Beta Amyloid in AD

A precise diagnostic tool is needed to reduce the time to accurate diagnosis

Diagnostic assessment of cognitive impairment during life is improved by detecting the presence or absence of β-amyloid neuritic plaques in the brain.

  • Structural imaging with MRI may not detect early disease or clearly distinguish the etiology of neuronal changes2

  • FDG-PET may not be able to detect cortical hypometabolism until several years after detectable β-amyloid pathology has occurred, and may not clarify the reason for the hypometabolism3,4

  • Structural and metabolic changes remain surrogate rather than direct markers of dementia pathology4

  • Determining if cognitive decline is due to AD relies on detecting the presence of β-amyloid neuritic plaques

  • β-amyloid neuritic plaques accumulate early, before the onset of symptoms—but historically could only be visualized via post-mortem histopathology1

  • Symptoms alone make the diagnostic interpretation challenging: up to 39% of patients will not have a typical cognitive profile and disparities across cognitive domains occur even between “typical” patients5

A typical patient experiences symptoms for >2 years and visits an average of 2.3 doctors before receiving a diagnosis6

Negative and positive scans with Neuraceq® help you clarify the clinical picture and plan the path ahead

Neuraceq® delivers valuable information for greater confidence in diagnosis and more personalized patient management.

  • Negative Neuraceq® PET scans allow you to consider alternative causes of cognitive impairment

  • A positive Neuraceq® PET scan indicates moderate to frequent amyloid neuritic plaques; neuropathological examination has shown this amount of amyloid neuritic plaque is present in patients with AD, but may also be present in patients with other types of neurologic conditions as well as older people with normal cognition7

  • Neuraceq® is an adjunct to other diagnostic evaluations and enables physicians and patients to plan accordingly

  • The safety and efficacy of Neuraceq® has not been fully established for the prediction of the development of dementia or other neurologic conditions and is not authorized for therapy monitoring

  • Symptoms alone make the diagnostic interpretation challenging: up to 39% of patients will not have a typical cognitive profile and disparities across cognitive domains occur even between “typical” patients3

FDG-PET, fludeoxyglucose positron emission tomography; MRI, magnetic resonance imaging. 1Fodero-Tavoletti MT, Brockschnieder D, Villemagne VL, et al. In vitro characterization of [18F]-florbetaben, an AB imaging radiotracer. Nucl Med Biol. 2012;39(7):1042-1048. 2Bloudek LM, Spackman DE, Blankenburg M, Sullivan SD. Review and meta-analysis of biomarkers and diagnostic imaging in Alzheimer’s disease. J Alzheimers Dis. 2011;26(4):627-645 3Prestia A, Caroli A, van der Flier WM, et al. Prediction of dementia in MCI patients based on core diagnostic markers for Alzheimer’s disease. Neurology. 2013;80(11):1048-1056. 4Mosconi L, Berti V, Glodzik L, Pupi A, DeSanti S, de Leon MJ. Pre-clinical detection of Alzheimer’s disease using FDG-PET, with or without amyloid imaging. J Alzheimers Dis. 2010;20(3)843-854 5Snowden JS, Stopford CL, Julien CL, et al. Cognitive phenotypes in Alzheimer’s disease and genetic risk. Cortex. 2007;43(7):835-845. 6Grossberg GT, Christensen DD, Griffith PA, Kerwin DR, Hung G, Hall EJ. The art of sharing the diagnosis and management of Alzheimer’s disease with patients and caregivers: recommendations of an expert consensus panel. Prim Care Companion J Clin Psychiatry. 2010;12:PCC.09cs00833. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882814, Accessed January 22, 2014. 7Neuraceq® (florbetaben F18 injection) prescribing information. Life Molecular Imaging; April 2025. Fareham, UK.