Amyloid Imaging: Poised for Integration into Medical Practice

Abstract

Amyloid imaging represents a significant advance as an adjunct in the diagnosis of Alzheimer's disease (AD) because it is the first imaging modality that identifies in vivo changes known to be associated with the pathogenesis. Initially, 11 C-PIB was developed, which was the prototype for many 18 F compounds, including florbetapir, florbetaben, and flutemetamol, among others. Despite the high sensitivity and specificity of amyloid imaging, it is not commonly used in clinical practice, mainly because it is not reimbursed under current Center for Medicare and Medicaid Services guidelines in the USA. To guide the field in who would be most appropriate for the utility of amyloid positron emission tomography, current studies are underway [Imaging Dementia Evidence for Amyloid Scanning (IDEAS) Study] that will inform the field on the utilization of amyloid positron emission tomography in clinical practice. With the advent of monoclonal antibodies that specifically target amyloid antibody, there is an interest, possibly a mandate, to screen potential treatment recipients to ensure that they are suitable for treatment. In this review, we summarize progress in the field to date.

MR elastography detection of early viscoelastic response of the murine hippocampus to amyloid β accumulation and neuronal cell loss due to Alzheimer's disease

“…Such histopathological changes cannot be detected early enough with conventional neuroimaging methods, leading to delayed diagnosis and hence ineffective treatment. At present, AD can only be diagnosed by a combination of multiple modalities, including MRI, [18F]‐fluorodeoxyglucose positron emission tomography (PET), cerebrospinal fluid biomarkers, clinical memory tests, and Amyloid‐PET . After diagnosis, medication to increase levels of glutamatergic and cholinergic neurotransmitters, regular physical exercise, as well as the involvement in daily life problem‐solving are known to decelerate disease progression .…”

“…At present, AD can only be diagnosed by a combination of multiple modalities, including MRI, [18F]-fluorodeoxyglucose positron emission tomography (PET), cerebrospinal fluid biomarkers, clinical memory tests, and Amyloid-PET. 25,26 After diagnosis, medication to increase levels of glutamatergic and cholinergic neurotransmitters, 27 regular physical exercise, as well as the involvement in daily life problem-solving are known to decelerate disease progression. 27,28 In animal studies, this physical and cognitive stimulation is induced by large environmentally enriched cages (ENR) with changing interior arrangements and larger animal groups.…”

An Appraisal of Novel Biomarkers for Evaluating and Monitoring Neurologic Diseases: Editorial Introduction

“…Tau and amyloid are being imaged in ongoing clinical trials in Alzheimer's disease (AD) [6][7][8]; it remains to be seen whether changes in protein burden correlate well with changes in clinical phenotype. However, such imaging studies have already enhanced our understanding of the distribution of disease burden in patients with AD, as well as the potential for therapeutic agents to ameliorate accumulation.…”

“…With respect to fluid markers, rapid developments are occurring in ALS, AD, and inflammatory neurological diseases [6,7,14,15]. In ALS, markers under current development probably reflect cell death or response to stress rather than specific disease pathways.…”

Neuroimaging in Dementias

“…The first of these was F-18 florbetapir (Amyvid, Avid Radiopharmaceuticals, Inc. and Eli Lilly and Company), approved in 2012, followed in subsequent years by F-18 flutemetamol (Vizamyl, GE Healthcare), and then F-18 florbetaben (Neuraceq, Piramal Life Science), all of which share the benefit of a longer half-life of 110 minutes from F-18. 52 F-18 florbetapir has been the most widely utilized radioligand, and its ability to reliably bind Aβ plaques has been validated with autopsy, with a sensitivity of 92% and specificity of 96% in the detection of moderate to frequent amyloid plaques. 53 Comparison of F-18 florbetapir with C-11 PiB compound in a cohort of patients who underwent imaging with both radioligands demonstrated similar highly significant group discrimination and correlation of regional uptake for both tracers.…”