Neuronavigation-guided Focused Ultrasound-induced Blood-brain Barrier Opening in Alzheimer's Disease Patients and Its Effects on Brain Amyloid and Tau

The primary purpose of this phase 1b study is to further assess the safety and reversibility of focused ultrasound induced blood-brain barrier opening (FUS-BBBO) in participants with Alzheimer´s Disease (AD) using a single-element transducer with neuronavigation guidance. Preliminary results from our phase 1a study demonstrate that our neuronavigation-guided FUS system was capable of safely and transiently open the BBB in participants with AD. The information collected in this new study may be used to design future clinical trials to ultimately provide a viable alternative for treatment of AD in a safe and noninvasive manner.
Our secondary objective includes the assessment of the therapeutic efficacy of FUS-BBBO in reducing amyloid beta and neurofibrillary tangles, the main hallmark pathologies of AD, using PET tracers. Based on our preclinical studies in AD transgenic mouse models, FUS-BBBO alone was able to reduce both the amyloid beta and tau protein load, resulting in improvements in behavioral tasks assessing memory. Therefore, in this new study, the effect of FUS-BBBO on the amyloid beta and tau protein load in patients with AD will be assessed through the use of PET tracers.

Start Date01 Aug 2026

Sponsor / Collaborator

Columbia University

CTIS2025-523264-21-00

/ Not yet recruitingPhase 2/3IIT

CIRAANO: Multimodal exploration (including radiopharmaceuticals Amyvid® and Tauvid®) of theater actors, memory athletes, and patients with various memory pathologies: evaluation of mnesic strategies and their cerebral substrates, and contribution to the treatment of memory pathologies.

Start Date01 Nov 2025

Sponsor / Collaborator

Institut National de la Santé et de la Recherche Médicale

NCT06790394

/ RecruitingPhase 1

A Test-retest Study to Evaluate the Reproducibility of [18F]Florbetaben PET Imaging in Patients With Cardiac Amyloidosis and Control Patients

This study is an open-label study to evaluate and characterize test-retest reliability of [18F]florbetaben PET in subjects with AL-CA and ATTR-CA compared to non-CA subjects. Quantification of the [18F]florbetaben parameters related to the deposition of amyloid in the heart (such as Myocardial Tracer Retention (MTR) or Retention Index (RI)), and the variability in these parameters after repeated imaging will be evaluated. Measurement of blood metabolites and comparison of invasive with non-invasive quantification of [18F]florbetaben uptake in the heart will be performed.

Start Date21 Oct 2025

Sponsor / Collaborator

Life Molecular Imaging Ltd.

[+1]

100 Clinical Results associated with Florbetapir F-18

100 Translational Medicine associated with Florbetapir F-18

100 Patents (Medical) associated with Florbetapir F-18

336

Literatures (Medical) associated with Florbetapir F-18

01 Dec 2025·Alzheimers & Dementia

Association of Occipital Amyloid PET Burden with ARIA‐E: Exploratory Analyses in Three Clinical Trials of Donanemab

Article

Author: Sims, John R. ; Collins, Emily C. ; Shcherbinin, Sergey ; Kim, Min Jung ; Lu, Ming ; Kennedy, Ian A. ; Mintun, Mark A.

Abstract:

Background:

Amyloid‐related imaging abnormalities including edema/effusions (ARIA‐E) occur with amyloid‐targeting therapies. Major risk factors for ARIA‐E include apolipoprotein (APOE) ε4 carrier status, microhemorrhages, and cerebral amyloid angiopathy (CAA). Though differential diagnosis between CAA and Alzheimer’s disease (AD) is challenging, amyloid plaque burden in occipital regions may be higher in CAA than AD. This work explores the association of ARIA‐E with occipital amyloid burden in donanemab‐treated participants with early symptomatic AD.

Method:

Data included donanemab‐treated participants with early symptomatic AD in TRAILBLAZER‐ALZ (NCT03367403), TRAILBLAZER‐ALZ 2 (NCT04437511), and TRAILBLAZER‐ALZ 4 (NCT05108922). Amyloid pathology was assessed with florbetapir or florbetaben positron emission tomography (PET). Baseline amyloid burden was calculated in the atlas‐based lateral occipital region referenced to the whole cerebellum. Participants were categorized as having lower, comparable, or elevated occipital uptake relative to 6 cortical regions included in global amyloid assessments; these thresholds were derived from the Imaging Dementia‐Evidence for Amyloid Scanning Study (NCT02420756) after region‐ and tracer‐specific pre‐processing. The association of baseline occipital burden level with ARIA‐E over 76 weeks was assessed with Cox proportional hazard modeling adjusted for APOE ε4 carrier status and their interaction.

