Skip to main content

Table 1 Network-predicted risk genes involved in four pathobiological pathways of Alzheimer’s disease (AD)

From: Artificial intelligence framework identifies candidate targets for drug repurposing in Alzheimer’s disease

Gene Protein Description
Neurotransmitter transport
MEF2Ca Myocyte-specific enhancer factor 2C MEF2C mRNA expression levels were correlated with AD pathology
RIMS1 Regulating synaptic membrane exocytosis protein 1 An altered protein expression in RIMS1 during AD pathology
Beta-amyloid-related biologic process
APOEa Apolipoprotein E Affect Aβ production, aggregation, and clearance
CHRNA7 Neuronal acetylcholine receptor subunit alpha-7 Bind to Aβ with very high affinity, providing therapeutic insight into AD
SORL1a Sortilin-related receptor Reduce Aβ generation by trafficking APP away from amyloidogenic cleavage sites
ADAM10a Disintegrin and metalloproteinase domain-containing protein 10 Constitutive α-secretase in the process of amyloid-β protein precursor (AβPP) cleavage
LRP2 Low-density lipoprotein receptor-related protein 2 rs3755166 polymorphism within LRP2 gene is associated with susceptibility to AD in the Chinese population
Long-term synaptic potentiation
MAPK1 Mitogen-activated protein kinase 1 Beta-amyloid activates the MAPK cascade via hippocampal CHRNA7
PTK2Ba Protein-tyrosine kinase 2-beta An in vivo modulator and early marker of Tau pathology
Oxidative stress  
FOXO3 Forkhead box protein O3 Activate BCL2L11 and FASLG to promote neuronal death and aberrant Aβ processing
NOS1 Nitric oxide synthase Loss of endothelial NOS promotes p25 production and Tau phosphorylation
NFKB1 Nuclear factor NF-kappa-B p105 subunit Involve in neuroinflammation, synaptic plasticity, learning, and memory implicated in AD
ESR1 Estrogen receptor Interact with tau protein in vivo, and prevent glutamate excitotoxic injury by Aβ through estrogen signaling mechanisms
  1. aGenes have experimental or functional evidence reported in AD transgenic animal models or human-derived samples (see Table S2 and Supplementary Method). The detailed literature data are provided in Table S2