Table 2. The source and the association of pro-inflammatory cytokine with AD pathogenesis.

Pro-inflammatory cytokine	CNS origin	Effects on neurons	Synaptic effects	Effects on Aβ	Effects on tau	References
TNF-α	Microglia, astrocytes neurons	Pro-apoptotic; prevent apoptosis	Synaptic excitotoxicity; LTP ↓	↑ Aβ synthesis; ↓ Aβ clearance	↑ tau hyperphosphorylation	(74,75)
IL-1β	Microglial, astrocytes	Neuronal death and damage↑	LTP ↓ synaptic plasticity↓	↑ Aβ synthesis	↑ tau phosphorylation	(76-79)
				↓ Aβ-related pathology	↓ tau pathology
IL-6	Microglial astrocytes endothelial cells	Rescue neurons	LTP ↓ prevents synaptic loss	↓ Aβ deposition	↑ tau phosphorylation	(80-82)
IL-18	Activated microglia, astrocytes and ependymal cells	Pro-apoptotic	↓ the induction of LTP	↑ production of APP ↑Aβ	↑ hyperphosphorylation of tau	(83-85)

CNS, central nervous system; TNF-α, tumour necrosis factor alpha; IL, interleukin; LTP, long term potentiation; Aβ, amyloid beta; ↑↓, increase or decrease.