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Article: The HPA - Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain.

Bellavance, Marc-André / Rivest, Serge

2014 Volume 5, Page(s) 136

Abstract: In response to physiological and psychogenic stressors, the hypothalamic-pituitary-adrenal (HPA) axis orchestrates the systemic release of glucocorticoids (GCs). By virtue of nearly ubiquitous expression of the GC receptor and the multifaceted metabolic, ...

Abstract	In response to physiological and psychogenic stressors, the hypothalamic-pituitary-adrenal (HPA) axis orchestrates the systemic release of glucocorticoids (GCs). By virtue of nearly ubiquitous expression of the GC receptor and the multifaceted metabolic, cardiovascular, cognitive, and immunologic functions of GCs, this system plays an essential role in the response to stress and restoration of an homeostatic state. GCs act on almost all types of immune cells and were long recognized to perform salient immunosuppressive and anti-inflammatory functions through various genomic and non-genomic mechanisms. These renowned effects of the steroid hormone have been exploited in the clinic for the past 70 years and synthetic GC derivatives are commonly used for the therapy of various allergic, autoimmune, inflammatory, and hematological disorders. The role of the HPA axis and GCs in restraining immune responses across the organism is however still debated in light of accumulating evidence suggesting that GCs can also have both permissive and stimulatory effects on the immune system under specific conditions. Such paradoxical actions of GCs are particularly evident in the brain, where substantial data support either a beneficial or detrimental role of the steroid hormone. In this review, we examine the roles of GCs on the innate immune system with a particular focus on the CNS compartment. We also dissect the numerous molecular mechanisms through which GCs exert their effects and discuss the various parameters influencing the paradoxical immunomodulatory functions of GCs in the brain.
Language	English
Publishing date	2014-03-31
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2014.00136
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Article ; Online: The neuroendocrine control of the innate immune system in health and brain diseases.

Bellavance, Marc-André / Rivest, Serge

Immunological reviews

2012 Volume 248, Issue 1, Page(s) 36–55

Abstract: The innate immune reaction takes place in the brain during immunogenic challenges, injury, and disease. Such a response is highly regulated by numerous anti-inflammatory mechanisms that may directly affect the ultimate consequences of such a reaction ... ...

Abstract	The innate immune reaction takes place in the brain during immunogenic challenges, injury, and disease. Such a response is highly regulated by numerous anti-inflammatory mechanisms that may directly affect the ultimate consequences of such a reaction within the cerebral environment. The neuroendocrine control of this innate immune system by glucocorticoids is critical for the delicate balance between cell survival and damage in the presence of inflammatory mediators. Glucocorticoids play key roles in regulating the expression of inflammatory genes, and they also have the ability to modulate numerous functions that may ultimately lead to brain damage or repair after injury. Here we review these mechanisms and discuss data supporting both neuroprotective and detrimental roles of the neuroendocrine control of innate immunity.
MeSH term(s)	Animals ; Brain Diseases/immunology ; Brain Diseases/metabolism ; Central Nervous System/drug effects ; Central Nervous System/immunology ; Glucocorticoids/pharmacology ; Humans ; Hypothalamo-Hypophyseal System/immunology ; Hypothalamo-Hypophyseal System/metabolism ; Immunity, Innate ; Microglia/immunology ; Microglia/metabolism ; Neurosecretory Systems/immunology ; Neurosecretory Systems/metabolism ; Pituitary-Adrenal System/immunology ; Pituitary-Adrenal System/metabolism ; Signal Transduction
Chemical Substances	Glucocorticoids
Language	English
Publishing date	2012-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/j.1600-065X.2012.01129.x
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Article ; Online: Role of adaptor protein MyD88 in TLR-mediated preconditioning and neuroprotection after acute excitotoxicity.

Larochelle, Antoine / Bellavance, Marc-André / Rivest, Serge

Brain, behavior, and immunity

2015 Volume 46, Page(s) 221–231

Abstract: Excitotoxic cell death is a crucial mechanism through which neurodegeneration occurs in numerous pathologies of the central nervous system (CNS), such as Alzheimer's disease, stroke and spinal cord injury. Toll-like receptors (TLRs) are strongly ... ...

