阿尔茨海默病表型变异中蓝斑核的早期改变。
Early alteration of the locus coeruleus in phenotypic variants of Alzheimer's disease.
机构信息
Unit of Neurology of Memory and Language, Université Paris Descartes, Sorbonne Paris Cité, GHU Paris Psychiatry and Neurosciences, Hôpital Sainte Anne, Paris, France.
UMR 1023, IMIV, Service Hospitalier Frédéric Joliot, CEA, Inserm, Université Paris Sud, CNRS, Université Paris-Saclay, Orsay, France.
出版信息
Ann Clin Transl Neurol. 2019 Jul;6(7):1345-1351. doi: 10.1002/acn3.50818. Epub 2019 Jun 23.
Neuropathological studies showed early locus coeruleus (LC) neuronal loss associated with tauopathy in Alzheimer's Disease (AD). We used the LC signal intensity (LC-I) on 3T MRI to assess the LC integrity in AD (n = 37) and controls (n = 17). The LC-I was decreased in AD regardless of typical (amnesic) and atypical presentation (logopenic aphasia/visuo-spatial deficit), from the prodromal stage, and independently of the amyloid load measured by PiB-PET. The LC-I was correlated with memory performance of typical AD. This supports the pathophysiological model in which the LC plays a critical role in AD and may thus be a potential therapeutic target.
神经病理学研究表明，阿尔茨海默病（AD）中存在与tau 病相关的蓝斑核（LC）神经元早期丢失。我们使用 3T MRI 上的 LC 信号强度（LC-I）来评估 AD（n=37）和对照组（n=17）的 LC 完整性。无论表现为典型（遗忘型）还是非典型（失语法性失语症/视觉空间缺陷），AD 患者的 LC-I 均降低，从前驱期开始，且与 PiB-PET 测量的淀粉样蛋白负荷无关。LC-I 与典型 AD 的记忆表现相关。这支持了 LC 在 AD 中起关键作用的病理生理学模型，因此可能是一个潜在的治疗靶点。
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