Sala Llonch, RoserIdland, Ane VictoriaBorza, TomWatne, Leiv OttoWyller, Torgeir BruunBrækhus, AnneZetterberg, HenrikBlennow, KajWalhovd, Kristine BeateFjell, Anders Martin2020-05-292020-05-292017-06-051387-2877https://hdl.handle.net/2445/163111Amyloid deposition occurs in aging, even in individuals free from cognitive symptoms, and is often interpreted as preclinical Alzheimer's disease (AD) pathophysiology. YKL-40 is a marker of neuroinflammation, being increased in AD, and hypothesized to interact with amyloid-B (AB ) in causing cognitive decline early in the cascade of AD pathophysiology. Whether and how A and YKL-40 affect brain and cognitive changes in cognitively healthy older adults is still unknown. We studied 89 participants (mean age: 73.1 years) with cerebrospinal fluid samples at baseline, and both MRI and cognitive assessments from two time-points separated by two years. We tested how baseline levels of AB 42 and YKL-40 correlated with changes in cortical thickness and cognition. Thickness change correlated with AB 42 only in AB 42+ participants (<600 pg/mL, n = 27) in the left motor and premotor cortices. AB 42 was unrelated to cognitive change. Increased YKL-40 was associated with less preservation of scores on the animal naming test in the total sample (r = -0.28, p = 0.012) and less preservation of a score reflecting global cognitive function for AB 42+ participants (r = -0.58, p = 0.004). Our results suggest a role for inflammation in brain atrophy and cognitive changes in cognitively normal older adults, which partly depended on AB accumulation.12 p.application/pdfeng(c) Sala Llonch, Roser et al., 2017EnvellimentEnvelliment cerebralInflamacióAgingAging brainInflammationinfo:eu-repo/semantics/article6782132020-05-29info:eu-repo/semantics/openAccess28505968