Possible effects of Porphyromonas gingivalis on the blood–brain barrier in Alzheimer’s disease

Figures & data

Figure 1. The blood–brain barrier (BBB) and the neurovascular unit (NVU). Pial arteries divide into smaller arteries, so-called penetrating arteries, which branch into capillaries. Pial and penetrating arteries are covered by vascular smooth cells and are separated from brain tissues through the parenchymal basement membrane (glia limitans). One layer of smooth muscle cells covers the parenchymal arterioles. The BBB is formed by endothelial cells in capillaries. BBB properties in these cells are further maintained and regulated through communications with the basement membranes and neighboring cells in the NVU such as pericytes, astrocytes and interneurons. Adopted from Ref. [1]

Figure 2. Physical and molecular properties of endothelial cells contributing to BBB integrity and function. Paracellular flux across the BBB is restricted by tight junction and adherens junction complexes. Some nutrients and essential molecules are selectively transported from luminal to abluminal membranes by specific influx systems. Most small lipophilic molecules passively diffused across the lipid layer are returned to the blood by ATP-dependent efflux transporters. P. gingivalis may cause vascular endothelial barrier disruption and increased permeability destroying intercellular junctions. This could promote the passage of this bacterium through the BBB to the AD brain where it has been found. ZO-1 = zonula occludens-1, JAM = junctional adhesion molecule, VE = cadherin (vascular endothelial-cadherin), IgG = immunoglobulin G. Adopted from Ref. [1]

Yamazaki Y, Kanekiyo T. Blood-brain barrier dysfunction and the pathogenesis of Alzheimer’s disease. Int J Mol Sci. 2017;18(9):1965.

 PubMed Web of Science ®Google Scholar