Authors: Anna Antonell, Adrià Tort‐Merino, José Ríos, Mircea Balasa, Sergi Borrego‐Écija, Josep M. Auge, Cristina Muñoz‐García, Beatriz Bosch, Neus Falgàs, Lorena Rami, Oscar Ramos‐Campoy, Kaj Blennow, Henrik Zetterberg, José L. Molinuevo, Albert Lladó, Raquel Sánchez‐Valle
Published: 2019-10-24
DOI: 10.1016/j.jalz.2019.09.001
Source: Full article
AbstractIntroductionSynaptic damage, axonal neurodegeneration, and neuroinflammation are common features in Alzheimer's disease (AD), frontotemporal dementia (FTD), and Creutzfeldt‐Jakob disease (CJD).MethodsUnicentric cohort of 353 participants included healthy control (HC) subjects, AD continuum stages, genetic AD and FTD, and FTD and CJD. We measured cerebrospinal fluid neurofilament light (NF‐L), neurogranin (Ng), 14‐3‐3, and YKL‐40 proteins.ResultsBiomarkers showed differences in HC subjects versus AD, FTD, and CJD. Disease groups differed between them except AD versus FTD for YKL‐40. Only NF‐L differed between all stages within the AD continuum. AD and FTD symptomatic mutation carriers presented differences with respect to HC subjects. Applying the AT(N) system, 96% subjects were positive for neurodegeneration if 14‐3‐3 was used, 94% if NF‐L was used, 62% if Ng was used, and 53% if YKL‐40 was used.DiscussionBiomarkers of synapse and neurodegeneration differentiate HC subjects from neurodegenerative dementias and between AD, FTD, and CJD. NF‐L and 14‐3‐3 performed similar to total tau when AT(N) system was applied.