Page 57 - TI Journal 18-1

Technology and Innovation, Vol. 18, pp. 51-61, 2016 ISSN 1949-8241 • E-ISSN 1949-825X
Printed in the USA. All rights reserved. http://dx.doi.org/10.21300/18.1.2016.51
Copyright © 2016 National Academy of Inventors. www.technologyandinnovation.org

USING PITTSBURGH COMPOUND B FOR PET IMAGING ACROSS

THE ALZHEIMER’S DISEASE SPECTRUM

Ann D. Cohen

Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

Use of biomarkers in the detection of early and preclinical Alzheimer’s disease (AD) has
become of central importance for the diagnosis of AD, mild cognitive impairment (MCI), and
preclinical AD following publication of the NIA-Alzheimer’s Association revised criteria for
diagnosis across the spectrum of AD pathogenesis. The use of in vivo PET amyloid imaging
agents, such as Pittsburgh Compound-B, allows early detection of AD pathological processes
and subsequent neurodegeneration. Imaging with PiB provides early, or perhaps even preclin-
ical, detection of disease and accurately distinguishes AD from dementias of other etiologies
in which the diagnostic distinction is difficult to make clinically. From a research perspective,
utilizing amyloid imaging agents allows us to study relationships between amyloid pathology
and changes in cognition, brain structure, and function across the continuum from normal
aging to MCI to AD. The present review focuses on use of PiB-PET across the spectrum of
AD pathogenesis.
Key words: Amyloid; Alzheimer’s disease; Pittsburgh Compound B; Neuroimaging

Alzheimer’s disease (AD) is the most common aminophenyl)-6-hydroxybenzothiazole (33)), is
cause of dementia and is pathologically characterized a thioflavin-T (ThT) derivative, a small molecule
by the presence of amyloid plaques containing amy- known to bind amyloid proteins aggregated into a
loid-beta (Aβ) and neurofibrillary tangles containing beta-pleated sheet structure (31). The development of
hyperphosphorylated tau, as well as significant loss of amyloid imaging PET tracers, such as PiB, have made
neurons and deficits in neurotransmitter systems. The the in vivo imaging of amyloid possible, with striking
“amyloid cascade hypothesis” points to deposition of differences in PiB retention observed between control
Aβ plaques as a central event in the pathogenesis of and AD subjects in brain areas known to contain sig-
AD (16,18). This states that overproduction of Aβ, or nificant amyloid deposits in AD (e.g., frontal cortex
failure to clear this peptide, leads to AD primarily and parietal cortex).
through amyloid deposition, by way of the produc- Imaging AD pathology, using amyloid PET imag-
tion of NFT, cell death, and, ultimately, the clinical ing agents such as PiB, has several potential clinical
symptoms such as memory loss and other domains benefits, including preclinical detection of disease
of cognitive impairment (17). and accurately distinguishing AD from non-AD
Pittsburgh Compound-B (PiB), also known as dementia in patients with mild or atypical symp-
[ C]6-OH-BTA-1 or [N-methyl- C]2-(4’-methyl- toms or confounding comorbidities (in which the
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Accepted December 10, 2015.
Ann D. Cohen, Ph.D., 1406 Western Psychiatric Institute and Clinic, 3811 O’Hara Street, Pittsburgh, PA 15213, USA. Tel: +1 (412) 246-6251;
Fax: +1 (412) 246-6466; E-mail: cohenad@upmc.edu

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