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      Gene expression and functional annotation of human choroid plexus epithelium failure in Alzheimer's disease.

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          Abstract

          Alzheimer's disease (AD) is the most common form of dementia. AD has a multifactorial disease etiology and is currently untreatable. Multiple genes and molecular mechanisms have been implicated in AD, including ß-amyloid deposition in the brain, neurofibrillary tangle accumulation of hyper-phosphorylated Tau, synaptic failure, oxidative stress and inflammation. Relatively little is known about the role of the blood-brain barriers, especially the blood-cerebrospinal fluid barrier (BCSFB), in AD. The BCSFB is involved in cerebrospinal fluid (CSF) production, maintenance of brain homeostasis and neurodegenerative disorders.

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          The blood-brain barrier in health and disease.

          Richard Daneman (2012)
          The blood-brain barrier (BBB) is a term used to describe a series of properties possessed by the vasculature of the central nervous system (CNS) that tightly regulate the movement of ions, molecules, and cells between the blood and the CNS. This barrier is crucial to provide the appropriate environment to allow for proper neural function, as well as protect the CNS from injury and disease. In this review, I discuss the cellular and molecular composition of the BBB and how the development and function of the BBB is regulated by interactions with the CNS microenvironment. I further discuss what is known about BBB dysfunction during CNS injury and disease, as well as methodology used to deliver drugs across the BBB to the CNS. Copyright © 2012 American Neurological Association.
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            Blood–brain-barriers in aging and in Alzheimer’s disease

            Fernanda Marques, Fernanda Marques, João Carlos Sousa … (2013)
            The aging process correlates with a progressive failure in the normal cellular and organ functioning; these alterations are aggravated in Alzheimer’s disease (AD). In both aging and AD there is a general decrease in the capacity of the body to eliminate toxic compounds and, simultaneously, to supply the brain with relevant growth and nutritional factors. The barriers of the brain are targets of this age related dysfunction; both the endothelial cells of the blood–brain barrier and the choroid plexus epithelial cells of the blood-cerebrospinal fluid barrier decrease their secretory capacity towards the brain and their ability to remove toxic compounds from the brain. Additionally, during normal aging and in AD, the permeability of the brain barriers increase. As such, a greater contact of the brain parenchyma with the blood content alters the highly controlled neural environment, which impacts on neural function. Of interest, the brain barriers are more than mere obstacles to the passage of molecules and cells, and therefore active players in brain homeostasis, which is still to be further recognized and investigated in the context of health and disease. Herein, we provide a review on how the brain barriers change during aging and in AD and how these processes impact on brain function.
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              Functional Characterisation of the Maturation of the Blood-Brain Barrier in Larval Zebrafish

              Angeleen Fleming, Heike Diekmann, Paul Goldsmith (2013)
              Zebrafish are becoming increasingly popular as an organism in which to model human disease and to study the effects of small molecules on complex physiological and pathological processes. Since larvae are no more than a few millimetres in length, and can live in volumes as small as 100 microliters, they are particularly amenable to high-throughput and high content compound screening in 96 well plate format. There is a growing literature providing evidence that many compounds show similar pharmacological effects in zebrafish as they do in mammals, and in particular humans. However, a major question regarding their utility for small molecule screening for neurological conditions is whether a molecule will reach its target site within the central nervous system. Studies have shown that Claudin-5 and ZO-1, tight-junction proteins which are essential for blood-brain barrier (BBB) integrity in mammals, can be detected in some cerebral vessels in zebrafish from 3 days post-fertilisation (d.p.f.) onwards and this timing coincides with the retention of dyes, immunoreactive tracers and fluorescent markers within some but not all cerebral vessels. Whilst these findings demonstrate that features of a BBB are first present at 3 d.p.f., it is not clear how quickly the zebrafish BBB matures or how closely the barrier resembles that of mammals. Here, we have combined anatomical analysis by transmission electron microscopy, functional investigation using fluorescent markers and compound uptake using liquid chromatography/tandem mass spectrometry to demonstrate that maturation of the zebrafish BBB occurs between 3 d.p.f. and 10 d.p.f. and that this barrier shares both structural and functional similarities with that of mammals.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): BMC Genomics
                Title: BMC genomics
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 1471-2164
                ISSN (Print): 1471-2164
                Publication date (Electronic): Nov 16 2015
                Volume: 16
                Affiliations
                [1 ] Department of Clinical Genetics, Academic Medical Centre, Amsterdam, AMC, Meibergdreef 9, 1105 AZ AMC, Amsterdam, The Netherlands. aabergen@amc.uva.nl.
                [2 ] The Netherlands Institute for Neurosciences (NIN-KNAW), Amsterdam, The Netherlands. aabergen@amc.uva.nl.
                [3 ] The Netherlands Institute for Neurosciences (NIN-KNAW), Amsterdam, The Netherlands.
                [4 ] Department of Clinical Genetics, Academic Medical Centre, Amsterdam, AMC, Meibergdreef 9, 1105 AZ AMC, Amsterdam, The Netherlands.
                [5 ] University Eye Clinic Maastricht, MUMC, Maastricht, The Netherlands.
                [6 ] Department of Ophthalmology, VUMC, Amsterdam, The Netherlands.
                Article
                Publisher Item ID: 10.1186/s12864-015-2159-z
                DOI: 10.1186/s12864-015-2159-z
                PMC ID: 4647590
                PubMed ID: 26573292
                SO-VID: 8486155c-8dd6-425e-a63e-1b3080cfe818
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