Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Typ-2-Diabetes und Adipositas Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende

Die Highlights vom Kongress des American College of Cardiology 2024

Im April diskutierten die Herz-Kreislauf-Spezialisten aus der ganzen Welt auf dem  Kongress des American College of Cardiology (ACC) u.a. neue Therapieansätze bei akutem Myokardinfarkt, koronarer Herzerkrankung, kardiogenem Schock oder Aortenklappenstenose. In unserem Kongress-Dossier haben wir für Sie Berichte über die „Late-Breaking Trials“ und andere wichtige Studien zusammengestellt. 
Erweiterte Suche
Anmelden
nach oben
Current Neurology and Neuroscience Reports
Erschienen in: Current Neurology and Neuroscience Reports 12/2018

01.12.2018 | Neuroimaging (N Pavese, Section Editor)

The Role of Tau Imaging in Parkinsonian Disorders

verfasst von: Jochen Hammes, Alexander Drzezga, Thilo van Eimeren

Erschienen in: Current Neurology and Neuroscience Reports | Ausgabe 12/2018

Einloggen, um Zugang zu erhalten

Abstract

Purpose of Review

Differential diagnosis of atypical Parkinson syndromes (APS) is difficult as clinical presentations may vary and as there is a strong overlap between disease entities. Aggregations of misfolded and hyperphosphorylated tau proteins are the common denominator of many of these diseases.

Recent Findings

Several tau targeting positron emission tomography (PET) tracers have been evaluated as possible biomarkers in APS in the recent years. For Parkinson’s disease, dementia with Lewy bodies, progressive supranuclear palsy, and corticobasal degeneration, promising results have been reported with regard to the ability to detect the presence of disease and to discriminate patients from controls. However, the discussion about the specificity of the first-generation radiotracers and their value in the clinical context is ongoing.

