Canna~Fangled Abstracts

Alternative approaches for PET radiotracer development in Alzheimer's disease: imaging beyond plaque

By December 12, 2013No Comments
 [Epub ahead of print]

pm8Alternative approaches for PET radiotracer development in Alzheimer’s disease: imaging beyond plaque.

Source

Division of Nuclear Medicine and Molecular Imaging, Massachusetts General Hospital, Department of Radiology, Harvard Medical School, 55 Fruit St., White 427, Boston, Massachusetts, 02114, USA; Life Sciences, Australian Nuclear Science and Technology Organisation, Kirrawee, New South Wales, 2232, Australia.

Abstract

Alzheimer’s disease (AD) and related dementias show increasing clinical prevalence, yet our understanding of the etiology and pathobiology of disease-related neurodegeneration remains limited. In this regard, noninvasive imaging with radiotracers for positron emission tomography (PET) presents a unique tool for quantifying spatial and temporal changes in characteristic biological markers of brain disease and for assessing potential drug efficacy. PET radiotracers targeting different protein markers are being developed to address questions pertaining to the molecular and/or genetic heterogeneity of AD and related dementias. For example, radiotracers including [11 C]-PiB and [18 F]-AV-45 (Florbetapir) are being used to measure the density of Aβ-plaques in AD patients and to interrogate the biological mechanisms of disease initiation and progression. Our focus is on the development of novel PET imaging agents, targeting proteins beyond Aβ-plaques, which can be used to investigate the broader mechanism of AD pathogenesis. Here, we present the chemical basis of various radiotracers which show promise in preclinical or clinical studies for use in evaluating the phenotypic or biochemical characteristics of AD. Radiotracers for PET imaging neuroinflammation, metal ion association with Aβ-plaques, tau protein, cholinergic and cannabinoidreceptors, and enzymes including glycogen-synthase kinase-3β and monoamine oxidase B amongst others, and their connection to AD are highlighted. Copyright © 2013 John Wiley & Sons, Ltd.
Copyright © 2013 John Wiley & Sons, Ltd.

KEYWORDS:

Alzheimer’s disease, Aβ plaque, FAAH, GSK-3β, MAO-B, acetyl cholinesterase, metals, neuroinflammation, positron emission tomography (PET), tau

PMID:

 

24327420

 

[PubMed – as supplied by publisher]