Consistent with this notion, prior studies have reported increased CSF GAP-43 concentrations, as a proxy of synaptic dysfunction, in those with low amyloid burden (Milà-Alomà et al., 2021) as well as those with pathogenic levels of amyloid-β but without tau pathology (Pereira et al., 2020), suggesting early alterations of GAP-43 in the progression of AD. This evidence concerns the gene GAP43 and Alzheimer disease.