Summary

A combined interpretation of signal strength and distribution pattern in PET scans with first- and second-generation tracers may be helpful in clinical diagnosis and follow-up of patients with APS.
Literatur
1.
Ling H. Untangling the tauopathies: current concepts of tau pathology and neurodegeneration. Parkinsonism Relat Disord. 2018;46(Suppl 1):S34–8.CrossRef
2.
McKee AC, Daneshvar DH, Alvarez VE, et al. The neuropathology of sport. Acta Neuropathol. 2014;127:29–51.CrossRef
3.
Bischof GN, Endepols H, van Eimeren T, Drzezga A. Tau-imaging in neurodegeneration. Methods. 2017;130:114–23.CrossRef
4.
5.
Hammes J, Bischof GN, Drzezga A. Molecular imaging in early diagnosis, differential diagnosis and follow-up of patients with neurodegenerative diseases. Clin Transl Imaging. 2017;5:465–71.CrossRef
6.
Tolosa E, Wenning G, Poewe W. The diagnosis of Parkinson’s disease. Lancet Neurol. 2006;5:75–86.CrossRef
7.
•• Höglinger GU, Respondek G, Stamelou M, Kurz C, Josephs KA, Lang AE, et al. Clinical diagnosis of progressive supranuclear palsy: the movement disorder society criteria. Mov Disord Off J Mov Disord Soc. 2017;32:853–64 Twenty years after the original “Litvan” criteria, the PSP research criteria have been adapted to incorporate earlier cases along the full spectrum of PSP phenotypes.CrossRef
8.
Williams DR, Lees AJ. Progressive supranuclear palsy: clinicopathological concepts and diagnostic challenges. Lancet Neurol. 2009;8:270–9.CrossRef
9.
McFarland NR. Diagnostic approach to atypical parkinsonian syndromes. Continumm (Minneap Minn). 2016;22:1117–42.
10.
Stamelou M, Höglinger G. A review of treatment options for progressive supranuclear palsy. CNS Drugs. 2016;30:629–36.CrossRef
11.
12.
Golde TE, Lewis J, McFarland NR. Anti-tau antibodies: hitting the target. Neuron. 2013;80:254–6.CrossRef
13.
Yanamandra K, Kfoury N, Jiang H, Mahan TE, Ma S, Maloney SE, et al. Anti-tau antibodies that block tau aggregate seeding in vitro markedly decrease pathology and improve cognition in vivo. Neuron. 2013;80:402–14.CrossRef
14.
Choi Y, Ha S, Lee Y-S, Kim YK, Lee DS, Kim DJ. Development of tau PET imaging ligands and their utility in preclinical and clinical studies. Nucl Med Mol Imaging. 2018;52:24–30.CrossRef
15.
• Villemagne VL, Doré V, Burnham SC, Masters CL, Rowe CC. Imaging tau and amyloid-β proteinopathies in Alzheimer disease and other conditions. Nat Rev Neurol. 2018;14:225–36 Comprehensive review on current status of specific molecular imaging of protein pathologies.CrossRef
16.
Honer M, Gobbi L, Knust H, Kuwabara H, Muri D, Koerner M, et al. Preclinical evaluation of 18F-RO6958948, 11C-RO6931643, and 11C-RO6924963 as novel PET radiotracers for imaging tau aggregates in Alzheimer disease. J Nucl Med. 2018;59:675–81.CrossRef
17.
Furumoto S, Tago T, Harada R, et al. 18F-Labeled 2-Arylquinoline derivatives for tau imaging: chemical, radiochemical, biological and clinical features. Curr Alzheimer Res. 2017;14:178–85.CrossRef
18.
Declercq L, Rombouts F, Koole M, Fierens K, Mariën J, Langlois X, et al. Preclinical evaluation of 18F-JNJ64349311, a novel PET tracer for tau imaging. J Nucl Med. 2017;58:975–81.CrossRef
19.
Respondek G, Kurz C, Arzberger T, Compta Y, Englund E, Ferguson LW, et al. Which ante mortem clinical features predict progressive supranuclear palsy pathology? Mov Disord Off J Mov Disord Soc. 2017;32:995–1005.CrossRef
20.
•• Kovacs GG. Invited review: neuropathology of tauopathies: principles and practice. Neuropathol Appl Neurobiol. 2015;41:3–23 Excellent review of the underlying neuropathological processes and histopathological findings in atypical Parkinson syndromes and other neurodegenerative diseases.CrossRef
21.
Marquié M, Normandin MD, Meltzer AC, Siao Tick Chong M, Andrea NV, Antón-Fernández A, et al. Pathological correlations of [F-18]-AV-1451 imaging in non-alzheimer tauopathies. Ann Neurol. 2017;81:117–28.CrossRef
22.
Smith R, Schain M, Nilsson C, Strandberg O, Olsson T, Hägerström D, et al. Increased basal ganglia binding of (18) F-AV-1451 in patients with progressive supranuclear palsy. Mov Disord. 2017;32:108–14.CrossRef
23.
