Abstract:
:The central nervous system is protected by barriers which control the entry of compounds into the brain, thereby regulating brain homeostasis. The blood-brain barrier, formed by the endothelial cells of the brain capillaries, restricts access to brain cells of blood-borne compounds and facilitates nutrients essential for normal metabolism to reach brain cells. This very tight regulation of the brain homeostasis results in the inability of some small and large therapeutic compounds to cross the blood-brain barrier (BBB). Therefore, various strategies are being developed to enhance the amount and concentration of therapeutic compounds in the brain. In this review, we will address the different approaches used to increase the transport of therapeutics from blood into the brain parenchyma. We will mainly concentrate on the physiologic approach which takes advantage of specific receptors already expressed on the capillary endothelial cells forming the BBB and necessary for the survival of brain cells. Among all the approaches used for increasing brain delivery of therapeutics, the most accepted method is the use of the physiological approach which takes advantage of the transcytosis capacity of specific receptors expressed at the BBB. The low density lipoprotein receptor related protein (LRP) is the most adapted for such use with the engineered peptide compound (EPiC) platform incorporating the Angiopep peptide in new therapeutics the most advanced with promising data in the clinic.
journal_name
Neurobiol Disjournal_title
Neurobiology of diseaseauthors
Gabathuler Rdoi
10.1016/j.nbd.2009.07.028subject
Has Abstractpub_date
2010-01-01 00:00:00pages
48-57issue
1eissn
0969-9961issn
1095-953Xpii
S0969-9961(09)00207-1journal_volume
37pub_type
杂志文章,评审abstract::Cerebral ischemia activates endogenous neurogenesis in the subventricular zone (SVZ) and the dentate gyrus. Consecutively, SVZ-derived neural precursors migrate towards ischemic lesions. However, functional relevance of activated neurogenesis is limited by poor survival of new-born precursors. We therefore employed th...
journal_title:Neurobiology of disease
pub_type: 杂志文章
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更新日期:2009-04-01 00:00:00
abstract::Loss of function mutations in the SCN1A gene, which encodes the voltage-gated sodium channel Nav1.1, have been described in the majority of Dravet syndrome patients presenting with epileptic seizures, hyperactivity, autistic traits, and cognitive decline. We previously reported predominant Nav1.1 expression in parvalb...
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1006/nbdi.2002.0507
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journal_title:Neurobiology of disease
pub_type: 杂志文章,评审
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journal_title:Neurobiology of disease
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journal_title:Neurobiology of disease
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2004.10.020
更新日期:2005-04-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2013.03.010
更新日期:2013-07-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章,评审
doi:10.1016/j.nbd.2015.10.012
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2013.12.002
更新日期:2014-03-01 00:00:00
abstract::Oculopharyngeal muscular dystrophy (OPMD) is a late-onset disorder caused by a (GCG)n trinucleotide repeat expansion in the poly(A) binding protein nuclear-1 (PABPN1) gene, which in turn leads to an expanded polyalanine tract in the protein. We generated transgenic mice expressing either the wild type or the expanded ...
journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2004.09.021
更新日期:2005-04-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2015.11.010
更新日期:2016-02-01 00:00:00
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journal_title:Neurobiology of disease
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doi:10.1016/j.nbd.2019.03.004
更新日期:2019-07-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2020.105224
更新日期:2021-02-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2003.11.004
更新日期:2004-03-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2010.01.005
更新日期:2010-04-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2014.02.001
更新日期:2014-07-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2004.02.011
更新日期:2004-08-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2016.03.013
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journal_title:Neurobiology of disease
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更新日期:2020-11-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2012.05.013
更新日期:2012-10-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2003.09.013
更新日期:2004-02-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2017.04.020
更新日期:2017-08-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2004.07.004
更新日期:2004-12-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2009.07.015
更新日期:2009-11-01 00:00:00
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pub_type: 杂志文章,评审
doi:10.1016/j.nbd.2019.104579
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2013.10.010
更新日期:2014-02-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2010.02.011
更新日期:2010-06-01 00:00:00
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journal_title:Neurobiology of disease
pub_type: 杂志文章
doi:10.1016/j.nbd.2006.08.024
更新日期:2007-01-01 00:00:00