| Title | Inflammation, Amyloid, and Atrophy in The Aging Brain: Relationships with Longitudinal Changes in Cognition. |
| Publication Type | Journal Article |
| Year of Publication | 2017 |
| Authors | Sala-Llonch, R, Idland, A-V, Borza, T, Watne, LOtto, Wyller, TBruun, Brækhus, A, Zetterberg, H, Blennow, K, Walhovd, KBeate, Fjell, AMartin |
| Journal | J Alzheimers Dis |
| Volume | 58 |
| Issue | 3 |
| Pagination | 829-840 |
| Date Published | 2017 |
| ISSN | 1875-8908 |
| 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-β (Aβ) in causing cognitive decline early in the cascade of AD pathophysiology. Whether and how Aβ 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 Aβ42 and YKL-40 correlated with changes in cortical thickness and cognition. Thickness change correlated with Aβ42 only in Aβ42+ participants ( |
| DOI | 10.3233/JAD-161146 |
| Alternate Journal | J. Alzheimers Dis. |
| PubMed ID | 28505968 |
