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. 2021 Apr 12;12:660087. doi: 10.3389/fneur.2021.660087

Figure 2.

Figure 2

Schematic representation of the pathophysiological mechanisms of SARS-CoV-2. (A) Peripheral pathological events triggered by SARS-CoV-2 infection. (B) Possible CNS pathological mechanisms caused by the severe peripheral hyperinflammation associated with COVID-19. ACE2, angiotensin-converting enzyme 2 receptor; AJs, adherent junctions; Aβ; amyloid-beta; BBB, blood-brain barrier; C1q, the complement component 1q; CASP1, caspase1; CCL, chemokine (C-C motif) ligand; CNS, central nervous system; CXCL10, C–X–C motif chemokine 10; GSDMD, gasdermin-D; IL, interleukin; MMPs, metalloproteinases; NETs, neutrophil extracellular traps; NF-κB, Nuclear factor Kappa B; N-GSDMD, N-terminal gasdermin; NLRP3, nucleotide-binding domain-, leucine-rich repeat-containing receptor, pyrin domain-containing 3; TJs, tight junctions; TLR3, toll-like receptor 3; TNF-α, tumor necrosis factor-alpha; α-syn, alpha-synuclein.