Skip to main content
. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: Metab Brain Dis. 2018 Oct 4;34(1):3–19. doi: 10.1007/s11011-018-0322-3

Figure 2. Role of tissue nonspecific alkaline phosphatase (TNAP) in the central nervous system:

Figure 2.

TNAP is expressed in neurons, microglia, astrocytes, oligodendrocytes, and is highly expressed in brain endothelial cells. TNAP is localized in the lipid rafts of the plasma membrane outer leaflet via its C-terminus to the GPI. It can also be found as a soluble protein in the serum or as a vesicle-associated protein in the extracellular space. TNAP may have a role in blood-brain barrier (BBB) breakdown, neuroinflammation, and vascular dysfunction in stroke and other neurological disorders. Inflammatory mediators such as reactive oxygen species (ROS), proteases, and inflammatory cytokines, promote the breakdown of junctional proteins at the BBB. The loss of junctional proteins weakens the BBB and allows activated T-cells, antigen-presenting cells (APC), other leukocytes, and pro-inflammatory mediators to traverse the BBB, with bidirectional movement between the brain parenchyma and cerebral circulation. These mechanisms play an important role in the pathophysiology of ischemic stroke and other neuroinflammatory disorders.