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.
|Number of pages||11|
|Publication status||Published - 2018 Feb|
Bibliographical noteFunding 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).
© 2017 International Parkinson and Movement Disorder Society
All Science Journal Classification (ASJC) codes
- Clinical Neurology