Result:

Analysis included N = 2087 baseline amyloid PET scans, with 741, 561, and 785 scans with lower, comparable, and elevated occipital amyloid burden relative to 6 cortical regions, respectively (Table 1). Baseline occipital burden was independently associated with ARIA‐E over 76 weeks (Table 2, Model 2). Compared with lower occipital burden, both comparable and elevated occipital burden were associated with statistically significantly higher risk of ARIA‐E, even when accounting for APOE ε4 carrier status (Figure, Model 2). Though the interaction of occipital burden with APOE ε4 status was not statistically significant (Table 2, Model 3), elevated occipital burden was associated with ARIA‐E within all APOE ε4 carrier groups (Figure, Model 3).

Conclusion:

Elevated occipital amyloid burden at baseline was statistically significantly associated with risk of ARIA‐E in donanemab‐treated participants with early symptomatic AD. The potential of occipital burden to predict ARIA‐E should be further validated with additional methodologies, subgroup analyses, and datasets.

01 Dec 2025·Alzheimers & Dementia

Wake slow waves during resting‐state EEG vary with current and two‐year changes in amyloid and neurodegeneration status in older adults with memory complaints

Article

Author: Chaumon, Maximilien ; Herzog, Rubén ; Champetier, Pierre ; Andrillon, Thomas ; Pereira, Filipa Raposo ; Albero, Claudia ; George, Nathalie ; Oudiette, Delphine ; Arnulf, Isabelle ; Houot, Marion

Abstract:

Background:

An increasing body of evidence has underscored the critical role of sleep slow waves in facilitating the clearance of brain waste, affecting the accumulation of Alzheimer's disease (AD) brain lesions. Recent studies have identified sleep‐like slow waves in wake EEG of young adults, often interpreted as intrusions of local sleep during wakefulness. The occurrence of these wake slow waves (wSW) is known to increase during sleep deprivation, and can predict behavioral errors across various tasks. This study aimed to compare wSW features based on 1) amyloid (A‐/A+) and neurodegeneration ( N ‐/N+) status, and 2) transitions to amyloid or neurodegeneration positivity (A+ or N+).

Method:

We included 314 elderly individuals with memory complaints from the INSIGHT‐preAD cohort (76.5 ± 3.5 years, range: 70‐85 years). Amyloid (A) and neurodegeneration (N) status were assessed at baseline and 2 years later using Florbetapir and 18 F‐FDG PET scans. wSW features (density and amplitude within delta and theta frequency bands) were extracted from 2 minutes of resting‐state high‐density EEG recordings (256 electrodes). ANOVA tests were performed on each EEG channel to compare wSW features based on 1) A and N status, and 2) transitions to A+ or N+ between the two sessions. All analyses were adjusted for age, sex, ApoE genotype and education level. Multiple comparisons were corrected using a cluster‐based permutation approach.

Result:

Compared to A‐N‐ participants, the other groups (A+N‐, n = 45; A‐N+, n = 44; and A+N+, n = 37) exhibited significantly lower delta wSW density. Moreover, A+N+ individuals showed significantly higher wSW amplitude in both delta and theta bands. Participants transitioning from A‐ to A+ over 2 years ( n = 16) had significantly higher wSW amplitude (delta and theta) than those remaining A‐, as well as compared to stable A+ individuals. Participants transitioning from N‐ to N+ ( n = 33) exhibited significantly lower delta wSW density compared to those remaining N‐.

Conclusion:

Our findings suggest that wSW features may serve as early EEG biomarkers for amyloid deposition and neurodegeneration in AD. These metrics, measurable during a simple and brief resting‐state EEG, show potential for identifying at‐risk individuals at very early stages of the disease, even before cognitive decline onset.

01 Dec 2025·Alzheimers & Dementia

The impact of AI correction on Centiloid in a same subject visual read comparison of ¹⁸ F‐Florbetapir and ¹⁸ F‐NAV4694 Aβ PET

Article

Author: Bourgeat, Pierrick ; Dore, Vincent ; Huang, Kun ; Feizpour, Azadeh ; Sutherland, Antony ; Toh, H. B. ; Poon, Aurora ; Kaewchur, Tawika ; Thientunyakit, Tanyaluck ; Villemagne, Victor L. ; Fripp, Jurgen ; Paranawithana, Ishara ; Rowe, Christopher C.

