Rare genetic variants prioritize molecular pathways for semaphorin interactions in Alzheimer’s disease patients

Figures & data

Figure 1. REACTOME pathways associated with Development Biology in: AD patients (А); FTD patients (В); Centenarians (С) and Young controls (D). The numbers denote enhanced pathways: 1. Semaphorin interactions, 2. NCAM1 interaction, 3.Interaction between La and Ankyrins, 4. Formation of cornified envelope, 5. Keratinization.

Figure 2. Molecular pathways indicated by the seven genes with pathogenic and VUSs.

Table 1. Significant pathways associated with developmental biology in AD patients.

Pathway name	Entities found	Entities Total	Entities ratio	Entities p-value	Entities FDR
1. CRMPs in Sema3A signaling	2	18	0.001	9.79E-5	4.36E-4
2. Other semaphorin interactions	7	19	0.001	1.11E-16	4.22E-14
3. SEMA3A-Plexin repulsion signaling by inhibiting Integrin adhesion	2	19	0,.01	1.1E-4	4.36E-4
4. Sema3A PAK dependent Axon repulsion	2	19	0.001	1.1E-5	4.36E-4
5. Sema4D induced cell migration and growth-cone collapse	1	26	0.002	2.1E-2	3.13E-2
6. Sema4D mediated inhibition of cell attachment and migration	1	14	0.001	1.14E-3	2.279E-2

Figure 3. Molecular network involving the TREM2 protein.

Figure 4. The molecular network which the PLXND1 gene is part of.

Data availability statement

Data are available upon reasonable request from the authors.