Open AccessDifferential effects of neurodegeneration biomarkers on subclinical cognitive decline
Author(s) -
Merluzzi Andrew P.,
Vogt Nicholas M.,
Norton Derek,
Jonaitis Erin,
Clark Lindsay R.,
Carlsson Cynthia M.,
Johnson Sterling C.,
Asthana Sanjay,
Blennow Kaj,
Zetterberg Henrik,
Bendlin Barbara B.
Publication year - 2019
Publication title -
alzheimer's and dementia: translational research and clinical interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.49
H-Index - 30
ISSN - 2352-8737
DOI - 10.1016/j.trci.2019.02.004
Subject(s) - neurodegeneration , neurogranin , subclinical infection , cognitive decline , cognition , medicine , psychology , neuropsychology , cognitive test , neuroscience , disease , dementia , biology , biochemistry , protein kinase c , enzyme
Neurodegeneration appears to be the biological mechanism most proximate to cognitive decline in Alzheimer's disease. We test whether t‐tau and alternative biomarkers of neurodegeneration—neurogranin and neurofilament light protein (NFL)—add value in predicting subclinical cognitive decline. Methods One hundred fifty cognitively unimpaired participants received a lumbar puncture for cerebrospinal fluid and at least two neuropsychological examinations (mean age at first visit = 59.3 ± 6.3 years; 67% female). Linear mixed effects models were used with cognitive composite scores as outcomes. Neurodegeneration interactions terms were the primary predictors of interest: age × NFL or age × neurogranin or age × t‐tau. Models were compared using likelihood ratio tests. Results Age × NFL accounted for a significant amount of variation in longitudinal change on preclinical Alzheimer's cognitive composite scores, memory composite scores, and learning scores, whereas age × neurogranin and age × t‐tau did not. Discussion These data suggest that NFL may be more sensitive to subclinical cognitive decline compared to other proposed biomarkers for neurodegeneration.