Abstract:

Background:

Visual read of Aβ PET remains standard clinical practice. 18 F‐NAV4694 (NAV) has high affinity for Aβ and low non‐specific binding so may be more accurate than older Aβ tracers. We compared visual read of NAV to 18 F‐Florbetapir (FBP) PET using standard and AI corrected Centiloid (CL) thresholds as gold standard.

Method:

150 participants (71.3±6.0 years) in the AIBL study underwent both scans within 2 years. Scans were read by 6 nuclear medicine physicians blinded to CL. Reader performance was compared against various CL thresholds. CL was measured with CapAIBL using a) the standard method, b) a composite cerebellum plus hemispheric white matter reference region for FBP and c) with an AI correction method for the CL SUVR (DeepSUVR). The DeepSUVR correction was learnt from a separate dataset of longitudinal scans where unexpected temporal changes were penalized and a tracer specific SUVR correction factor was developed for application to single scans.

Result:

CL frequency distribution graphs differed for NAV and FBP. Applying the DeepSUVR correction improved the correlation (R 2 ) between NAV and FBP CL from 0.82 to 0.94, predominantly by boosting many mid‐range FBP CL values and reducing FBP variance around zero CL (Figure 1). The FBP composite reference region had a similar though less marked effect. The thresholds that produced peak visual read accuracy with standard and DeepSUVR CL methods were 15CL and 11CL for NAV, and 29CL and 21CL for FBP (Figure 2). Mean sensitivity at peak accuracy thresholds was higher in NAV with 97% for standard and 96% for DeepSUVR methods compared to 93% for both methods in FBP. Mean specificity at the same thresholds was similar with 95% for NAV and FBP with standard CL while DeepSUVR produced a specificity of 97% for both tracers.

Conclusion:

Visual read of amyloid PET can accurately detect levels of amyloid below the traditional thresholds of 20 or 25CL for a positive scan. Visual read thresholds vary by tracer and reader experience. AI correction of CL with the DeepSUVR method significantly improves the performance of Florbetapir but NAV4694 remains more sensitive to low amyloid levels.

News (Medical) associated with Florbetapir F-18

09 Dec 2025

·pmlive.com

Novo Nordisk presents new findings on semaglutide in Alzheimer’s disease

Novo Nordisk has presented new findings from its phase 3 Evoke and Evoke+ trials on using semaglutide as part of Alzheimer’s disease (AD) treatment. The trials did not meet their primary endpoints; however, they still highlighted important biomarker findings. Semaglutide demonstrated reductions of up to 10% in biomarkers linked to AD and neuroinflammation that, despite not being a large enough change to have clinical impact, is still a notable result. Semaglutide is a glucagon-like peptide-1 (GLP-1) drug currently used in the treatment of type 2 diabetes, and as a weight management medication. Research into other possible indications of GLP-1 drugs is ongoing. There is high unmet medical need for treatment in AD, a progressive neurodegenerative disease which currently has no cure. The Alzheimer’s Drug Discovery Foundation (ADDF) made early investments in the science that led to the Evoke trials, stressing that the full pathophysiology of AD needs to be addressed in order to discover possible treatment. From 2011, the ADDF provided nearly $1m to Paul Edison’s phase 2 study of liraglutide, another injectable GLP-1 drug. Edison, a professor of neuroscience in the Faculty of Medicine at Imperial College London, said: “The metabolic pathway remains a compelling area of investigation, and we will continue to pursue rigorous studies to determine how therapies targeting these mechanisms can be optimised and combined to achieve greater impact for patients.” Founded in 1998, the ADDF is a foundation focused on accelerating the discovery and development of drugs to treat AD. It is the only public charity with this focus, and its funding has assisted in bringing to market the first Alzheimer’s PET scan (Amyvid) and blood test (PrecivityAD). “With more than 70% of the Alzheimer’s drug pipeline now focused on non-amyloid targets, the field is moving steadily toward an era of precision medicine and combination therapies,” said Howard Fillit, co-founder and chief science officer of the ADDF. “The Evoke trials are an important part of this progress, demonstrating how large-scale studies of novel pathways can deepen our understanding of Alzheimer’s biology.”

