These alterations compromise the synthesis and release of neuronal support factors and result in the build-up of neurotoxic and pro-inflammatory factors, including tumor necrosis factor (TNF-α), interleukin (IL)-1α, IL-1β, monocyte chemoattractant protein-1 (MCP-1), and CXCL2, which in turn contribute to endothelial dysfunction, axonal degeneration, and neuronal damage [93,94,95]. Here, CCL2 is linked to endothelial dysfunction.