| Literature DB >> 25865441 |
Daniel Alcolea1, Eduard Vilaplana1, Jordi Pegueroles1, Victor Montal1, Pascual Sánchez-Juan2, Andrea González-Suárez2, Ana Pozueta2, Eloy Rodríguez-Rodríguez2, David Bartrés-Faz3, Dídac Vidal-Piñeiro3, Sofía González-Ortiz4, Santiago Medrano4, María Carmona-Iragui1, MaBelén Sánchez-Saudinós1, Isabel Sala1, Sofía Anton-Aguirre1, Frederic Sampedro5, Estrella Morenas-Rodríguez1, Jordi Clarimón1, Rafael Blesa1, Alberto Lleó1, Juan Fortea6.
Abstract
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.Entities:
Keywords: CSF biomarkers; Cortical thickness; Neuroinflammation; Preclinical Alzheimer's disease; Structural MRI; YKL-40
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Year: 2015 PMID: 25865441 DOI: 10.1016/j.neurobiolaging.2015.03.001
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673