未经证实：路易体病的病理特征是α-突触核蛋白病理学。阿尔茨海默病(AD)共病可影响表型。体内AD生物标志物可以提示在不寻常的情况下存在这种共病，但病理验证仍然是必不可少的。
UNASSIGNED：该患者最初表现为皮质基底综合征，后来出现视觉幻觉和帕金森病，与突触核蛋白病一致。病人接受了脑脊液取样,18F-flortaucipirPET扫描，和双侧区域的大脑捐赠可用于数字组织学分析。
未经证实：CSFAβ42和t-tau在AD范围内。18F-flortaucipir扫描显示所有叶中的右侧保留（t=4.3-10.0，P<.006）。尸检时出现新皮质阶段的路易体病理和高水平的AD神经病理变化。α-突触核蛋白和tau病理右侧化（分别为T值=3.1，P值=.007和T值=3.3，P值=.004）。
UNASSIGNED：该病例具有重叠tau蛋白病和突触核蛋白病的临床特征，具有深入的生物标志物特征，罕见的双侧尸检采样显示，tu蛋白和α-突触核蛋白病理显示可能的协同关系。
UNASSIGNED: Lewy body diseases are pathologically characterized by α-synuclein pathology. Alzheimer\'s disease (AD) co-pathology can influence phenotypes. In vivo AD biomarkers can suggest the presence of this co-pathology in unusual cases, but pathological validation remains essential.
UNASSIGNED: This patient originally presented with corticobasal syndrome and later developed visual hallucinations and parkinsonism consistent with a synucleinopathy. The patient underwent CSF sampling, 18F-flortaucipir PET scanning, and brain donation with bilateral regions available for digital histological analysis.
UNASSIGNED: CSF Aβ42 and t-tau were in the AD range. 18F-flortaucipir scanning showed right-lateralized retention in all lobes (t = 4.3-10.0, P < .006). Neocortical stage Lewy body pathology and high levels of AD neuropathological changes were present at autopsy. There was right lateralization of α-synuclein and tau pathology (T value = 3.1, P value = .007 and T value = 3.3, P value = .004 respectively).
UNASSIGNED: This
case with overlapping tauopathy and synucleinopathy clinical features had in-depth biomarker characterization and rare bilateral post-mortem sampling showing lateralized tau and α-synuclein pathology suggesting possible synergistic relationships.
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