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I n t e r n a t i o n a l C o n f e r e n c e o n
Nuclear Medicine &
Radiation Therapy
Journal of Medical Physics and Applied Sciences
ISSN: 2574-285X
O c t o b e r 0 1 - 0 2 , 2 0 1 8
S t o c k h o l m , S w e d e n
Nuclear Medicine & Radiation Therapy 2018
Page 16
Biography
Stephens AndrewWhas received anMD and a PhD in Biochem-
istry, Biophysics and Genetics from the University of Colorado.
He was Board certified in Internal Medicine and had a Clinical
Practice before entering Pharmaceutical Development. He is
a Founder and the Chief Medical Officer at Piramal Imaging,
GmbH, responsible for all clinical research and development
activities including the approval of
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F-florbetaben (NeuraCeq).
He has more than 25 years of experience in the Pharmaceu-
tical Industry, primarily in the areas of translational medicine,
and diagnostic imaging of neurodegenerative, oncological and
cardiovascular diseases. He began his pharmaceutical industry
career investigating RNA Aptamers at NeXagen/NeXstar, and
Gilead. As a Senior Director of Translational Medicine at OSI
Pharmaceuticals, he was responsible for early clinical studies
of a number of anti-cancer oral signal transduction inhibitors.
Most recently, he was VP, Head of Experimental Medicine On-
cology/Diagnostic Imaging for Bayer Pharma.
andrew.stephens@piramal.comPET imaging of proteinopathies in
neurodegenerative disease
Andrew W Stephens
Life Molecular Imaging GmbH, Germany
Andrew W Stephens, J. med phys & appl sci 2018, Volume: 3
DOI: 10.21767/2574-285X-C1-001
T
raditional nuclear medicine ligands were designed to target cellular receptors
or transporters with a binding pocket and a defined structure activity
relationship. More recently, tracers have been developed to target pathological
protein aggregations. Aggregations of proteins such as tau, α-synuclein, and
β-amyloid (Aβ) have been identified in neurodegenerative diseases, including
Alzheimer’s disease (AD) and other dementias, and Parkinson’s disease (PD).
Indeed, Aβ deposition is a hallmark of AD, and detection methods have evolved
from coloured dyes to modern
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F-labelled positron emission tomography (PET)
tracers. Such tracers are becoming increasingly established in routine clinical
practice for evaluation of Aβ neuritic plaque density in the brains of adults who are
being evaluated for AD and other causes of cognitive impairment. While similar
in structure, there are key differences between the available compounds in terms
of dosing/dosimetry, pharmacokinetics, and interpretation of visual reads. In the
future, quantification of Aβ-PET may further improve its utility. Tracers are now
being developed for evaluation of tau protein, which is associated with decreased
cognitive function and neurodegenerative changes in AD, and is implicated in the
pathogenesis of other neurodegenerative diseases. While no compound has yet
been approved for tau imaging in clinical use, it is a very active area of research.
Development of tau tracers comprises in-depth characterisation of existing
radiotracers, clinical validation, a better understanding of uptake patterns, test-
retest/dosimetry data, and neuropathological correlations with PET. Tau imaging
may allow early, more accurate diagnosis, and monitoring of disease progression,
in a range of conditions. In conclusion, several PET tracers for detection of
pathological protein depositions are now available for clinical use, particularly
PET tracers that bind to Aβ plaques. Tau-PET tracers are currently in clinical
development. These tracers will continue to change our understanding of complex
disease processes.