Review Article
Computational and Pharmacological Target of Neurovascular Unit for Drug Design and Delivery
Table 1
Pathological consequences of NVU disorder.
| Diseases | BBB proteins and affected mechanisms |
| Alzheimer’s disease | BBB disruption and permit peripheral IgG to brain. Decrease P-gp and accumulate amyloid-β in brain [67]. |
| Parkinson’s disease | BBB disruption increases therapeutic agent concentration and reduces efficacy of Pgp [6]. |
| Stroke | Astrocytes secrete TGFβ that downregulates tissue plasminogen activator (tPA) and anticoagulant thrombomodulin (TM) [68]. |
| Epilepsy | Transient BBB opening and upregulation of multiple drug resistance (MRD1) Pgp [69]. |
| Trauma | Opening of BBB, release of IL-6 from astrocytes, and neuroinflammation [70]. |
| HIV | BBB TJ disruption. Loss of glycoproteins and apoptosis of endothelial cell lead to increase diameter of cortical vessels [71]. |
| Infectious processes | Increase CSF/serum albumin ratio. Bacterial lipopolysaccharides affect BBB TJ [72]. |
| Brain tumours | Breakdown of BBB TJ, overexpress folate, insulin, and transferrin receptor, and downregulation of claudin 1/3 [73]. |
| Ischaemic brain oedema | BBB breakdown due to MMP9 release by neutrophils and degradation of occludin, claudins, and JAM [74]. |
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