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|Title:||Inflammation, amyloid, and atrophy in the aging brain: relationships with longitudinal changes in cognition|
|Author:||Sala Llonch, Roser|
Idland, Ane V.
Watne, Leiv O.
Wyller, Torgeir B.
Walhovd, Kristine B.
Fjell, Anders M.
|Abstract:||Amyloid 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.|
|Note:||Reproducció del document publicat a: https://doi.org/10.3233/JAD-161146|
|It is part of:||Journal of Alzheimer's Disease, 2017, vol. 58, num. 3, p. 829-840|
|Appears in Collections:||Articles publicats en revistes (Biomedicina)|
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