Abstract	Excitotoxic cell death is a crucial mechanism through which neurodegeneration occurs in numerous pathologies of the central nervous system (CNS), such as Alzheimer's disease, stroke and spinal cord injury. Toll-like receptors (TLRs) are strongly expressed on microglial cells and are key regulators of the innate immune response to neuronal damage. However, it is still unclear whether their stimulation is protective or harmful in excitotoxic contexts. In this study, we demonstrate that systemic administration of lipopolysaccharide (LPS) or Pam3CSK4 24h prior to an intrastriatal injection of kainic acid (KA) significantly protected cortical neurons in the acute phase of injury. Protection could not be detected with the TLR3 ligand poly-IC. Histological analyses revealed that microglia of LPS and Pam3CSK4 pre-conditioned group were primed to react to injury and exhibited a stronger expression of Tnf and Tlr2 mRNA. We also found that mice deficient for MyD88, a critical adaptor protein for most TLR, were more vulnerable than WT mice to KA-induced excitotoxicity at early (12h and 24h) and late (10days) time points. Finally, bone-marrow chimeric mice revealed that MyD88 signaling in CNS resident cells, but not in cells of hematopoietic origin, mediates the protective effect. This study unravels the potential of TLR2 and TLR4 agonists to induce a protective state of preconditioning against KA-mediated excitotoxicity and further highlights the beneficial role of cerebral MyD88 signaling in this context.
MeSH term(s)	Animals ; Cell Death/drug effects ; Cell Death/physiology ; Kainic Acid/toxicity ; Lipopeptides/pharmacology ; Lipopolysaccharides ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotection/physiology ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Toll-Like Receptors/genetics ; Toll-Like Receptors/metabolism
Chemical Substances	Lipopeptides ; Lipopolysaccharides ; Myeloid Differentiation Factor 88 ; Pam(3)CSK(4) peptide ; Toll-Like Receptors ; Kainic Acid (SIV03811UC)
Language	English
Publishing date	2015-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2015.02.019
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Article: Bone marrow-derived macrophages and the CNS: An update on the use of experimental chimeric mouse models and bone marrow transplantation in neurological disorders.

Larochelle, Antoine / Bellavance, Marc-André / Michaud, Jean-Philippe / Rivest, Serge

Biochimica et biophysica acta

2015 Volume 1862, Issue 3, Page(s) 310–322

Abstract: ... the landmark studies that used chimeric mice to characterize the roles of microglia and BMDM ... and Markus Schwaninger. ...

Abstract	The central nervous system (CNS) is a very unique system with multiple features that differentiate it from systemic tissues. One of the most captivating aspects of its distinctive nature is the presence of the blood brain barrier (BBB), which seals it from the periphery. Therefore, to preserve tissue homeostasis, the CNS has to rely heavily on resident cells such as microglia. These pivotal cells of the mononuclear lineage have important and dichotomous roles according to various neurological disorders. However, certain insults can overwhelm microglia as well as compromising the integrity of the BBB, thus allowing the infiltration of bone marrow-derived macrophages (BMDMs). The use of myeloablation and bone marrow transplantation allowed the generation of chimeric mice to study resident microglia and infiltrated BMDM separately. This breakthrough completely revolutionized the way we captured these 2 types of mononuclear phagocytic cells. We now realize that microglia and BMDM exhibit distinct features and appear to perform different tasks. Since these cells are central in several pathologies, it is crucial to use chimeric mice to analyze their functions and mechanisms to possibly harness them for therapeutic purpose. This review will shed light on the advent of this methodology and how it allowed deciphering the ontology of microglia and its maintenance during adulthood. We will also compare the different strategies used to perform myeloablation. Finally, we will discuss the landmark studies that used chimeric mice to characterize the roles of microglia and BMDM in several neurological disorders. This article is part of a Special Issue entitled: Neuro Inflammation edited by Helga E. de Vries and Markus Schwaninger.
MeSH term(s)	Animals ; Bone Marrow Transplantation/methods ; Brain/metabolism ; Brain/pathology ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Disease Models, Animal ; Humans ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Mice, Transgenic ; Microglia/metabolism ; Microglia/pathology ; Nervous System Diseases/genetics ; Nervous System Diseases/pathology
Language	English
Publishing date	2015-10-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2015.09.017
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Article: IL-1RAcPb signaling regulates adaptive mechanisms in neurons that promote their long-term survival following excitotoxic insults.

Gosselin, David / Bellavance, Marc-André / Rivest, Serge

Frontiers in cellular neuroscience

2013 Volume 7, Page(s) 9

Abstract: Excitotoxicity is a major component of neurodegenerative diseases and is typically accompanied by an inflammatory response. Cytokines IL-1alpha and IL-1beta are key regulators of this inflammatory response and modulate the activity of numerous cell types, ...