Phase 2Phase 3Clinical Result

13 Nov 2025

·www.prnewswire.com

Landmark JPAD Special Issue Highlights How Combination Therapies, Underpinned by New Era of Research, Are Poised to Redefine Alzheimer's Treatment

Innovative science convened by the Alzheimer's Drug Discovery Foundation is paving the way for a new, revolutionary era of precision care NEW YORK, Nov. 13, 2025 /PRNewswire/ -- The Journal of Prevention of Alzheimer's Disease (JPAD) today published a special edition in collaboration with the Alzheimer's Drug Discovery Foundation (ADDF), titled, "Combination Therapies for Alzheimer's Disease: Charting the Future of New Treatments and Prevention." This landmark issue builds upon the rapidly growing evidence that combination therapies will be essential to effectively treating Alzheimer's and provides a roadmap for advancing this critical research. "This JPAD issue arrives at a pivotal moment for the field," said Howard Fillit, MD, Co-Founder and Chief Science Officer at the ADDF. "The drug development landscape is changing, with multiple anti-amyloid therapies available and more than 70% of the Alzheimer's pipeline now aimed at novel targets informed by the disease's pathobiology. Alzheimer's is a complex condition that will ultimately require a precision approach, and it is crucial that we offer guidance to chart the path forward for a new generation of biomarker-powered clinical trials to evaluate drugs in combination." Combination therapies are already the gold standard in cancer care. The new JPAD edition provides a blueprint for expanding this approach to Alzheimer's disease and designing the next wave of combination trials – whether that be combining novel drugs with anti-amyloids, multiple novel drugs, or drugs with lifestyle interventions – to accelerate progress toward effective, personalized treatments. "With Alzheimer's science advancing at an unprecedented speed, this JPAD issue is especially timely," said Bruno Vellas, MD, PhD, President and Founder of IHU HealthAge in Toulouse. "The field is at a turning point – we now have the tools and the science to design the combination trials that will define the next era of Alzheimer's treatment. This issue provides the framework to do just that." Key highlights of the JPAD special issue include: Drug repurposing opportunities: Existing therapies from other disease areas, such as metabolic disease and schizophrenia, are being evaluated for use in Alzheimer's, opening new avenues for treatment. Integration of lifestyle interventions: Growing evidence from studies such as the landmark FINGER trial, led by Goodes Prize recipient Dr. Miia Kivipelto, demonstrates how combining drugs with diet, exercise, and other lifestyle changes can further prevent or slow disease progression. Emerging role of artificial intelligence: AI is increasingly being leveraged to identify promising drug combinations, optimize trial design, and accelerate discovery. Biomarker innovation: Developing and validating new biomarkers is essential to enable precision medicine and ensure patients receive the therapies most likely to benefit them as early as possible. "A critical next step is to further build out our biomarker guidance, as these tools will be vital to designing and running rigorous combination trials," said Suzanne Schindler, MD, PhD, Associate Professor of Neurology at the Washington University School of Medicine in St. Louis. "We now have multiple blood tests approved by the FDA to aid in Alzheimer's diagnosis, and this is only the beginning. Continuing to develop a diverse toolkit of biomarkers reflecting different pathologies and advancing digital technologies will be key to opening the door for precision care." There are already 20 ongoing trials evaluating combination therapy approaches in today's drug development pipeline, comprising 11% of all current trials. And many promising candidates remain on the horizon, including GLP-1 drugs like semaglutide. "We have entered a new era in Alzheimer's research, one that is embracing the complexity of the disease to build the foundations for personalized prevention and treatment," said Aaron Burstein, PharmD, Head of Search and Evaluation at the ADDF. "Combination therapy has already proven successful in other complex diseases, and this issue provides critical considerations for applying that strategy to Alzheimer's – offering hope for more effective treatments and better outcomes for patients worldwide." About The Alzheimer's Drug Discovery Foundation (ADDF) Founded in 1998 by Leonard A. and Ronald S. Lauder, the Alzheimer's Drug Discovery Foundation is dedicated to rapidly accelerating the development of drugs to prevent, treat, and cure Alzheimer's disease. The ADDF is the only public charity solely focused on funding the development of drugs for Alzheimer's, employing a venture philanthropy model to support research in academia and the biotech industry. The ADDF's leadership and contributions to the field have played a pivotal role in bringing the first Alzheimer's PET scan (Amyvid®) and blood test (PrecivityAD®) to market, as well as fueling the current robust and diverse drug pipeline. Through the generosity of its donors, the ADDF has awarded more than $370 million to fund 765 Alzheimer's drug development, biomarker, and prevention programs in 21 countries. To learn more, please visit: . SOURCE Alzheimer's Drug Discovery Foundation 21% more press release views with Request a Demo