Brendel M, Schönecker S, Höglinger G, et al. [18F]-THK5351 PET correlates with topology and symptom severity in progressive supranuclear palsy. Front Aging Neurosci. 2017;9:440.CrossRef
24.
Cope TE, Rittman T, Borchert RJ, Jones PS, Vatansever D, Allinson K, et al. Tau burden and the functional connectome in Alzheimer’s disease and progressive supranuclear palsy. Brain J Neurol. 2018;141:550–67.CrossRef
25.
Schonhaut DR, McMillan CT, Spina S, et al. 18 F-flortaucipir tau positron emission tomography distinguishes established progressive supranuclear palsy from controls and Parkinson disease: a multicenter study. Ann Neurol. 2017;82:622–34.CrossRef
26.
Perez-Soriano A, Arena JE, Dinelle K, Miao Q, McKenzie J, Neilson N, et al. PBB3 imaging in parkinsonian disorders: evidence for binding to tau and other proteins. Mov Disord Off J Mov Disord Soc. 2017;32:1016–24.CrossRef
27.
Cho H, Choi JY, Hwang MS, Lee SH, Ryu YH, Lee MS, et al. Subcortical (18) F-AV-1451 binding patterns in progressive supranuclear palsy. Mov Disord. 2017;32:134–40.CrossRef
28.
Ishiki A, Harada R, Okamura N, Tomita N, Rowe CC, Villemagne VL, et al. Tau imaging with [18 F]THK-5351 in progressive supranuclear palsy. Eur J Neurol. 2017;24:130–6.CrossRef
29.
Hammes J, Bischof GN, Giehl K, Faber J, Drzezga A, Klockgether T, et al. Elevated in vivo [18F]-AV-1451 uptake in a patient with progressive supranuclear palsy. Mov Disord Off J Mov Disord Soc. 2017;32:170–1.CrossRef
30.
Coakeley S, Cho SS, Koshimori Y, Rusjan P, Ghadery C, Kim J, et al. [18F]AV-1451 binding to neuromelanin in the substantia nigra in PD and PSP. Brain Struct Funct. 2018;223:589–95.CrossRef
31.
Whitwell JL, Lowe VJ, Tosakulwong N, Weigand SD, Senjem ML, Schwarz CG, et al. [18 F]AV-1451 tau positron emission tomography in progressive supranuclear palsy. Mov Disord Off J Mov Disord Soc. 2017;32:124–33.CrossRef
32.
Williams DR, Holton JL, Strand C, Pittman A, de Silva R, Lees AJ, et al. Pathological tau burden and distribution distinguishes progressive supranuclear palsy-parkinsonism from Richardson’s syndrome. Brain J Neurol. 2007;130:1566–76.CrossRef
33.
Smith R, Schöll M, Widner H, van Westen D, Svenningsson P, Hägerström D, et al. In vivo retention of 18F-AV-1451 in corticobasal syndrome. Neurology. 2017;89:845–53.CrossRef
34.
Kikuchi A, Okamura N, Hasegawa T, Harada R, Watanuki S, Funaki Y, et al. In vivo visualization of tau deposits in corticobasal syndrome by 18F-THK5351 PET. Neurology. 2016;87:2309–16.CrossRef
35.
Josephs KA, Whitwell JL, Tacik P, Duffy JR, Senjem ML, Tosakulwong N, et al. [18F]AV-1451 tau-PET uptake does correlate with quantitatively measured 4R-tau burden in autopsy-confirmed corticobasal degeneration. Acta Neuropathol. 2016;132:931–3.CrossRef
36.
McMillan CT, Irwin DJ, Nasrallah I, et al. Multimodal evaluation demonstrates in vivo 18F-AV-1451 uptake in autopsy-confirmed corticobasal degeneration. Acta Neuropathol. 2016;132:935–7.CrossRef
37.
Fodero-Tavoletti MT, Furumoto S, Taylor L, McLean CA, Mulligan RS, Birchall I, et al. Assessing THK523 selectivity for tau deposits in Alzheimer’s disease and non-Alzheimer’s disease tauopathies. Alzheimers Res Ther. 2014;6:11.CrossRef
38.
Schweyer K, Busche MA, Hammes J, Zwergal A, Buhmann C, van Eimeren T, et al. Pearls & Oy-sters: ocular motor apraxia as essential differential diagnosis to supranuclear gaze palsy: eyes up. Neurology. 2018;90:482–5.CrossRef
39.
Cho H, Baek MS, Choi JY, Lee SH, Kim JS, Ryu YH, et al. 18F-AV-1451 binds to motor-related subcortical gray and white matter in corticobasal syndrome. Neurology. 2017;89:1170–8.CrossRef
40.
Hansen AK, Knudsen K, Lillethorup TP, Landau AM, Parbo P, Fedorova T, et al. In vivo imaging of neuromelanin in Parkinson’s disease using 18F-AV-1451 PET. Brain J Neurol. 2016;139:2039–49.CrossRef
41.
Aldridge GM, Birnschein A, Denburg NL, Narayanan NS. Parkinson’s disease dementia and dementia with Lewy bodies have similar neuropsychological profiles. Front Neurol. 2018;9:123.CrossRef
42.
Jellinger KA, Korczyn AD. Are dementia with Lewy bodies and Parkinson’s disease dementia the same disease? BMC Med. 2018;16:34.CrossRef
43.
Irwin DJ, Lee VM-Y, Trojanowski JQ. Parkinson’s disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies. Nat Rev Neurosci. 2013;14:626–36.CrossRef
