Table 1.

ADRD risk/pathology genes

Gene	Expression in COVID-19	Function	Reference
CCL20	predicted activation	recruitment of leukocytes	Goldeck et al.32
CTCFL	increased	controls gene expression in myeloid cells	Corces et al.,33 Novikova et al.34
CXCL8	increased	neuroinflammation	Zuena et al.35
EGFR	increased	astrocyte activation, inflammation	Mansour et al.36
GFAP	increased	astroglial activation	Cicognola et al.37
IFI16	increased	interferon-induced DNA sensor	Velez et al.38
IL-17	predicted activation	neuroinflammation	Brigas et al.39
IL-18	increased	neuroinflammation/amyloid processing	Ojala et al.40
IL-6R	increased	neuroinflammation	Haddick et al.41
KLF4	increased	regulates neuronal apoptosis and axon regeneration	Cheng et al.42
LGALS3	increased	microglia-mediated inflammation, amyloid aggregation	Tan et al.,43 Tao et al.44
TAC1	decreased	vasodilator	Dharshini et al.45
CAV1	increased	endocytosis and protein trafficking	Gaudreault et al.46
FKBP5	increased	tau phosphorylation, tau oligomerization, glucose metabolism	Wang et al.,47 Fuji et al.,48 Blair et al.49
HSP90	decreased	protein folding	Blair et al.50
HSPA8	decreased	autophagy/tau regulation	Loeffler et al.51
IFITM3	increased	modulates γ-secretase	Hur et al.52
C3/4	increased	complement activation, association with plaques	Tenner et al.53
C5AR1	increased	C5a receptor on myeloid cells	Hernandez et al.54
CR1	predicted activation	phagocytosis of immune complexes, inflammation	Zhu et al.55
CALB1	decreased	calcium sequestration	Sanfillipo et al.56
CAMKK2	decreased	regulatory kinase Ca-dependent signaling	Sabbir et al.,57 Mairet-Coello et al.58
BDNF	decreased	protects against tau-related neurodegeneration	Elliott et al.59
CCK/BR	decreased/ predicted decrease	hormone, maintaining memory	Plagman et al.60
PLAT	increased	tissue plasminogen activator, cleaves pro-BDNF, cleaves amyloid plaques	Shibata et al.61