Figure 5.

A proposed mechanism for TGF-β activation in the VaD. The figure represents the proposed hypothesis that interaction between neuroblasts and activated microglial cells might lead to the production of the inactive form of the TGF-β attached with latent transforming growth factor-β binding protein (LTBP) through latency-associated peptide (LAP). The inactive form of TGF-β has generally been stored in the extracellular matrix (ECM). Vascular damage upon mitochondrial defects, release of free radical and acidification of the local microenvironment might be underlying mechanisms of the pathological activation and release of TGF-β in VaD.