Editing Blood–brain barrier (section)

===Damage in injury and disease===
The blood–brain barrier may become damaged in certain [[neurological disease]]s, as indicated by [[neuroimaging]] studies of [[Alzheimer's disease]], [[amyotrophic lateral sclerosis]], [[epilepsy]], ischemic stroke,<ref name="Blood-brain barrier dysfunction in"/><ref>{{cite journal | vauthors = Turner RJ, Sharp FR | title = Implications of MMP9 for Blood Brain Barrier Disruption and Hemorrhagic Transformation Following Ischemic Stroke | journal = Frontiers in Cellular Neuroscience | volume = 10 | pages = 56 | date = 2016-03-04 | pmid = 26973468 | doi = 10.3389/fncel.2016.00056 | pmc = 4777722 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Mracsko E, Veltkamp R | title = Neuroinflammation after intracerebral hemorrhage | journal = Frontiers in Cellular Neuroscience | volume = 8 | pages = 388 | date = 2014-11-20 | pmid = 25477782 | doi = 10.3389/fncel.2014.00388 | pmc = 4238323 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Alluri H, Wiggins-Dohlvik K, Davis ML, Huang JH, Tharakan B | title = Blood-brain barrier dysfunction following traumatic brain injury | journal = Metabolic Brain Disease | volume = 30 | issue = 5 | pages = 1093–1104 | date = October 2015 | pmid = 25624154 | doi = 10.1007/s11011-015-9651-7 | s2cid = 17688028 }}</ref> and [[Traumatic brain injury|brain trauma]],<ref name=sweeney/> and in [[systemic disease]]s, such as [[liver failure]].<ref name=daneman/> Effects such as impaired glucose transport and endothelial degeneration may lead to metabolic dysfunction within the brain, and an increased permeability of the BBB to [[Inflammation|proinflammatory]] factors, potentially allowing antibiotics and [[phagocytes]] to move across the BBB.<ref name=daneman/><ref name=sweeney/> However, in many neurodegenerative diseases, the exact cause and pathology remains unknown. It is still unclear whether the BBB dysfunction in the disease is a causative agent, a result of the disease, or somewhere in the middle.