It's well known that borrelia burgdorferi causes blood-brain-barrier dysfunction.
The blood–brain barrier acts very effectively to protect the brain from many common bacterial infections. Thus, infections of the brain are very rare. Infections of the brain that do occur are often very serious and difficult to treat. Antibodies are too large to cross the blood–brain barrier, and only certain antibiotics are able to pass. In some cases a drug has to be administered directly into the cerebrospinal fluid (CSF). However, drugs delivered directly to the CSF do not effectively penetrate into the brain tissue itself, possibly due to the tortuous nature of the interstitial space in the brain. The blood–brain barrier becomes more permeable during inflammation. This allows some antibiotics and phagocytes to move across the BBB. However, this also allows bacteria and viruses to infiltrate the BBB. An exception to the bacterial exclusion is the diseases caused by spirochetes, such as Borrelia, which causes Lyme disease, Group B streptococci which causes meningitis in newborns and Treponema pallidum, which causes syphilis. These harmful bacteria gain access by releasing cytotoxins like pneumolysin which have a direct toxic effect on brain microvascular endothelium and tight junctions.
Blood brain barrier dysfunction can lead to neurdegenrative and psychiatric disorders.
The role of the blood brain barrier in neurodegenerative disorders and their treatment.
Neurodegenerative disorders represent a major medical challenge that is set to increase substantially in the decades ahead with the massive increase in the number of people in the world aged 65 or more. Neuroprotective therapeutics have the potential to play a key role in helping manage this growing global burden of long-term neurological care. However, neuropharmaceutical research is associated with significant challenges including: (1) the complexity of the brain (the cause of the majority of neurodegenerative disorders remains unknown); (2) the liability of central nervous system (CNS) drugs to cause CNS side effects (which limits their use); and (3) the requirement of neuropharmaceuticals to cross the blood-brain barrier (BBB). The BBB itself also plays a key role in most (if not all) neurodegenerative disorders since BBB dysfunction inevitably leads to inflammatory change including the movement of immune cells and immune mediators into the brain, which then contribute to the process of neurodegeneration. This review focuses on the role of the BBB in both neurodegenerative disorders and neuropharmaceutical research.
Breaching the Blood-Brain Barrier as a Gate to Psychiatric Disorder
Role of blood-brain barrier in temporal lobe epilepsy and pharmacoresistance.The mechanisms underlying the development and progression of psychiatric illnesses are only partially known. Clinical data suggest blood-brain barrier (BBB) breakdown and inflammation are involved in some patients groups. Here we put forward the “BBB hypothesis” and abnormal blood-brain communication as key mechanisms leading to neuronal dysfunction underlying disturbed cognition, mood, and behavior. Based on accumulating clinical data and animal experiments, we propose that events within the “neurovascular unit” are initiated by a focal BBB breakdown, and are associated with dysfunction of brain astrocytes, a local inflammatory response, pathological synaptic plasticity, and increased network connectivity. Our hypothesis should be validated in animal models of psychiatric diseases and BBB breakdown. Recently developed imaging approaches open the opportunity to challenge our hypothesis in patients. We propose that molecular mechanisms controlling BBB permeability, astrocytic functions, and inflammation may become novel targets for the prevention and treatment of psychiatric disorders.
Temporal lobe epilepsy (TLE) is the most common form of focal epilepsies in adults. It is often initiated by an insult or brain injury which triggers a series of alterations which ultimately lead to seizures (epilepsy). In 50-70% of people with TLE the condition cannot be adequately treated by the present antiepileptic drugs. During the last decade the blood-brain barrier (BBB) has received renewed interest as a potential target to treat TLE or its progression. BBB changes have been observed in brain tissue of people with epilepsy as well as in experimental models at the structural, cellular and molecular level that could explain its role in the development and progression of epilepsy (epileptogenesis) as well as the development of drug resistance. Here, we will discuss the role of the BBB in TLE and drug resistance and summarize potential new therapies that may restore normal BBB function in order to put a brake on epileptogenesis and/or to improve drug treatment.
Does anybody have information if it's possible to restore blood brain barrier function (heal)?