Abstract	Excitotoxicity is a major component of neurodegenerative diseases and is typically accompanied by an inflammatory response. Cytokines IL-1alpha and IL-1beta are key regulators of this inflammatory response and modulate the activity of numerous cell types, including neurons. IL-1RAcPb is an isoform of IL-1RAcP expressed specifically in neurons and promotes their survival during acute inflammation. Here, we investigated in vivo whether IL-1RAcPb also promotes neuronal survival in a model of excitotoxicity. Intrastriatal injection of kainic acid (KA) in mice caused a strong induction of IL-1 cytokines mRNA in the brain. The stress response of cortical neurons at 12 h post-injection, as measured by expression of Atf3, FoxO3a, and Bdnf mRNAs, was similar in WT and AcPb-deficient mice. Importantly however, a delayed upregulation in the transcription of calpastatin was significantly higher in WT than in AcPb-deficient mice. Finally, although absence of AcPb signaling had no effect on damage to neurons in the cortex at early time points, it significantly impaired their long-term survival. These data suggest that in a context of excitotoxicity, stimulation of IL-1RAcPb signaling may promote the activity of a key neuroprotective mechanism.
Language	English
Publishing date	2013-02-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2013.00009
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Article ; Online: Real-Time In Vivo Imaging Reveals the Ability of Monocytes to Clear Vascular Amyloid Beta

Jean-Philippe Michaud / Marc-André Bellavance / Paul Préfontaine / Serge Rivest

Cell Reports, Vol 5, Iss 3, Pp 646-

2013 Volume 653

Abstract: Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aβ) that is assumed to result from impaired elimination of this neurotoxic peptide. Most patients with AD also exhibit cerebral amyloid angiopathy, which consists of Aβ ... ...

Abstract	Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aβ) that is assumed to result from impaired elimination of this neurotoxic peptide. Most patients with AD also exhibit cerebral amyloid angiopathy, which consists of Aβ deposition within the cerebral vasculature. The contribution of monocytes in AD has so far been limited to macrophage precursors. In this study, we aimed to investigate whether circulating monocytes could play a role in the elimination of Aβ. With live intravital two-photon microscopy, we demonstrate that patrolling monocytes are attracted to and crawl onto the luminal walls of Aβ-positive veins, but not on Aβ-positive arteries or Aβ-free blood vessels. Additionally, we report the presence of crawling monocytes carrying Aβ in veins and their ability to circulate back into the bloodstream. Selective removal of Ly6Clo monocytes in APP/PS1 mice induced a significant increase of Aβ load in the cortex and hippocampus. These data uncover the ability of Ly6Clo monocytes to naturally target and eliminate Aβ within the lumen of veins and constitute a potential therapeutic target in AD.
Keywords	Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2013-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Real-time in vivo imaging reveals the ability of monocytes to clear vascular amyloid beta.

Michaud, Jean-Philippe / Bellavance, Marc-André / Préfontaine, Paul / Rivest, Serge

Cell reports

2013 Volume 5, Issue 3, Page(s) 646–653

Abstract: Alzheimer's disease (AD) is characterized by the accumulation of amyloid beta (Aβ) that is assumed to result from impaired elimination of this neurotoxic peptide. Most patients with AD also exhibit cerebral amyloid angiopathy, which consists of Aβ ... ...

Abstract	Alzheimer's disease (AD) is characterized by the accumulation of amyloid beta (Aβ) that is assumed to result from impaired elimination of this neurotoxic peptide. Most patients with AD also exhibit cerebral amyloid angiopathy, which consists of Aβ deposition within the cerebral vasculature. The contribution of monocytes in AD has so far been limited to macrophage precursors. In this study, we aimed to investigate whether circulating monocytes could play a role in the elimination of Aβ. With live intravital two-photon microscopy, we demonstrate that patrolling monocytes are attracted to and crawl onto the luminal walls of Aβ-positive veins, but not on Aβ-positive arteries or Aβ-free blood vessels. Additionally, we report the presence of crawling monocytes carrying Aβ in veins and their ability to circulate back into the bloodstream. Selective removal of Ly6C(lo) monocytes in APP/PS1 mice induced a significant increase of Aβ load in the cortex and hippocampus. These data uncover the ability of Ly6C(lo) monocytes to naturally target and eliminate Aβ within the lumen of veins and constitute a potential therapeutic target in AD.
MeSH term(s)	Alzheimer Disease/blood ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/blood ; Animals ; Blood Vessels/metabolism ; Blood Vessels/pathology ; Image Processing, Computer-Assisted/methods ; Leukocytes, Mononuclear/metabolism ; Mice ; Mice, Inbred C57BL ; Microscopy, Fluorescence, Multiphoton/methods
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2013-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2013.10.010
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Article ; Online: Patrolling monocytes play a critical role in CX3CR1-mediated neuroprotection during excitotoxicity.

