{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:21:39Z","timestamp":1790727699617,"version":"4.1.0"},"reference-count":409,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[2018,9,19]],"date-time":"2018-09-19T00:00:00Z","timestamp":1537315200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Aust N Z J Psychiatry"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>The blood\u2013brain barrier acts as a highly regulated interface; its dysfunction may exacerbate, and perhaps initiate, neurological and neuropsychiatric disorders.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>In this narrative review, focussing on redox, inflammatory and mitochondrial pathways and their effects on the blood\u2013brain barrier, a model is proposed detailing mechanisms which might explain how increases in blood\u2013brain barrier permeability occur and can be maintained with increasing inflammatory and oxidative and nitrosative stress being the initial drivers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Peripheral inflammation, which is causatively implicated in the pathogenesis of major psychiatric disorders, is associated with elevated peripheral pro-inflammatory cytokines, which in turn cause increased blood\u2013brain barrier permeability. Reactive oxygen species, such as superoxide radicals and hydrogen peroxide, and reactive nitrogen species, such as nitric oxide and peroxynitrite, play essential roles in normal brain capillary endothelial cell functioning; however, chronically elevated oxidative and nitrosative stress can lead to mitochondrial dysfunction and damage to the blood\u2013brain barrier. Activated microglia, redox control of which is mediated by nitric oxide synthases and nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, secrete neurotoxic molecules such as reactive oxygen species, nitric oxide, prostaglandin, cyclooxygenase-2, quinolinic acid, several chemokines (including monocyte chemoattractant protein-1 [MCP-1], C-X-C motif chemokine ligand 1 [CXCL-1] and macrophage inflammatory protein 1\u03b1 [MIP-1\u03b1]) and the pro-inflammatory cytokines interleukin-6, tumour necrosis factor-\u03b1 and interleukin-1\u03b2, which can exert a detrimental effect on blood\u2013brain barrier integrity and function. Similarly, reactive astrocytes produce neurotoxic molecules such as prostaglandin E2 and pro-inflammatory cytokines, which can cause a \u2018leaky brain\u2019.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Chronic inflammatory and oxidative and nitrosative stress is associated with the development of a \u2018leaky gut\u2019. The following evidence-based approaches, which address the leaky gut and blood\u2013brain barrier dysfunction, are suggested as potential therapeutic interventions for neurological and neuropsychiatric disorders: melatonin, statins, probiotics containing Bifidobacteria and Lactobacilli, N-acetylcysteine, and prebiotics containing fructo-oligosaccharides and galacto-oligosaccharides.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/0004867418796955","type":"journal-article","created":{"date-parts":[[2018,9,20]],"date-time":"2018-09-20T02:14:28Z","timestamp":1537409668000},"page":"924-948","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":129,"title":["Leaky brain in neurological and psychiatric disorders: Drivers and consequences"],"prefix":"10.1177","volume":"52","author":[{"given":"Gerwyn","family":"Morris","sequence":"first","affiliation":[{"name":"IMPACT Strategic Research Centre, Deakin University School 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