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Inflammation, amyloid, and atrophy in the aging brain: relationships with longitudinal changes in cognition

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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.

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SALA LLONCH, Roser, IDLAND, Ane victoria, BORZA, Tom, WATNE, Leiv otto, WYLLER, Torgeir bruun, BRÆKHUS, Anne, ZETTERBERG, Henrik, BLENNOW, Kaj, WALHOVD, Kristine beate, FJELL, Anders martin. Inflammation, amyloid, and atrophy in the aging brain: relationships with longitudinal changes in cognition. _Journal of Alzheimer's Disease_. 2017. Vol. 58, núm. 3, pàgs. 829-840. [consulta: 28 de gener de 2026]. ISSN: 1387-2877. [Disponible a: https://hdl.handle.net/2445/163111]

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