- Tau Positron Emission Tomography Imaging in Degenerative Parkinsonisms
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Chul Hyoung Lyoo, Hanna Cho, Jae Yong Choi, Young Hoon Ryu, Myung Sik Lee
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J Mov Disord. 2018;11(1):1-12. Published online January 23, 2018
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DOI: https://doi.org/10.14802/jmd.17071
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 Abstract
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- In recent years, several radiotracers that selectively bind to pathological tau proteins have been developed. Evidence is emerging that binding patterns of in vivo tau positron emission tomography (PET) studies in Alzheimer’s disease (AD) patients closely resemble the distribution patterns of known neurofibrillary tangle pathology, with the extent of tracer binding reflecting the clinical and pathological progression of AD. In Lewy body diseases (LBD), tau PET imaging has clearly revealed cortical tau burden with a distribution pattern distinct from AD and increased cortical binding within the LBD spectrum. In progressive supranuclear palsy, the globus pallidus and midbrain have shown increased binding most prominently. Tau PET patterns in patients with corticobasal syndrome are characterized by asymmetrical uptake in the motor cortex and underlying white matter, as well as in the basal ganglia. Even in the patients with multiple system atrophy, which is basically a synucleinopathy, 18F-flortaucipir, a widely used tau PET tracer, also binds to the atrophic posterior putamen, possibly due to off-target binding. These distinct patterns of tau-selective radiotracer binding in the various degenerative parkinsonisms suggest its utility as a potential imaging biomarker for the differential diagnosis of parkinsonisms.
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Citations
Citations to this article as recorded by  - Current directions in tau research: Highlights from Tau 2020
Claire Sexton, Heather Snyder, Dirk Beher, Adam L. Boxer, Pat Brannelly, Jean‐Pierre Brion, Luc Buée, Angela M. Cacace, Gaël Chételat, Martin Citron, Sarah L. DeVos, Kristophe Diaz, Howard H. Feldman, Bess Frost, Alison M. Goate, Michael Gold, Bradley Hym
Alzheimer's & Dementia.2022; 18(5): 988. CrossRef - 18F‐Florzolotau Tau Positron Emission Tomography Imaging in Patients with Multiple System Atrophy–Parkinsonian Subtype
Feng‐Tao Liu, Xin‐Yi Li, Jia‐Ying Lu, Ping Wu, Ling Li, Xiao‐Niu Liang, Zi‐Zhao Ju, Fang‐Yang Jiao, Ming‐Jia Chen, Jing‐Jie Ge, Yi‐Min Sun, Jian‐Jun Wu, Tzu‐Chen Yen, Jian‐Feng Luo, Chuantao Zuo, Jian Wang
Movement Disorders.2022; 37(9): 1915. CrossRef - Imaging pathological tau in atypical parkinsonisms: A review
Anastassia M. Mena, Antonio P. Strafella
Clinical Parkinsonism & Related Disorders.2022; 7: 100155. CrossRef - Integrated 18F-T807 Tau PET, Structural MRI, and Plasma Tau in Tauopathy Neurodegenerative Disorders
Cheng-Hsuan Li, Ta-Fu Chen, Ming-Jang Chiu, Ruoh-Fang Yen, Ming-Chieh Shih, Chin-Hsien Lin
Frontiers in Aging Neuroscience.2021;[Epub] CrossRef - Dual-Phase 18F-FP-CIT PET in Corticobasal Syndrome
Je Hong Min, Dong Gyu Park, Jung Han Yoon, Young Sil An
Clinical Nuclear Medicine.2019; 44(1): e49. CrossRef - Tau Positron-Emission Tomography in Former National Football League Players
Robert A. Stern, Charles H. Adler, Kewei Chen, Michael Navitsky, Ji Luo, David W. Dodick, Michael L. Alosco, Yorghos Tripodis, Dhruman D. Goradia, Brett Martin, Diego Mastroeni, Nathan G. Fritts, Johnny Jarnagin, Michael D. Devous, Mark A. Mintun, Michael
New England Journal of Medicine.2019; 380(18): 1716. CrossRef
- Relationship Between the Striatal and Cerebellar Glucose Metabolism and the Response to Levodopa Treatment in Patients With Multiple System Atrophy
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Chul Hyoung Lyoo, Seung Hun Oh, Ki Ook Lee, Seung Yeob Lee, Young Hoon Ryu, Myung Sik Lee
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J Mov Disord. 2008;1(1):26-32.
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DOI: https://doi.org/10.14802/jmd.08005
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Abstract
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Introduction:
About two thirds of the patients with multiple system atrophy (MSA) do not respond to levodopa treatment. Postmortem pathological studies and one retrospective [18F]-deoxyglucose positron emission tomography (FDGPET) study attributed such poor response to the striatal degeneration. We prospectively investigated the relationship between levodopa responsiveness and the metabolic activities of the striatum and cerebellum in MSA patients.
Methods:
In 39 patients with MSA, the UPDRS motor score was assessed and two sets of timed motor tests were perform ed before and after the levodopa treatment. After quantitative FDG PET and baseline evaluation, treatment w as started with 3 tablets of Sinemet® 25/250 mg a day. Clinical assessments were performed monthly for three months. Metabolic activities of the caudate, anterior putamen, posterior putamen, cerebellar cortex and cerebellar vermis were measured. We compared the measurements with mean percentage changes of motor function. Also, using statistical parametric mapping (SPM) analysis, we tried to find brain areas in which metabolism correlated with the clinical changes.
Results:
Mean percentage improvements of UPDRS motor scores w ere correlated with glucose metabolism in the posterior putamen and cerebellar vermis. The mean percentage improvements of performance in Purdue peg board test correlated with the glucose metabolism in the cerebellar cortex and vermis. In SPM analysis, cerebellar glucose metabolism correlated with the improvement of UPDRS motor score and the performance of two timed motor tests.
Conclusion:
The integrity of cerebellum, as well as posterior putamen, may be an important factor for showing the response to levodopa.
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