Bellavance, Marc-André / Gosselin, David / Yong, V Wee / Stys, Peter K / Rivest, Serge

Brain structure & function

2015 Volume 220, Issue 3, Page(s) 1759–1776

Abstract: ... following sterile excitotoxicity. Cx3cr1 disruption also markedly altered the blood levels of patrolling ...

Abstract	Excitotoxicity underlies neuronal death in many neuropathological disorders, such as Alzheimer's disease and multiple sclerosis. In murine models of these diseases, disruption of CX3CR1 signaling has thus far generated data either in favor or against a neuroprotective role of this crucial regulator of microglia and monocyte functions. In this study, we investigated the recruitment of circulating PU.1-expressing cells following sterile excitotoxicity and delineated the CX3CR1-dependent neuroprotective functions of circulating monocytes versus that of microglia in this context. WT, Cx3cr1-deficient and chimeric mice were subjected to a sterile excitotoxic insult via an intrastriatal injection of kainic acid (KA), a conformational analog of glutamate. Following KA administration, circulating monocytes physiologically engrafted the brain and selectively accumulated in the vicinity of excitotoxic lesions where they gave rise to activated macrophages depicting strong Iba1 and CD68 immunoreactivity 7 days post-injury. Monocyte-derived macrophages completely vanished upon recovery and did thus not permanently seed the brain. Furthermore, Cx3cr1 deletion significantly exacerbated neuronal death, behavioral deficits and activation of microglia cells following sterile excitotoxicity. Cx3cr1 disruption also markedly altered the blood levels of patrolling monocytes 24 h after KA administration. The specific elimination of patrolling monocytes using Nr4a1(-/-) chimeric mice conditioned with chemotherapy provided direct evidence that these circulating monocytes are essential for neuroprotection. Taken together, these data support a beneficial role of CX3CR1 signaling during excitotoxicity and highlight a novel and pivotal role of patrolling monocytes in neuroprotection. These findings open new research and therapeutic avenues for neuropathological disorders implicating excitotoxicity.
MeSH term(s)	Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; CX3C Chemokine Receptor 1 ; Calcium-Binding Proteins/metabolism ; Cell Death/drug effects ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Disease Models, Animal ; Kainic Acid/administration & dosage ; Kainic Acid/toxicity ; Macrophages/cytology ; Macrophages/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microfilament Proteins/metabolism ; Microglia/cytology ; Microglia/drug effects ; Microinjections/methods ; Monocytes/cytology ; Monocytes/drug effects ; Neurons/drug effects ; Neuroprotection/drug effects ; Nuclear Receptor Subfamily 4, Group A, Member 1/deficiency ; Nuclear Receptor Subfamily 4, Group A, Member 1/genetics ; Receptors, Chemokine/deficiency ; Receptors, Chemokine/genetics
Chemical Substances	Aif1 protein, mouse ; Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD68 antigen, human ; CX3C Chemokine Receptor 1 ; Calcium-Binding Proteins ; Cx3cr1 protein, mouse ; Microfilament Proteins ; Nr4a1 protein, mouse ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Receptors, Chemokine ; Kainic Acid (SIV03811UC)
Language	English
Publishing date	2015
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2273162-3
ISSN	1863-2661 ; 1863-2653
ISSN (online)	1863-2661
ISSN	1863-2653
DOI	10.1007/s00429-014-0759-z
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Article ; Online: Uptake and intracellular release kinetics of liposome formulations in glioma cells.

Bellavance, Marc-André / Poirier, Marie-Belle / Fortin, David

International journal of pharmaceutics

2010 Volume 395, Issue 1-2, Page(s) 251–259

Abstract: Glioblastoma (GBM) is the most malignant primary brain tumor in adults, and its prognosis remains very limited despite decades of research. Enhanced drug delivery to GBM using liposomes represents a promising therapeutic strategy. In this study, we ... ...

