Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases

Seung Ha Lee; Hanna Cho; Jae Yong Choi; Jae Hoon Lee; Young Hoon Ryu; Myung Sik Lee; Chul Hyoung Lyoo

doi:10.1002/mds.27252

Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases

Seung Ha Lee, Hanna Cho, Jae Yong Choi, Jae Hoon Lee, Young Hoon Ryu, Myung Sik Lee, Chul Hyoung Lyoo

Department of Neurology

Research output: Contribution to journal › Article › peer-review

34 Citations (Scopus)

Abstract

Background: In addition to Lewy body pathology, amyloid-β plaques and neurofibrillary tangles that are characteristic for Alzheimer's disease are also frequently found in Lewy body diseases. Objectives: The objective of this study was to investigate tau accumulation patterns in dementia with Lewy bodies and other Lewy body diseases using in vivo ¹⁸F-AV-1451 PET. Methods: The study included 12 Parkinson's disease (PD) patients with normal cognition, 22 PD patients with cognitive impairment, and 18 dementia with Lewy bodies patients. In addition, 25 Alzheimer's disease patients and 25 healthy controls were included for comparison. All participants underwent ¹⁸F-AV-1451 and ¹⁸F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group. Results: When compared with the controls, dementia with Lewy bodies patients showed slightly increased ¹⁸F-AV-1451 binding in the primary sensorimotor and visual cortices and the parieto-temporal cortices, which failed to survive multiple comparisons. Amyloid-positive dementia with Lewy bodies patients showed significantly increased binding in the same regions when compared with controls, and even greater binding in the primary sensorimotor and visual cortices than Alzheimer's disease. Meanwhile, binding in the lateral and medial temporal cortices was less prominent than in Alzheimer's disease. In dementia with Lewy bodies, ¹⁸F-AV-1451 binding in the occipital cortex correlated with ¹⁸F-florbetaben binding. Amyloid-negative patients with normal cognition, patients with cognitive impairment, and dementia with Lewy bodies patients did not show increased ¹⁸F-AV-1451 binding. Conclusions: Dementia with Lewy bodies patients may harbor ¹⁸F-AV-1451 binding patterns distinct from Alzheimer's disease, with greater involvement of the primary cortices and less involvement of the temporal cortex. Tau burden increases in the Lewy body disease spectrum, and amyloid may play an important role in the accumulation of neocortical tau in Lewy body diseases.

Original language	English
Pages (from-to)	262-272
Number of pages	11
Journal	Movement Disorders
Volume	33
Issue number	2
DOIs	https://doi.org/10.1002/mds.27252
Publication status	Published - 2018 Feb

Bibliographical note

Funding Information:
Funding agencies: This study was financially supported by the “Mirae Medical” Faculty Research Assistance Program of Yonsei University College of Medicine (Grant 6-2016-0162), a National Research Foundation of Korea grant funded by the Korean government (MSIP; no. 2015R1C1A2A01054507), and the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (2017R1A2B2006694).

Publisher Copyright:
© 2017 International Parkinson and Movement Disorder Society

All Science Journal Classification (ASJC) codes

Neurology
Clinical Neurology

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10.1002/mds.27252

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@article{105435c7ce4c4d6bbb48e647d76b9721,

title = "Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases",

abstract = "Background: In addition to Lewy body pathology, amyloid-β plaques and neurofibrillary tangles that are characteristic for Alzheimer's disease are also frequently found in Lewy body diseases. Objectives: The objective of this study was to investigate tau accumulation patterns in dementia with Lewy bodies and other Lewy body diseases using in vivo 18F-AV-1451 PET. Methods: The study included 12 Parkinson's disease (PD) patients with normal cognition, 22 PD patients with cognitive impairment, and 18 dementia with Lewy bodies patients. In addition, 25 Alzheimer's disease patients and 25 healthy controls were included for comparison. All participants underwent 18F-AV-1451 and 18F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group. Results: When compared with the controls, dementia with Lewy bodies patients showed slightly increased 18F-AV-1451 binding in the primary sensorimotor and visual cortices and the parieto-temporal cortices, which failed to survive multiple comparisons. Amyloid-positive dementia with Lewy bodies patients showed significantly increased binding in the same regions when compared with controls, and even greater binding in the primary sensorimotor and visual cortices than Alzheimer's disease. Meanwhile, binding in the lateral and medial temporal cortices was less prominent than in Alzheimer's disease. In dementia with Lewy bodies, 18F-AV-1451 binding in the occipital cortex correlated with 18F-florbetaben binding. Amyloid-negative patients with normal cognition, patients with cognitive impairment, and dementia with Lewy bodies patients did not show increased 18F-AV-1451 binding. Conclusions: Dementia with Lewy bodies patients may harbor 18F-AV-1451 binding patterns distinct from Alzheimer's disease, with greater involvement of the primary cortices and less involvement of the temporal cortex. Tau burden increases in the Lewy body disease spectrum, and amyloid may play an important role in the accumulation of neocortical tau in Lewy body diseases.",

