GAP-43 in cerebrospinal fluid (CSF) has previously been shown to be increased in AD and was correlated with the magnitude of Aβ plaques in the hippocampus, amygdala, and cortex, but was not associated with the α-synuclein or TDP-43 neuropathic molecules (Sandelius et al., 2019; Qiang et al., 2022; Zhu et al., 2022), supporting the notion that GAP-43 might be a marker for hippocampal neuronal cell degeneration, which are most vulnerable to AD pathogens. Here, GAP43 is linked to Alzheimer disease.