Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Department of Nuclear Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Mov Disord. 2018 Feb;33(2):262-272. doi: 10.1002/mds.27252. Epub 2017 Nov 23.
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.
The objective of this study was to investigate tau accumulation patterns in dementia with Lewy bodies and other Lewy body diseases using in vivo F-AV-1451 PET.
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 F-AV-1451 and F-florbetaben PET scans, and cortical binding values were compared between the controls and each disease group.
When compared with the controls, dementia with Lewy bodies patients showed slightly increased F-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, F-AV-1451 binding in the occipital cortex correlated with F-florbetaben binding. Amyloid-negative patients with normal cognition, patients with cognitive impairment, and dementia with Lewy bodies patients did not show increased F-AV-1451 binding.
Dementia with Lewy bodies patients may harbor F-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. © 2017 International Parkinson and Movement Disorder Society.
除路易体病理学外,淀粉样β斑块和神经原纤维缠结也是阿尔茨海默病的特征,在路易体疾病中也经常发现。
本研究旨在使用体内 F-AV-1451 PET 研究路易体痴呆和其他路易体疾病中的 tau 积累模式。
该研究纳入 12 名认知正常的帕金森病(PD)患者、22 名认知障碍的 PD 患者和 18 名路易体痴呆患者。此外,还纳入了 25 名阿尔茨海默病患者和 25 名健康对照者作为比较。所有参与者均接受了 F-AV-1451 和 F-florbetaben PET 扫描,并比较了对照组和每个疾病组的皮质结合值。
与对照组相比,路易体痴呆患者的初级感觉运动和视觉皮质以及顶颞皮质的 F-AV-1451 结合略有增加,但未通过多重比较检验。与对照组相比,淀粉样阳性路易体痴呆患者在相同区域的结合显著增加,并且在初级感觉运动和视觉皮质中的结合甚至大于阿尔茨海默病。同时,外侧和内侧颞叶皮质的结合不如阿尔茨海默病明显。在路易体痴呆中,枕叶皮质的 F-AV-1451 结合与 F-florbetaben 结合相关。认知正常的非淀粉样阴性患者、认知障碍患者和路易体痴呆患者均未出现 F-AV-1451 结合增加。
路易体痴呆患者可能具有与阿尔茨海默病不同的 F-AV-1451 结合模式,其初级皮质的受累程度更大,而颞叶皮质的受累程度较小。在路易体疾病谱中,tau 负担增加,淀粉样蛋白可能在路易体疾病中神经原纤维缠结的皮质 tau 积累中发挥重要作用。© 2017 国际帕金森病和运动障碍学会。