author = "Lee, {Seung Ha} and Hanna Cho and Choi, {Jae Yong} and Lee, {Jae Hoon} and Ryu, {Young Hoon} and Lee, {Myung Sik} and Lyoo, {Chul Hyoung}",

note = "Funding Information: Funding agencies: This study was financially supported by the “Mirae Medical” Faculty Research Assistance Program of Yonsei University College of Medicine (Grant 6-2016-0162), a National Research Foundation of Korea grant funded by the Korean government (MSIP; no. 2015R1C1A2A01054507), and the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (2017R1A2B2006694). Publisher Copyright: {\textcopyright} 2017 International Parkinson and Movement Disorder Society",

year = "2018",

month = feb,

doi = "10.1002/mds.27252",

language = "English",

volume = "33",

pages = "262--272",

journal = "Movement Disorders",

issn = "0885-3185",

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T1 - Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases

AU - Lee, Seung Ha

AU - Cho, Hanna

AU - Choi, Jae Yong

AU - Lee, Jae Hoon

AU - Ryu, Young Hoon

AU - Lee, Myung Sik

AU - Lyoo, Chul Hyoung

N1 - Funding Information: Funding agencies: This study was financially supported by the “Mirae Medical” Faculty Research Assistance Program of Yonsei University College of Medicine (Grant 6-2016-0162), a National Research Foundation of Korea grant funded by the Korean government (MSIP; no. 2015R1C1A2A01054507), and the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (2017R1A2B2006694). Publisher Copyright: © 2017 International Parkinson and Movement Disorder Society

PY - 2018/2

Y1 - 2018/2

N2 - Background: In addition to Lewy body pathology, amyloid-β plaques and neurofibrillary tangles that are characteristic for Alzheimer's disease are also frequently found in Lewy body diseases. Objectives: The objective of this study was to investigate tau accumulation patterns in dementia with Lewy bodies and other Lewy body diseases using in vivo 18F-AV-1451 PET. Methods: The study included 12 Parkinson's disease (PD) patients with normal cognition, 22 PD patients with cognitive impairment, and 18 dementia with Lewy bodies patients. In addition, 25 Alzheimer's disease patients and 25 healthy controls were included for comparison. All participants underwent 18F-AV-1451 and 18F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group. Results: When compared with the controls, dementia with Lewy bodies patients showed slightly increased 18F-AV-1451 binding in the primary sensorimotor and visual cortices and the parieto-temporal cortices, which failed to survive multiple comparisons. Amyloid-positive dementia with Lewy bodies patients showed significantly increased binding in the same regions when compared with controls, and even greater binding in the primary sensorimotor and visual cortices than Alzheimer's disease. Meanwhile, binding in the lateral and medial temporal cortices was less prominent than in Alzheimer's disease. In dementia with Lewy bodies, 18F-AV-1451 binding in the occipital cortex correlated with 18F-florbetaben binding. Amyloid-negative patients with normal cognition, patients with cognitive impairment, and dementia with Lewy bodies patients did not show increased 18F-AV-1451 binding. Conclusions: Dementia with Lewy bodies patients may harbor 18F-AV-1451 binding patterns distinct from Alzheimer's disease, with greater involvement of the primary cortices and less involvement of the temporal cortex. Tau burden increases in the Lewy body disease spectrum, and amyloid may play an important role in the accumulation of neocortical tau in Lewy body diseases.

AB - Background: In addition to Lewy body pathology, amyloid-β plaques and neurofibrillary tangles that are characteristic for Alzheimer's disease are also frequently found in Lewy body diseases. Objectives: The objective of this study was to investigate tau accumulation patterns in dementia with Lewy bodies and other Lewy body diseases using in vivo 18F-AV-1451 PET. Methods: The study included 12 Parkinson's disease (PD) patients with normal cognition, 22 PD patients with cognitive impairment, and 18 dementia with Lewy bodies patients. In addition, 25 Alzheimer's disease patients and 25 healthy controls were included for comparison. All participants underwent 18F-AV-1451 and 18F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group. Results: When compared with the controls, dementia with Lewy bodies patients showed slightly increased 18F-AV-1451 binding in the primary sensorimotor and visual cortices and the parieto-temporal cortices, which failed to survive multiple comparisons. Amyloid-positive dementia with Lewy bodies patients showed significantly increased binding in the same regions when compared with controls, and even greater binding in the primary sensorimotor and visual cortices than Alzheimer's disease. Meanwhile, binding in the lateral and medial temporal cortices was less prominent than in Alzheimer's disease. In dementia with Lewy bodies, 18F-AV-1451 binding in the occipital cortex correlated with 18F-florbetaben binding. Amyloid-negative patients with normal cognition, patients with cognitive impairment, and dementia with Lewy bodies patients did not show increased 18F-AV-1451 binding. Conclusions: Dementia with Lewy bodies patients may harbor 18F-AV-1451 binding patterns distinct from Alzheimer's disease, with greater involvement of the primary cortices and less involvement of the temporal cortex. Tau burden increases in the Lewy body disease spectrum, and amyloid may play an important role in the accumulation of neocortical tau in Lewy body diseases.

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Distinct patterns of amyloid-dependent tau accumulation in Lewy body diseases

Abstract

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