Alcolea Daniel, Vilaplana Eduard, Pegueroles Jordi, Montal Victor, Sánchez-Juan Pascual, González-Suárez Andrea, Pozueta Ana, Rodríguez-Rodríguez Eloy, Bartrés-Faz David, Vidal-Piñeiro Dídac, González-Ortiz Sofía, Medrano Santiago, Carmona-Iragui María, Sánchez-Saudinós MaBelén, Sala Isabel, Anton-Aguirre Sofía, Sampedro Frederic, Morenas-Rodríguez Estrella, Clarimón Jordi, Blesa Rafael, Lleó Alberto, Fortea Juan
Department of Neurology, Institut d'Investigacions Biomèdiques Sant Pau-Hospital de Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red en enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Centro de Investigación Biomédica en Red en enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain; Department of Neurology, Hospital Universitario Marqués de Valdecilla-IDIVAL, Santander, Spain.
Neurobiol Aging. 2015 Jun;36(6):2018-23. doi: 10.1016/j.neurobiolaging.2015.03.001. Epub 2015 Mar 9.
Cerebrospinal fluid YKL-40 has been described as a marker of glial inflammation. We aimed to study the relationship between YKL-40 and brain structure and its interactions with core Alzheimer's disease (AD) biomarkers. We measured cortical thickness (CTh) and cerebrospinal fluid biomarkers (amyloid-β 1-42 [Aβ42], total tau, p-tau, and YKL-40) of 80 cognitively normal controls and 27 patients with amnestic mild cognitive impairment. Subjects were classified as Aβ42+ (<550 pg/mL) or Aβ42- (>550 pg/mL). CTh difference maps were derived from the interaction and correlation analyses in the whole sample and within clinical groups. There was a strong correlation between YKL-40 and markers of neurodegeneration (total tau and p-tau). In the whole sample, we found a negative correlation between YKL-40 and CTh in AD vulnerable areas in Aβ42+ subjects but not in Aβ42 participants. Our results suggest that YKL-40 could track the inflammatory processes associated to tau-related neurodegeneration in the presence of the AD pathophysiological process.
脑脊液YKL-40已被描述为胶质细胞炎症的标志物。我们旨在研究YKL-40与脑结构之间的关系及其与核心阿尔茨海默病（AD）生物标志物的相互作用。我们测量了80名认知正常对照者和27名遗忘型轻度认知障碍患者的皮质厚度（CTh）和脑脊液生物标志物（淀粉样β蛋白1-42 [Aβ42]、总tau蛋白、磷酸化tau蛋白和YKL-40）。受试者被分类为Aβ42+（<550 pg/mL）或Aβ42-（>550 pg/mL）。CTh差异图来自于整个样本以及临床组内的相互作用和相关性分析。YKL-40与神经退行性变标志物（总tau蛋白和磷酸化tau蛋白）之间存在强相关性。在整个样本中，我们发现Aβ42+受试者中AD易损区域的YKL-40与CTh呈负相关，而在Aβ42-受试者中则无此相关性。我们的结果表明，在AD病理生理过程存在的情况下，YKL-40可以追踪与tau相关神经退行性变相关的炎症过程。