Clinical Study

07 Oct 2025

·www.fiercebiotech.com

Lilly calls for \'urgent improvements\' in Europe to boost diagnostic testing for Alzheimer\'s

Eli Lilly says Alzheimer\'s disease experts are warning the disease “remains critically underdiagnosed\" across Europe. \n Eli Lilly is calling on European countries to make “urgent improvements” to their Alzheimer’s disease diagnostic testing practices just weeks after nabbing a new approval on the continent for its Alzheimer\'s therapy Kisunla.The Indianapolis Big Pharma has teamed up with leading Alzheimer\'s experts at this year\'s Alzheimer Europe Conference to call for “urgent improvements to diagnostic pathways to ensure people in Europe can benefit from new therapeutic innovation.”Lilly points to a recent survey, published in the Journal of Alzheimer’s Disease, that found 70% of clinicians believe biomarker tests, which can find evidence of Alzheimer\'s or dementia, are “important or extremely important.\" Still, such tests remain \"underutilized,\" according to Lilly\'s Oct. 7 release.The survey questioned clinicians who treat patients with mild cognitive impairment (MCI) and Alzheimer\'s in France, Germany, Italy, Spain, the U.K., Japan and the U.S. The team found that across these countries, fewer than 1 in 5 patients (15.2%) received biomarker testing to confirm the specific pathology, with those in Germany and the U.K. the least likely to receive these tests, according to the journal.As a result, experts warn Alzheimer\'s and dementia “remain critically underdiagnosed,” Lilly said in the release, which has the effect of \"denying patients the opportunity to access treatment and care options.\"Lilly markets Kisunla, which works as an amyloid-plaque-targeting therapy and has an FDA approval for early symptomatic Alzheimer\'s, which includes the MCI or the mild dementia stages of the disease.The drug was approved by the FDA last year and received a final European sign-off just last month.To qualify for the drugs, patients must have a confirmed amyloid pathology, which can be done via several routes including a PET scan, a blood test or an MRI.Lilly also markets Amyvid, which works as an injectable prescription imaging agent to find high level of plaques. These are a buildup of a protein called amyloid beta in the brain that, if found, can be ultimately used by patients or their doctors to help prescribe Alzheimer\'s meds such as Kisunla. More diagnoses of Alzheimer\'s also mean potentially more uptake for medicines. Rival drug Leqembi, marketed by Biogen and Eisai, was also approved in the EU earlier this year.“Emerging therapies that target the pathology of Alzheimer\'s disease offer hope to slow progression and delay the need for care services,” said Stéphane Epelbaum, M.D., Ph.D., associate vice president for international medical affairs at Eli Lilly, in a statement.“But this possibility hinges on early detection, as approximately one-third of individuals in early symptomatic stages of the disease will progress to more advanced clinical stages within one year. Timely and accurate diagnosis is essential to ensure patients can access the next generation of Alzheimer\'s disease care.”

$Lilly calls for \'urgent improvements\' in Europe to boost diagnostic testing for Alzheimer\'s$

Drug Approval

100 Deals associated with Florbetapir F-18

External Link

KEGG	Wiki	ATC	Drug Bank
D09617	Florbetapir F-18	V09AX05	DB09149

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Alzheimer Disease	European Union	Eli Lilly Nederland BV	14 Jan 2013
Alzheimer Disease	Iceland	Eli Lilly Nederland BV	14 Jan 2013
Alzheimer Disease	Liechtenstein	Eli Lilly Nederland BV	14 Jan 2013
Alzheimer Disease	Norway	Eli Lilly Nederland BV	14 Jan 2013
Contrast agents	United States	Avid Radiopharmaceuticals, Inc.	06 Apr 2012

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Dementia due to Alzheimer's disease (disorder)	Phase 3	China	JYAMS PET Research & Development Ltd.	20 Oct 2022
Cognitive Dysfunction	Phase 3	United States	Avid Radiopharmaceuticals, Inc.	01 Jul 2011
Mild cognitive disorder	Phase 3	-	Avid Radiopharmaceuticals, Inc.	01 Feb 2011
Chronic Traumatic Encephalopathy	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Jun 2014
Lewy Body Disease	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Mar 2010
Striatonigral Degeneration	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Mar 2010
Frontotemporal Dementia	Phase 2	United Kingdom	Avid Radiopharmaceuticals, Inc.	01 Sep 2009
Parkinson Disease	Phase 2	United States	Avid Radiopharmaceuticals, Inc.	01 Jan 2009

