominant AD to those of late-onset "sporadic" AD (using the data sets established by ADNI and by NACC). 4. Maintain the DIAN Central Archive, an integrated database incorporating all information obtained from individuals in the registry to permit analyses within, between, and among the various data domains and also to disseminate the data to qualified investigators in a user-friendly manner. 5. All DIAN participants who wish to know their mutation status will have the costs of genetic counseling and clinical mutation testing paid for by the grant. The clinical genetic counseling and testing is provided as an optional participant benefit and is not part of the DIAN research design.

    NCT ID:

    NCT00869817

    Who can I contact for additional information about this study?



    Jacksonville: Dana Haley, MPH CCRP 904-953-9680
                        
  5. A Randomized, Placebo Controlled, Parallel-Group, Double Blind Efficacy and Safety Trial of MK-8931 With a Long Term Double-Blind Extension in Subjects With Mild to Moderate Alzheimer s Disease (Protocol No. MK-8931-017-08)(Also Known as SCH 900931, P07738)

    Phoenix/Scottsdale, Ariz. View Summary

    A Randomized, Placebo Controlled, Parallel-Group, Double Blind Efficacy and Safety Trial of MK-8931 With a Long Term Double-Blind Extension in Subjects With Mild to Moderate Alzheimer s Disease (Protocol No. MK-8931-017-08)(Also Known as SCH 900931, P07738)

    Location:

    Phoenix/Scottsdale, Ariz.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Two substudies are included in Part I of the study: 1) a medical imaging substudy to evaluate changes in brain amyloid protein load using positron emission tomography (PET) and an amyloid tracer ([18F]flutemetamol); and 2) a cerebrospinal fluid (CSF) biomarker substudy to evaluate changes in CSF concentrations of amyloid-β related peptides, total tau, and phosphorylated tau (p-tau). The substudies will be conducted only at designated investigational sites. Participants are not required to take part in a substudy in order to take part in the larger trial.

    NCT ID:

    NCT01739348

    IRB Number:

    13-000419

    Who can I contact for additional information about this study?

  6. Longitudinal Study of Cognition With Niemann-Pick Disease, Type C

    Rochester, Minn. View Summary

    Longitudinal Study of Cognition With Niemann-Pick Disease, Type C

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Niemann-Pick Disease, Type C (NPC) is a rare neurodegenerative disorder with a wide clinical spectrum and variable age of onset. Classically, children with NPC demonstrate neurological dysfunction with cerebellar ataxia (an inability to coordinate balance, gait, extremity and eye movements), dysarthria (difficulty speaking), seizures, vertical gaze palsy (ability to move eyes in the same direction) motor impairment, dysphagia (trouble swallowing), psychotic episodes, and progressive dementia. There is no curative treatment for NPC and it is a lethal disorder. The purpose of this protocol is to obtain both baseline and rate of progression data on a clinical and biochemical markers that may later be used as outcome measures in a clinical trial. Specifically, this study will examine and characterize the longitudinal progression of neurocognitive symptoms of NPC with the goal of identifying early markers of disease progression that may be utilized in later trials to evaluate treatment efficacy.

    NCT ID:

    NCT01899950

    IRB Number:

    11-003868

    Who can I contact for additional information about this study?

    Rochester: Marc Patterson, MD 507-284-3351
                        


  7. PiB PET Scanning in Speech and Language Based Dementias

    Rochester, Minn. View Summary

    PiB PET Scanning in Speech and Language Based Dementias

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Speech and language based dementias (SLDs) (often referred to as primary progressive aphasias or PPA) are neurodegenerative diseases in which speech or language impairments are the most salient features of the disease and explain deficits in activities of daily living. Patients with SLDs may have poor grammar, prominent anomia, comprehension deficits, speech production and articulation problems, difficulty with repetition of words or sentences, word finding pauses, or a combination of all these features. The SLDs can be further divided into different subtypes. Up to 50% of patients with SLDs that go on to autopsy have shown Alzheimer type pathology where beta-amyloid deposition is observed; the rest have pathology consistent with frontotemporal lobar degeneration where beta-amyloid deposition is absent. Future disease modifying treatments that target beta-amyloid will most likely differ from treatments that do not target beta-amyloid. As a consequence, biomarkers are needed to differentiate patients with SLDs with and without beta-amyloid deposition. Little research has been done to identify biomarkers that could differentiate patients with SLDs with and without beta-amyloid, mainly because the gold standard to identify the presence of beta-amyloid has been pathological examination, which does not always occur, and may not occur until more than 10 years after onset. The recent development of [N-methyl-11C]2-(4'-methylaminophenyl)-6-hydroxybenzothiazole also known as 11C Pittsburgh Compound B or PiB is a solution to this problem since PiB allows the in vivo detection of beta-amyloid. Unfortunately, PiB is very expensive. The long term goal of our research is to develop a cost effective algorithmic approach to the evaluation and diagnosis of patients presenting with SLDs. The objective of the studies outlined in this proposal is to identify clinical, neuropsychological, or imaging biomarkers that are readily available, relatively inexpensive, and non-invasive that will allow the differentiation of patients with SLDs with and without beta-amyloid deposition. We will use PiB as an indicator of beta-amyloid pathology. Our proposal is predicated upon our strong preliminary data showing that clinical, neuropsychological and radiological features differ between patients with SLDs with and without beta-amyloid deposition. Our central hypothesis is that temporo-parietal lobe findings such as memory loss, visuospatial/perceptual impairment, parietal lobe atrophy on magnetic resonance imaging (MRI), and parietal lobe hypometabolism on [18-F]-fluoro-deoxy-glucose positron emission tomography (FDG-PET), will be associated with beta-amyloid deposition (PiB positive status). On-the-other hand, frontal lobe features, such as apraxia of speech and behavioral and executive dysfunction, as well as extrapyramidal features such as Parkinsonism, will be associated with absence of beta-amyloid deposition (PiB negative status). The rationale for examining these clinical-imaging relationships is that successful predictions will provide a solid scientific foundation for the ultimate development of a cost effective algorithm to guide the diagnosis of SLDs. Patients found to be eligible and willing to enroll in this study will be asked to undergo a Neurologic Examination, a Speech Pathology Consultation, Neuropsychometric testing, an MRI scan, an FDG PET scan and a PiB PET scan of the brain. This will be done over a period of two days at the Mayo Clinic in Rochester, MN.

