进行性核上麻痹
皮质基底变性
神经退行性变
神经科学
萎缩
陶氏病
路易氏体型失智症
病理
医学
心理学
化学
疾病
痴呆
作者
Elijah Mak,Negin Holland,P Simon Jones,George Savulich,Audrey Low,Maura Malpetti,Sanne S. Kaalund,Luca Passamonti,Timothy Rittman,Rafael Romero-García,Roido Manavaki,Guy B. Williams,Young T. Hong,Tim D. Fryer,Franklin I. Aigbirhio,John O’Brien,James B. Rowe
标识
DOI:10.1016/j.neurobiolaging.2021.01.016
摘要
Understanding the cellular underpinnings of neurodegeneration remains a challenge; loss of synapses and dendritic arborization are characteristic and can be quantified in vivo, with [11C]UCB-J PET and MRI-based Orientation Dispersion Imaging (ODI), respectively. We aimed to assess how both measures are correlated, in 4R-tauopathies of progressive supranuclear palsy - Richardson's Syndrome (PSP-RS; n = 22) and amyloid-negative (determined by [11C]PiB PET) Corticobasal Syndrome (Cortiobasal degeneration, CBD; n =14), as neurodegenerative disease models, in this proof-of-concept study. Compared to controls (n = 27), PSP-RS and CBD patients had widespread reductions in cortical ODI, and [11C]UCB-J non-displaceable binding potential (BPND) in excess of atrophy. In PSP-RS and CBD separately, regional cortical ODI was significantly associated with [11C]UCB-J BPND in disease-associated regions (p < 0.05, FDR corrected). Our findings indicate that reductions in synaptic density and dendritic complexity in PSP-RS and CBD are more severe and extensive than atrophy. Furthermore, both measures are tightly coupled in vivo, furthering our understanding of the pathophysiology of neurodegeneration, and applicable to studies of early neurodegeneration with a safe and widely available MRI platform.
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