44.
Gomperts SN, Locascio JJ, Makaretz SJ, Schultz A, Caso C, Vasdev N, et al. Tau positron emission tomographic imaging in the Lewy body diseases. JAMA Neurol. 2016;73:1334–41.CrossRef
45.
Lee SH, Cho H, Choi JY, Lee JH, Ryu YH, Lee MS, et al. Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases. Mov Disord Off J Mov Disord Soc. 2018;33:262–72.CrossRef
46.
Kantarci K, Lowe VJ, Boeve BF, Senjem ML, Tosakulwong N, Lesnick TG, et al. AV-1451 tau and β-amyloid positron emission tomography imaging in dementia with Lewy bodies. Ann Neurol. 2017;81:58–67.CrossRef
47.
Fanciulli A, Wenning GK. Multiple-system atrophy. N Engl J Med. 2015;372:249–63.CrossRef
48.
Uchikado H, DelleDonne A, Uitti R, Dickson DW. Coexistence of PSP and MSA: a case report and review of the literature. Acta Neuropathol. 2006;111:186–92.CrossRef
49.
Nagaishi M, Yokoo H, Nakazato Y. Tau-positive glial cytoplasmic granules in multiple system atrophy. Neuropathol Off J Jpn Soc Neuropathol. 2011;31:299–305.CrossRef
50.
Jellinger K. Unusual tau in MSA. Neuropathol Off J Jpn Soc Neuropathol. 2012;32:110–1.CrossRef
51.
Cho H, Choi JY, Lee SH, et al. 18 F-AV-1451 binds to putamen in multiple system atrophy. Mov Disord Off J Mov Disord Soc. 2017;32:171–3.CrossRef
52.
Wooten DW, Guehl NJ, Verwer EE, et al. Pharmacokinetic evaluation of the tau PET radiotracer 18F-T807 (18F-AV-1451) in human subjects. J Nucl Med Off Publ Soc Nucl Med. 2017;58:484–91.
53.
Shcherbinin S, Schwarz AJ, Joshi A, et al. Kinetics of the tau PET tracer 18F-AV-1451 (T807) in subjects with normal cognitive function, mild cognitive impairment, and Alzheimer disease. J Nucl Med Off Publ Soc Nucl Med. 2016;57:1535–42.
54.
Marshall VL, Reininger CB, Marquardt M, Patterson J, Hadley DM, Oertel WH, et al. Parkinson’s disease is overdiagnosed clinically at baseline in diagnostically uncertain cases: a 3-year European multicenter study with repeat [123I]FP-CIT SPECT. Mov Disord Off J Mov Disord Soc. 2009;24:500–8.CrossRef
55.
Siderowf A, Keene C, Beach T, et al. Comparison of regional flortaucipir PET SUVr values to quantitative tau histology and quantitative tau immunoassay in patients with Alzheimer’s disease pathology: a clinico-pathological study. J Nucl Med. 2017;58:629.
56.
Wren MC, Lashley T, Årstad E, Sander K. Large inter- and intra-case variability of first generation tau PET ligand binding in neurodegenerative dementias. Acta Neuropathol Commun. 2018;6:34.CrossRef
57.
•• Ng KP, Pascoal TA, Mathotaarachchi S, Therriault J, Kang MS, Shin M, et al. Monoamine oxidase B inhibitor, selegiline, reduces 18F-THK5351 uptake in the human brain. Alzheimers Res Ther. 2017;9:25 Important paper proving that THK-5351 imaging is largely influenced by tracer binding to MAO-B and that signal intensity can be modulated by application of MAO-B inhibitors.CrossRef
58.
Xia C-F, Arteaga J, Chen G, Gangadharmath U, Gomez LF, Kasi D, et al. [(18)F]T807, a novel tau positron emission tomography imaging agent for Alzheimer’s disease. Alzheimers Dement J Alzheimers Assoc. 2013;9:666–76.CrossRef
59.
Vermeiren C, Motte P, Viot D, Mairet-Coello G, Courade JP, Citron M, et al. The tau positron-emission tomography tracer AV-1451 binds with similar affinities to tau fibrils and monoamine oxidases. Mov Disord Off J Mov Disord Soc. 2018;33:273–81.CrossRef
60.
61.
• Hammes J, Leuwer I, Bischof GN, Drzezga A, van Eimeren T. Multimodal correlation of dynamic [18F]-AV-1451 perfusion PET and neuronal hypometabolism in [18F]-FDG-PET. Eur J Nucl Med Mol Imaging. 2017;44:2249–56 This paper demonstrates that dynamic [18F]-AV-1451 is able to provide information about the underlying pathology, while at the same time delivering information on regional (hypo-)metabolism equivalent to FDG-PET.CrossRef
Metadaten
Titel
The Role of Tau Imaging in Parkinsonian Disorders
verfasst von
Jochen Hammes
Alexander Drzezga
Thilo van Eimeren
Publikationsdatum
01.12.2018
Verlag
Springer US
Erschienen in
Current Neurology and Neuroscience Reports / Ausgabe 12/2018
Print ISSN: 1528-4042
Elektronische ISSN: 1534-6293
DOI
https://doi.org/10.1007/s11910-018-0898-3

