A very puzzling aspect of Long COVID is that symptoms appear to be aligned along two axes. One being neurodegeneration, the other being cancer cachexia. If you examine the interactions of SARS-CoV-2 and ACE-2, downregulation of ACE-2 causes an multi-fold increase in MMP13 expression (and many other Matrix Metalloproteinases). 

COVID-19 is theorized to increase α-Synuclein, a readily misfolded protein. An increase in α-Synuclein upregulates MMP13 expression. Misfolded A53T increases quantitative measures of amoeboid cell (microglia) morphology. MMP13 remodels the extracellular matrix and directly alters microglia. This may be the mechanism causing the microglia to destroy neurons in the brain.

On the tumorigenesis front, MMP13 is involved in many forms of cancer and its overexpression is a marker for poor prognosis in several cancers.

Further investigation is needed into the role of MMP13 and other Matrix Metalloproteinases. It is likely that dysregulation of MMP13 is also responsible for the aberrant tissue remodeling (especially fibrotic) seen in COVID patients.