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Issue title: Imaging the Alzheimer Brain
Guest editors: J. Wesson Ashford, Allyson Rosen, Maheen Adamson, Peter Bayley, Osama Sabri, Ansgar Furst, Sandra E. Black and Michael Weiner
Article type: Research Article
Authors: Shin, Jonghana; b; c | Kepe, Vladimirb | Barrio, Jorge R.b | Small, Gary W.c; *
Affiliations: [a] Neuroscience Research Institute, Gachon University of Medicine and Science, Incheon, Republic of Korea | [b] Department of Molecular and Medical Pharmacology, The University of California, Los Angeles David Geffen School of Medicine, Los Angeles, CA, USA | [c] Department of Psychiatry and Biobehavioral Sciences and Semel Institute for Neuroscience and Human Behavior, The University of California, Los Angeles David Geffen School of Medicine, Los Angeles, CA, USA
Correspondence: [*] Correspondence to: Gary W. Small, M.D., Department of Psychiatry and Biobehavioral Sciences and Semel Institute for Neuroscience and Human Behavior, The University of California, Los Angeles David Geffen School of Medicine, Los Angeles, CA 90095 6948, USA. Tel.: +310 825 0291; Fax: +310 825 3910; E-mail: [email protected].
Abstract: 2-(1-{6-[(2-[fluorine-18]fluoroethyl)(methyl)amino]-2-naphthyl}-ethylidene)malononitrile (FDDNP) is the first positron emission tomography (PET) molecular imaging probe to visualize Alzheimer's disease (AD) pathology in living humans. The most unique features of FDDNP are that (1) it is the only currently available radiotracer to image neurofibrillary tangles, beside amyloid aggregates, in living humans; and (2) it is also the only radiotracer to visualize AD pathology in the hippocampal region of living humans. In this article, we discuss FDDNP's unique ability to image tau pathology in living humans. Emphasizing tau pathology imaging capability using FDDNP in AD, as well as other tauopathies, is timely and beneficial considering that (1) post mortem histopathological studies using human specimens have consistently demonstrated that neurofibrillary tangles, compared with amyloid plaques, are better correlated with the disease severity and neuronal death; and (2) recently reported clinical trial failures of disease-modifying drugs in development, based on the amyloid-cascade hypothesis, suggest that some of the basic assumptions of AD causality warrant reassessment and redirection.
DOI: 10.3233/JAD-2011-0008
Journal: Journal of Alzheimer's Disease, vol. 26, no. s3, pp. 135-145, 2011
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