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      Characteristics of Tau and Its Ligands in PET Imaging

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          Abstract

          Tau deposition is one of the neuropathological hallmarks in Alzheimer’s disease as well as in other neurodegenerative disorders called tauopathies. Recent efforts to develop selective tau radiopharmaceuticals have allowed the visualization of tau deposits in vivo. In vivo tau imaging allows the assessment of the regional distribution of tau deposits in a single human subject over time for determining the pathophysiology of tau accumulation in aging and neurodegenerative conditions as well as for application in drug discovery of anti-dementia drugs as surrogate markers. However, tau deposits show complicated characteristics because of different isoform composition, histopathology, and ultrastructure in various neurodegenerative conditions. In addition, since tau radiopharmaceuticals possess different chemotype classes, they may show different binding characteristics with heterogeneous tau deposits. In this review, we describe the characteristics of tau deposits and their ligands that have β-sheet binding properties, and the status of tau imaging in clinical studies.

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          Most cited references79

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          Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease.

          P Arriagada, J H Growdon, E T Hedley-Whyte … (1992)
          We studied the accumulation of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 10 Alzheimer's disease patients who had been examined during life. We counted NFTs and SPs in 13 cytoarchitectural regions representing limbic, primary sensory, and association cortices, and in subcortical neurotransmitter-specific areas. The degree of neuropathologic change was compared with the severity of dementia, as assessed by the Blessed Dementia Scale and duration of illness. We found that (1) the severity of dementia was positively related to the number of NFTs in neocortex, but not to the degree of SP deposition; (2) NFTs accumulate in a consistent pattern reflecting hierarchic vulnerability of individual cytoarchitectural fields; (3) NFTs appeared in the entorhinal cortex, CA1/subiculum field of the hippocampal formation, and the amygdala early in the disease process; and (4) the degree of SP deposition was also related to a hierarchic vulnerability of certain brain areas to accumulate SPs, but the pattern of SP distribution was different from that of NFT.
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            Tau-mediated neurodegeneration in Alzheimer's disease and related disorders.

            Carlo Ballatore, Virginia M-Y Lee, John Trojanowski (2007)
            Advances in our understanding of the mechanisms of tau-mediated neurodegeneration in Alzheimer's disease (AD) and related tauopathies, which are characterized by prominent CNS accumulations of fibrillar tau inclusions, are rapidly moving this previously underexplored disease pathway to centre stage for disease-modifying drug discovery efforts. However, controversies abound concerning whether or not the deleterious effects of tau pathologies result from toxic gains-of-function by pathological tau or from critical losses of normal tau function in the disease state. This Review summarizes the most recent advances in our knowledge of the mechanisms of tau-mediated neurodegeneration to forge an integrated concept of those tau-linked disease processes that drive the onset and progression of AD and related tauopathies.
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              Primary age-related tauopathy (PART): a common pathology associated with human aging.

              John F Crary, John Q Trojanowski, Julie A Schneider … (2014)
              We recommend a new term, "primary age-related tauopathy" (PART), to describe a pathology that is commonly observed in the brains of aged individuals. Many autopsy studies have reported brains with neurofibrillary tangles (NFTs) that are indistinguishable from those of Alzheimer's disease (AD), in the absence of amyloid (Aβ) plaques. For these "NFT+/Aβ-" brains, for which formal criteria for AD neuropathologic changes are not met, the NFTs are mostly restricted to structures in the medial temporal lobe, basal forebrain, brainstem, and olfactory areas (bulb and cortex). Symptoms in persons with PART usually range from normal to amnestic cognitive changes, with only a minority exhibiting profound impairment. Because cognitive impairment is often mild, existing clinicopathologic designations, such as "tangle-only dementia" and "tangle-predominant senile dementia", are imprecise and not appropriate for most subjects. PART is almost universally detectable at autopsy among elderly individuals, yet this pathological process cannot be specifically identified pre-mortem at the present time. Improved biomarkers and tau imaging may enable diagnosis of PART in clinical settings in the future. Indeed, recent studies have identified a common biomarker profile consisting of temporal lobe atrophy and tauopathy without evidence of Aβ accumulation. For both researchers and clinicians, a revised nomenclature will raise awareness of this extremely common pathologic change while providing a conceptual foundation for future studies. Prior reports that have elucidated features of the pathologic entity we refer to as PART are discussed, and working neuropathological diagnostic criteria are proposed.
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                Author and article information

                Contributors
                Claude M. Wischik: Role: Academic Editor
                Charles Harrington: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Biomolecules
                Journal ID (iso-abbrev): Biomolecules
                Journal ID (publisher-id): biomolecules
                Title: Biomolecules
                Publisher: MDPI
                ISSN (Electronic): 2218-273X
                Publication date (Electronic): 06 January 2016
                Publication date Collection: March 2016
                Volume: 6
                Issue: 1
                Electronic Location Identifier: 7
                Affiliations
                [1 ]Division of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan; dragon1@ 123456med.tohoku.ac.jp (R.H.); kudoyk3y7k3@ 123456med.tohoku.ac.jp (Y.K.)
                [2 ]Department of Pharmacology, Tohoku University School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan; yanai@ 123456med.tohoku.ac.jp
                [3 ]Division of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, 6-3Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan; furumoto@ 123456cyric.tohoku.ac.jp (S.F.); tago@ 123456cyric.tohoku.ac.jp (T.T.)
                [4 ]Department of Geriatrics and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan; hiroyuki.arai.b5@ 123456tohoku.ac.jp
                Author notes
                [* ]Correspondence: nookamura@ 123456med.tohoku.ac.jp ; Tel.: +81-022-717-8058; Fax: +81-022-717-8060
                Article
                Publisher ID: biomolecules-06-00007
                DOI: 10.3390/biom6010007
                PMC ID: 4808801
                PubMed ID: 26751494
                SO-VID: 5fb075f1-27c8-464b-8d98-61ce1b79e182
                Copyright © © 2016 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 03 November 2015
                Date accepted : 28 December 2015
                Categories
                Subject: Review

                Keywords: alzheimer’s disease,tau deposits,positron emission tomography,radiotracer
                Data availability:
                Keywords: alzheimer’s disease, tau deposits, positron emission tomography, radiotracer

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