uu.seUppsala University Publications
Change search
ReferencesLink to record
Permanent link

Direct link
Blood–Central Nervous System Barriers: The Gateway to Neurodegeneration, Neuroprotection and Neuroregeneration
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
2009 (English)In: Handbook of Neurochemistry and Molecular Neurobiology: Brain and Spinal Cord Trauma / [ed] Abel Lajtha, Naren Banik & Swapan K. Ray, Springer, 2009, 363-457 p.Chapter in book (Other academic)
Abstract [en]

The microenvironment of the central nervous system (CNS) is precisely and meticulously maintained by a set of dynamic physiological barriers located within the cerebral microvessels of the brain (blood–brain barrier, BBB) and the spinal cord (blood–spinal cord barrier, BSCB), as well as within the epithelial cells of the choroid plexus separating the blood and cerebrospinal fluid (CSF) interface (blood–CSF barrier, BCSFB). The physicochemical properties of these cellular barriers are quite comparable to that of an extended plasma membrane. The BBB and the BSCB are quite tight to small molecules (12 Å, Lanthanum ion), whereas BCSFB is less restrictive in nature. On the other hand, the ependymal cell linings of the cerebral ventricles and spinal canal referred to as CSF–brain barrier do not normally restrict passage of several molecules of small sizes. However, protein transport across these blood–CNS barriers (BCNSB) is severely restricted. Entry of proteins into the CNS microenvironment induces vasogenic edema formation that is primarily responsible for cell and tissue injury. These BCNSB are often compromised under a wide variety of psychological, traumatic, metabolic, ischemic, environmental, or chemical insults leading to neuronal, glial, and axonal damage. Opening of the BCSNB to various endogenous or exogenous substances and proteins alters the molecular, cellular, biochemical, immunological, and metabolic environment of the CNS leading to abnormal neuronal function and/or brain pathology. This review is focused on current status of the BCSNB breakdown in experimental models of emotional stress, traumatic injuries, psychostimulants as well as key environmental health hazards, i.e., nanoparticles and heat exposure. Breakdown of the BCNSB in these conditions altered gene expression and induced brain pathology leading to neurodegeneration. Attenuation of the BCNSB disruption with drugs or antibodies affecting neurochemical metabolism and/or neurotrophic factors markedly reduced the development of brain pathology. Taken together, these novel observations strongly point out the role of BCNSB as a “gateway” to the neurodegeneration, neuroprotection, and/or neuroregeneration in neurological diseases.

Place, publisher, year, edition, pages
Springer, 2009. 363-457 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-171275DOI: 10.1007/978-0-387-30375-8_17ISBN: 978-0-387-30343-7OAI: oai:DiVA.org:uu-171275DiVA: diva2:510379
Available from: 2012-03-16 Created: 2012-03-16Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full text

Search in DiVA

By author/editor
Sharma, Hari Shanker
By organisation
Anaesthesiology and Intensive Care
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 169 hits
ReferencesLink to record
Permanent link

Direct link