NTRK3 was the most significantly upregulated protein for Aβ, demonstrating that NTRK3 signaling is associated with AD by promoting synaptic plasticity and interacting with Aβ-related pathways [50], while GFRA1 indicated the highest degree of upregulation in both MTA and WMH, where GFRA1 has known to bind with the glial cell line-derived neurotrophic factor (GDNF) [51], and the GDNF-GFRA1 complex has revealed to affect hippocampal-related neurological disorders and cerebral white matter damages [52, 53]. The gene discussed is NTRK3; the disease is nervous system disorder.