Imaging of amyloid β in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism

  title={Imaging of amyloid $\beta$ in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism},
  author={Christopher C. Rowe and Uwe Ackerman and William Browne and Rachel S. Mulligan and Kerryn L Pike and Graeme J. O'Keefe and Henry Tochon-Danguy and Gordon Chan and Salvatore U. Berlangieri and Gareth Jones and Kerryn L Dickinson-Rowe and Hank P Kung and Wei Zhang and Mei-Ping T. Kung and Daniel M. Skovronsky and Thomas Dyrks and Gerhard Holl and Sabine Krause and Matthias Friebe and Lutz Lehman and Stefanie Lindemann and Ludger M. Dinkelborg and Colin L. Masters and Victor L. Villemagne},
  journal={The Lancet Neurology},

Individualized quantification of brain β-amyloid burden: results of a proof of mechanism phase 0 florbetaben PET trial in patients with Alzheimer’s disease and healthy controls

Results indicate florbetaben to be a safe and efficacious β-amyloid-targeted tracer with favourable brain kinetics, which appeared valuable as a surrogate marker of disease severity.

Amyloid imaging in Alzheimer's disease: comparison of florbetapir and Pittsburgh compound-B positron emission tomography

These data support the hypothesis that florbetapir-F18 provides comparable information with Pittsburgh Compound-B, and show highly significant group discrimination and correlation of regional uptake.

In Vivo Imaging of Amyloid Deposition in Alzheimer Disease Using the Radioligand 18F-AV-45 (Flobetapir F 18)

18F-AV-45 was well tolerated, and PET showed significant discrimination between AD patients and HCs, using either a parametric reference region method (DVR) or a simplified SUVR calculated from 10 min of scanning 50–60 min after 18F- AV-45 administration.

Amyloid Imaging in Alzheimer’s Disease and Other Dementias

Observations suggest that Aβ deposition is not part of normal ageing, supporting the hypothesis that Αβ deposition occurs well before the onset of symptoms and is likely to represent preclinical AD.

Performance Characteristics of Amyloid PET with Florbetapir F 18 in Patients with Alzheimer's Disease and Cognitively Normal Subjects

Florbetapir F 18 appears to have a wide effective dose range and a high test–retest reliability for both quantitative (SUVr) values and visual assessment of the ligand, and these imaging performance properties provide important technical information on the use of florbetapIR F 18 and PET to detect cerebral amyloid aggregates.

18F-labeled radiopharmaceuticals for the molecular neuroimaging of amyloid plaques in Alzheimer's disease.

Molecular imaging of beta-amyloid deposits, with positron emission tomography (PET) and 18F-labeled radiopharmaceuticals such as 18f-florbetapir,18F- florbetaben, and 18 F-flutemetamol, has emerged as potential powerful tool for aiding AD diagnosis.

FDG- and amyloid-PET in Alzheimer's disease: is the whole greater than the sum of the parts?

  • L. MosconiP. McHugh
  • Biology
    The quarterly journal of nuclear medicine and molecular imaging : official publication of the Italian Association of Nuclear Medicine (AIMN) [and] the International Association of Radiopharmacology (IAR), [and] Section of the Society of...
  • 2011
The potential of combining symptoms-sensitive FDG-PET measures with pathology-specific Aβ-PET to improve the early detection of AD is discussed.

18F-Florbetaben Amyloid PET Imaging: A Chinese Study in Cognitive Normal Controls, Mild Cognitive Impairment, and Alzheimer’s Disease Patients

18F-FBB is a useful tracer for the evaluation of amyloid-β deposition in vivo and that global SUVR of 18F- FBB PET might be a reliable tool in the diagnosis of AD is suggested.



In-vivo imaging of Alzheimer disease beta-amyloid with [11C]SB-13 PET.

  • N. VerhoeffAlan A. Wilson S. Houle
  • Biology, Medicine
    The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry
  • 2004
Preliminary PET data indicate that [11C]SB-13 is an effective PET tracer for fibrillar Abeta imaging in vivo, with similar performance as [ 11C]PIB, and the two radiotracers demonstrated similar binding properties.

β-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease

Abeta deposition in the asymptomatic elderly is associated with episodic memory impairment, and this finding, together with the strong relationship between PIB binding and the severity of memory impairment in MCI, suggests that individuals with increased cortical P IB binding are on the path to Alzheimer's disease.

Kinetic Modeling of Amyloid Binding in Humans using PET Imaging and Pittsburgh Compound-B

  • J. PriceW. Klunk C. Mathis
  • Medicine, Biology
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2005
It was shown that it is feasible to perform quantitative PIB PET imaging studies that are needed to validate simpler methods for routine use across the AD disease spectrum and the Logan analysis was the method-of-choice for the PIBPET data as it proved stable, valid, and promising for future larger studies and voxel-based statistical analyses.

Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B

The results suggest that PET imaging with the novel tracer, PIB, can provide quantitative information on amyloid deposits in living subjects.

11C-PIB PET imaging in Alzheimer disease and frontotemporal lobar degeneration

PET imaging with 11C-labeled Pittsburgh Compound-B (11C-PIB) helps discriminate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD).

Imaging β-amyloid burden in aging and dementia

Pittsburgh Compound B PET findings match histopathologic reports of β-amyloid (Aβ) distribution in aging and dementia, and suggest that Aβ may influence the development of dementia with Lewy bodies, and therefore strategies to reduce A β may benefit this condition.

PIB is a non-specific imaging marker of amyloid-beta (Abeta) peptide-related cerebral amyloidosis.

The data provide a molecular explanation for PIB's limited specificity in diagnosing and monitoring disease progression in AD and instead indicate that the ligand is primarily a non-specific marker of Abeta-peptide related cerebral amyloidosis.

PET of brain amyloid and tau in mild cognitive impairment.

FDDNP-PET scanning can differentiate persons with mild cognitive impairment from those with Alzheimer's disease and those with no cognitive impairment, and this technique is potentially useful as a noninvasive method to determine regional cerebral patterns of amyloid plaques and tau neurofibrillary tangles.