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04118764 (CTgov)	Not Applicable	Alzheimer Disease	6	Neuronavigation-guided single-element focused ultrasound transducer+Amyvid+Definity	eligvcxmss = pyxnfvxqkw qiyldynsiw (dxfemyywxf, hvawiqwjpe - raykbrmjtx) View more	-	26 Aug 2024
NCT03977584 (CTgov)	Phase 2	Alzheimer Disease	114	Crenezumab (Crenezumab - Mutation Carriers)	srzpvbueee(tqiljejotn) = einaxfsnca xppcrffzmr (quvrjneqab, 0.00752) View more	-	15 Mar 2024
NCT03977584 (CTgov)	Phase 2	Alzheimer Disease	114	placebo+\[\^18F\]GTP1+crenezumab (Placebo - Mutation Carriers)	srzpvbueee(tqiljejotn) = ylzwvqefcy xppcrffzmr (quvrjneqab, 0.00768)	-	15 Mar 2024
NCT01683825 (CTgov)	Phase 4	Senile cardiac amyloidosis	23	florbetapir+F	btebbzyqjo(jnzzjcuwgj) = mjklsuwuzj bqqvkqwqgm (sqrirnrrsf, djmcoduozs - bvwjcimpey) View more	-	13 Apr 2022
NCT01767493 (CTgov)	Phase 4	Multiple Sclerosis, Relapsing-Remitting	19	[18F]Florbetapir PET imaging	shwnmltzdi = apgultuseu taihlpujvl (tmbxxpftbc, fbmrsqsuxk - nzzcezmlag) View more	-	27 Aug 2021
NCT01518374 (CTgov)	Phase 2	Alzheimer Disease \| Mild cognitive disorder	1,768	Florbetapir F 18	gqehpidybc = trmslebrbj cpzhzaqrvz (dxqamkpvyy, yuxvumfnez - alacpwrckd) View more	-	14 Jun 2018
NCT02051790 (CTgov)	Phase 4	Alzheimer Disease	241	florbetapir F 18	rupvlyggkp = zrcqkouapv zfncaterod (ncbltzgsgs, qganykerol - eegyuwnfbs) View more	-	28 Sep 2015
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F+18F-FDG (Frontotemporal Disorder)	vuwkodoqgm = tbwzbmmhqh maftocyhlt (btfqqbukga, uhfgdcxeup - pfurtsyvhf) View more	-	17 Sep 2014
NCT01890343 (CTgov)	Phase 2	Alzheimer Disease \| Frontotemporal Dementia	34	florbetapir 18F (Cognitively Normal)	vuwkodoqgm = orxlcedywv maftocyhlt (btfqqbukga, vtqfpvhaui - rckuwqbsxr) View more	-	17 Sep 2014
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (AD Subjects)	lizjifevdp = jnnjrynist esjdwmrlmc (bgutcztunc, nbbcmsqsid - wjlxlfeavc) View more	-	19 Sep 2013
NCT01662882 (CTgov)	Phase 2/3	Alzheimer Disease \| Mild cognitive disorder	48	florbetapir (18F) (Healthy Controls)	lizjifevdp = ugxhjniaef esjdwmrlmc (bgutcztunc, vlkzukouix - bimwbzrfju) View more	-	19 Sep 2013
NCT00857415 \| NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	Florbetapir PET imaging	xwjpxuyzet(vikoznaooi) = sfmxhcsawm tsjyswuqoq (kxckhpxnko, 78 - 98) View more	-	01 Aug 2012
NCT00857415 \| NCT01447719 (Pubmed \| Lancet Neurol)	Phase 3	Plaque, Amyloid	59	florbetapir (Autopsy)	xwjpxuyzet(vikoznaooi) = oldjmjjrln tsjyswuqoq (kxckhpxnko, 80 - 100) View more	-	01 Aug 2012
NCT01565382 (CTgov)	Phase 3	Alzheimer Disease \| Mild cognitive disorder	40	Florbetapir	iaryitsfqj = nfuhrobyog vyerksgimh (yaplvttgzz, ybbllqoowb - dggcyzjaid) View more	-	27 Jun 2012

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