    NCT ID:

    NCT01623284

    IRB Number:

    09-008772

    Who can I contact for additional information about this study?

    Rochester: Sarah Boland 507-293-4707
                        


  8. Effect of Passive Immunization on the Progression of Mild Alzheimer s Disease: Solanezumab (LY2062430) Versus Placebo

    Jacksonville, Fla. View Summary

    Effect of Passive Immunization on the Progression of Mild Alzheimer s Disease: Solanezumab (LY2062430) Versus Placebo

    Location:

    Jacksonville, Fla.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    To test the idea that solanezumab will slow the cognitive and functional decline of Alzheimer's Disease (AD) as compared with placebo in participants with mild AD.

    NCT ID:

    NCT01900665

    IRB Number:

    13-005818

    Who can I contact for additional information about this study?



    Jacksonville: 904-953-7103
                        
  9. Anti-Amyloid Treatment in Asymptomatic Alzheimer s Disease (A4 Study)

    Jacksonville, Fla., Rochester, Minn. View Summary

    Anti-Amyloid Treatment in Asymptomatic Alzheimer s Disease (A4 Study)

    Location:

    Jacksonville, Fla., Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    The A4 study is a clinical trial for older individuals who have evidence of amyloid plaque build-up in their brains who may be at risk for memory loss and cognitive decline due to Alzheimer's disease. The A4 study will test an anti-amyloid investigational drug in older individuals who do not yet show symptoms of Alzheimer's disease cognitive impairment or dementia with the aim of slowing memory and cognitive decline. The A4 study will also test whether anti-amyloid treatment can delay the progression of AD related brain injury on imaging and other biomarkers.

    NCT ID:

    NCT02008357

    IRB Number:

    13-008325

    Who can I contact for additional information about this study?

    Rochester: 507-293-4711
                        

    Jacksonville: 904-953-9680
                        
  10. Amyloid-related Imaging Abnormalities (Microbleeds) in Atypical AD

    Rochester, Minn. View Summary

    Amyloid-related Imaging Abnormalities (Microbleeds) in Atypical AD

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Alzheimer's disease (AD) is associated with amyloid-related imaging abnormalities (ARIA). Microbleeds (MBs) represent part of the spectrum of ARIA and can be identified as small hypointense lesions on gradient-recalled echo (GRE) T2*-weighted MRI. They are thought to represent hemosiderin deposits (and hence have been classified as ARIA-H1) and occur as a consequence of leakage of blood products out of vessels that have been damaged by deposition of the protein β-amyloid in cerebral vessels; cerebral amyloid angiopathy (CAA). However, it is also possible that cerebrovascular disease could contribute to the presence of MBs in AD. Subjects with MBs are at a greater risk of bleeds which could impact the use of anti-coagulation treatment approaches. The presence of CAA has been particularly associated with AD and studies have demonstrated that MBs occur in 12-33% of subjects with typical Alzheimer's dementia, with a large proportion of subjects showing multiple MBs. The presence of MBs has been associated with older age and a greater degree of white matter hyperintensities (WMH) in Alzheimer's dementia. The association between MBs and WMH, a marker of cerebrovascular disease, suggests cerebrovascular disease may also play a role in the etiology of MBs in AD. However, approximately 16% of AD subjects do not present with episodic memory loss, but instead display language problems such as poor naming and impaired sentence repetition, or visuospatial and visual perceptual deficits, and are referred to as atypical AD. Since AD is associated with CAA, one would assume that CAA and hence MBs, would also occur in atypical AD, although no studies have assessed MBs in atypical AD. Amyloid-binding ligands, such as Pittsburgh Compound B (PiB), that can be detected using PET scanning have now been developed and provide an invaluable biomarker to infer the presence of β-amyloid. The presence of CAA has been shown to be associated with elevated PiB uptake, and hence the assessment of PiB-PET in subjects with MBs will provide important information on the association of MBs and β-amyloid deposition in AD. The goal of the study is to assess the associations between MBs and demographic/clinical features, assess the associations between MBs and imaging features as well as a possible correlate to the number of MBs a subject has in atypical AD. Patients found to be eligible and willing to enroll in this study will be asked to undergo a Neurologic Examination, Neuropsychometric testing, an MRI scan, and a PiB PET scan of the brain. This will be done over a period of two days at the Mayo Clinic in Rochester, Minnesota.

    NCT ID:

    NCT01723553

    IRB Number:

    12-007139

    Who can I contact for additional information about this study?

    Rochester: Sarah Boland 507-293-4707
                        


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