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Network, Dominantly Inherited Alzheimer

Mayo Clinic

Washington University in St. Louis

Citations 1

Emerging cerebrospinal fluid biomarkers in autosomal dominant Alzheimer's disease
Schindler, Suzanne E. , Li, Yan , Todd, Kaitlin , Herries, Elizabeth, Henson, Rachel L. , Gray, Julia, Wang, Guoqiao , Graham, Danielle , Shaw, Leslie M. , Trojanowski, John Q. , Hassenstab, Jason , Benzinger, Tammie L.S. , Cruchaga, Carlos , Xiong, Chengjie , Chhatwal, Jasmeer P. , Noble, James M. , Ringman, John M. , Graff‐Radford, Neill R. , Ladenson, Jack H., Morris, John C. , Bateman, Randall J. , Fagan, Anne M. , Network, Dominantly Inherited Alzheimer, Fox, Nick C. , Cruchaga, Carlos , Bateman, Randall J , Xiong, Chengjie , Benzinger, Tammie L S , Fox, Nick C , Hassenstab, Jason , Morris, John C , Jucker, Mathias , Holtzman, David M. , Xiong, Chengjie , Network, Dominantly Inherited Alzheimer, Noble, James M

Alzheimer's & Dementia | March 4, 2019 | Volume: 15 | Issue: 5 | Pages: 655-665

10.1016/j.jalz.2018.12.019 Get It

AbstractIntroductionFour less well‐studied but promising “emerging” cerebrospinal fluid (CSF) biomarkers are elevated in late‐onset Alzheimer disease (AD): neurogranin, synaptosomal‐associated protein‐25 (SNAP‐25), visinin‐like protein 1 (VILIP‐1), and chitinase‐3‐like protein 1 (YKL‐40).MethodsCSF neurogranin, SNAP‐25, VILIP‐1, and YKL‐40 were measured in families carrying autosomal‐dominant AD mutations.ResultsThe four emerging CSF biomarkers were significantly elevated in the mutation carriers (n = 235) versus noncarriers (n = 145). CSF SNAP‐25, VILIP‐1, and YKL‐40 were altered very early in the AD time course, approximately 15–19 years before estimated symptom onset. All CSF biomarkers predicted important AD‐related outcomes including performance on a cognitive composite, brain amyloid burden as measured by amyloid positron emission tomography, and the estimated years from symptom onset.DiscussionEarly abnormalities in CSF tTau, pTau, SNAP‐25, VILIP‐1, and YKL‐40 suggest that synaptic damage, neuronal injury, and neuroinflammation begin shortly after the commencement of brain amyloid accumulation.