Abstract	Glioblastoma (GBM) is the most malignant primary brain tumor in adults, and its prognosis remains very limited despite decades of research. Enhanced drug delivery to GBM using liposomes represents a promising therapeutic strategy. In this study, we describe a novel cationic and pH-sensitive liposome formulation composed of DPPC:DC-Chol:DOPE:DHPE Oregon Green producing efficient internalization and intracellular delivery to F98 and U-118 GBM cells. With a series of derived modifications of the lipid composition, we investigated the impact of membrane fluidity, steric stabilization and loss of both cationic and pH-sensitive components on cellular uptake and intracellular release kinetics by flow cytometry and confocal microscopy, respectively. DPPC:DC-Chol:DOPE:DHPE Oregon Green liposomes were strongly internalized in both cell lines within 6h. Following cellular uptake, liposomes traveled towards the nucleus (12h) and gradually released their cargo in the cytosol (over 24h). Modifications in liposomal composition of our original formulation had detrimental consequences on both the uptake and intracellular release kinetics in the two tested cell lines. Thus, we report a novel potent liposomal formulation for efficient cytosolic delivery of intracellular therapeutics such as chemotherapy agents and siRNAs to GBM cells.
MeSH term(s)	1,2-Dipalmitoylphosphatidylcholine/metabolism ; Animals ; Biological Transport ; Brain Neoplasms/metabolism ; Carboxylic Acids/metabolism ; Cell Line, Tumor ; Chemistry, Pharmaceutical ; Cholesterol/analogs & derivatives ; Cholesterol/metabolism ; Flow Cytometry ; Glioma/metabolism ; Humans ; Hydrogen-Ion Concentration ; Kinetics ; Lipid Metabolism ; Liposomes ; Membrane Fluidity ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Particle Size ; Phosphatidylethanolamines/metabolism ; Phosphatidylglycerols/metabolism ; Polyethylene Glycols/metabolism ; Rats
Chemical Substances	1,2-dioleoyl-glycero-3-phosphatidyl ethanolamine ; Carboxylic Acids ; DPPE-PEG2000 ; Liposomes ; Oregon Green 488 carboxylic acid ; Phosphatidylethanolamines ; Phosphatidylglycerols ; 3-(N-(N',N'-dimethylaminoethane)carbamoyl)cholesterol (137056-72-5) ; 1,2-Dipalmitoylphosphatidylcholine (2644-64-6) ; Polyethylene Glycols (30IQX730WE) ; 1,2-didodecanoyl-glycero-3-phosphocholine (63644-55-3) ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2010-08-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	428962-6
ISSN	1873-3476 ; 0378-5173
ISSN (online)	1873-3476
ISSN	0378-5173
DOI	10.1016/j.ijpharm.2010.05.017
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Article ; Online: Recent advances in blood-brain barrier disruption as a CNS delivery strategy.

Bellavance, Marc-André / Blanchette, Marie / Fortin, David

The AAPS journal

2008 Volume 10, Issue 1, Page(s) 166–177

Abstract: The blood-brain barrier (BBB) is a complex functional barrier composed of endothelial cells, pericytes, astrocytic endfeets and neuronal cells. This highly organized complex express a selective permeability for molecules that bear, amongst other ... ...

Abstract	The blood-brain barrier (BBB) is a complex functional barrier composed of endothelial cells, pericytes, astrocytic endfeets and neuronal cells. This highly organized complex express a selective permeability for molecules that bear, amongst other parameters, adequate molecular weight and sufficient liposolubility. Unfortunately, very few therapeutic agents currently available do cross the BBB and enters the CNS. As the BBB limitation is more and more acknowledged, many innovative surgical and pharmacological strategies have been developed to circumvent it. This review focuses particularly on the osmotic opening of the BBB, a well-documented approach intended to breach the BBB. Since its inception by Rapoport in 1972, pre-clinical studies have provided important information on the extent of BBB permeation. Thanks to Neuwelt and colleagues, the osmotic opening of the BBB made its way to the clinic. However, many questions remain as to the detailed physiology of the procedure, and its best application to the clinic. Using different tools, amongst which MRI as a real-time in vivo characterization of the BBB permeability and CNS delivery, we attempt to better define the osmotic BBB permeabilization physiology. These ongoing studies are described, and data related to spatial and temporal distribution of a molecule after osmotic BBB breaching, as well as the window of BBB permeabilization, are discussed. We also summarize recent clinical series highlighting promising results in the application of this procedure to maximize delivery of chemotherapy in the treatment of brain tumor patients.
MeSH term(s)	Animals ; Blood-Brain Barrier/diagnostic imaging ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Central Nervous System/diagnostic imaging ; Central Nervous System/drug effects ; Central Nervous System/metabolism ; Humans ; Pharmaceutical Preparations/administration & dosage ; Pharmaceutical Preparations/metabolism ; Radiography
Chemical Substances	Pharmaceutical Preparations
Language	English
Publishing date	2008-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1550-7416
ISSN (online)	1550-7416
DOI	10.1208/s12248-008-9018-7
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