Weitere Artikel der Ausgabe 12/2018

Current Neurology and Neuroscience Reports 12/2018 Zur Ausgabe

Stroke (H Diener, Section Editor)

Management of Blunt Cerebrovascular Injury

Genetics (V Bonifati, Section Editor)

Using Patient-Derived Induced Pluripotent Stem Cells to Identify Parkinson’s Disease-Relevant Phenotypes

Nerve and Muscle (L H Weimer, Section Editor)

Hereditary Motor Neuropathies and Amyotrophic Lateral Sclerosis: a Molecular and Clinical Update

Neuroimaging (N Pavese, Section Editor)

Novel Imaging Biomarkers for Huntington’s Disease and Other Hereditary Choreas

Neurotrauma (D Sandsmark, Section Editor)

Cerebral Microdialysis in Neurocritical Care

Genetics (V Bonifati, Section Editor)

Relation Between Stress Granules and Cytoplasmic Protein Aggregates Linked to Neurodegenerative Diseases

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Kostenlos registrieren

Neu im Fachgebiet Neurologie

Sozialer Aufstieg verringert Demenzgefahr

24.05.2024 Demenz Nachrichten

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

17.05.2024 Direkte orale Antikoagulanzien Nachrichten

Kommt es zu einer nichttraumatischen Hirnblutung, spielt es keine große Rolle, ob die Betroffenen zuvor direkt wirksame orale Antikoagulanzien oder Marcumar bekommen haben: Die Prognose ist ähnlich schlecht.

Was nützt die Kraniektomie bei schwerer tiefer Hirnblutung?

17.05.2024 Hirnblutung Nachrichten

Eine Studie zum Nutzen der druckentlastenden Kraniektomie nach schwerer tiefer supratentorieller Hirnblutung deutet einen Nutzen der Operation an. Für überlebende Patienten ist das dennoch nur eine bedingt gute Nachricht.

Thrombektomie auch bei großen Infarkten von Vorteil

16.05.2024 Ischämischer Schlaganfall Nachrichten

Auch ein sehr ausgedehnter ischämischer Schlaganfall scheint an sich kein Grund zu sein, von einer mechanischen Thrombektomie abzusehen. Dafür spricht die LASTE-Studie, an der Patienten und Patientinnen mit einem ASPECTS von maximal 5 beteiligt waren.

Update Neurologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen
Bildnachweise