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Article ; Online: Local and remote interactions between macrophages and microglia in neurological conditions.

Boillée, Séverine

2021 Volume 74, Page(s) 118–124

Abstract: In the central nervous system (CNS) parenchymal macrophages are called microglial cells and have a distinct developmental origin and can self-renew. However, during pathological conditions, when the blood-brain-barrier becomes leaky, including after ... ...

Abstract	In the central nervous system (CNS) parenchymal macrophages are called microglial cells and have a distinct developmental origin and can self-renew. However, during pathological conditions, when the blood-brain-barrier becomes leaky, including after injury, in multiple sclerosis or with glioblastoma, monocyte-derived macrophages (MDM) infiltrate the CNS and cohabit with microglia. In neurodegenerative diseases such as Alzheimer's disease or ALS, MDM mostly do not enter the CNS, and instead microglia take several identities. In the specific case of ALS, the affected motor neurons are even surrounded locally by microglia, while along the peripheral nerves, by MDM-derived macrophages. The specific functions and interactions of these different myeloid cells are only starting to be recognized, but hold high promise for more targeted therapies.
MeSH term(s)	Alzheimer Disease ; Amyotrophic Lateral Sclerosis/pathology ; Central Nervous System ; Humans ; Macrophages/pathology ; Microglia
Language	English
Publishing date	2021-12-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2021.11.006
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Zs.A 2773: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 13: Show issues

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Article ; Online: The contribution of the peripheral immune system to neurodegeneration.

Berriat, Félix / Lobsiger, Christian S / Boillée, Séverine

Nature neuroscience

2023 Volume 26, Issue 6, Page(s) 942–954

Abstract: Microglial cells are the major immune cells of the central nervous system (CNS), and directly react to neurodegeneration, but other immune cell types are also able to react to pathology and can modify the course of neurodegenerative processes. These ... ...

Abstract	Microglial cells are the major immune cells of the central nervous system (CNS), and directly react to neurodegeneration, but other immune cell types are also able to react to pathology and can modify the course of neurodegenerative processes. These mainly include monocytes/macrophages and lymphocytes. While these peripheral immune cells were initially considered to act only after infiltrating the CNS, recent evidence suggests that some of them can also act directly from the periphery. We will review the existing and emerging evidence for a role of peripheral immune cells in neurodegenerative diseases, both with and without CNS infiltration. Our focus will be on amyotrophic lateral sclerosis, but we will also compare to Alzheimer's disease and Parkinson's disease to highlight similarities or differences. Peripheral immune cells are easily accessible, and therefore may be an attractive therapeutic target for neurodegenerative diseases. Thus, understanding how these peripheral immune cells communicate with the CNS deserves deeper investigation.
MeSH term(s)	Humans ; Central Nervous System ; Alzheimer Disease/metabolism ; Neurodegenerative Diseases/pathology ; Amyotrophic Lateral Sclerosis/pathology ; Leukocytes/metabolism
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-023-01323-6
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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Article ; Online: New insights on the disease contribution of neuroinflammation in amyotrophic lateral sclerosis.

Chiot, Aude / Lobsiger, Christian S / Boillée, Séverine

Current opinion in neurology

2019 Volume 32, Issue 5, Page(s) 764–770

Abstract: Purpose of review: Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron disease with a strong neuroinflammatory component. This review summarizes how the connection between neurodegeneration and the immune system is strengthened by new ... ...

Abstract	Purpose of review: Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron disease with a strong neuroinflammatory component. This review summarizes how the connection between neurodegeneration and the immune system is strengthened by new discoveries from ALS genetics and the analysis of subpopulations of immune cells in ALS. Recent findings: Recent genes identified in ALS encode for proteins with direct immune roles, which when mutated lead to deregulation of immune functions, potentially influencing the disease. Although neuroinflammation in the central nervous system (CNS) of ALS patients has been well documented, new evidence suggests also direct malfunctions of immune cells in the CNS and at the periphery. Although CD4+ T-regulatory lymphocytes are protective in ALS, their number and function are altered over the disease course. CD8+ T cells are detrimental for motor neurons in the CNS but show some protective roles at the periphery. Similarly, the presence of mast cells in muscles of ALS models and patients and impairments of monocyte functions reveal potential new players in ALS disease progression. Summary: Although motor neuron degeneration is considered the prime event in ALS, dysfunctions in immune processes can impact the disease, highlighting that targeting specific immune components is a strategy for developing biomarkers and ultimately new drugs.
MeSH term(s)	Animals ; Humans ; Myasthenic Syndromes, Congenital/drug therapy ; Myasthenic Syndromes, Congenital/genetics ; Myasthenic Syndromes, Congenital/pathology ; Myasthenic Syndromes, Congenital/physiopathology
Language	English
Publishing date	2019-07-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1182686-1
ISSN	1473-6551 ; 1350-7540
ISSN (online)	1473-6551
ISSN	1350-7540
DOI	10.1097/WCO.0000000000000729
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Zs.A 2524: Show issues

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Article ; Online: Effects of a Single Head Exposure to GSM-1800 MHz Signals on the Transcriptome Profile in the Rat Cerebral Cortex: Enhanced Gene Responses Under Proinflammatory Conditions.

Lameth, Julie / Arnaud-Cormos, Delia / Lévêque, Philippe / Boillée, Séverine / Edeline, Jean-Marc / Mallat, Michel

Neurotoxicity research

2020 Volume 38, Issue 1, Page(s) 105–123

Abstract: Mobile communications are propagated by electromagnetic fields (EMFs), and since the 1990s, they operate with pulse-modulated signals such as the GSM-1800 MHz. The biological effects of GSM-EMF in humans affected by neuropathological processes remain ... ...

Abstract	Mobile communications are propagated by electromagnetic fields (EMFs), and since the 1990s, they operate with pulse-modulated signals such as the GSM-1800 MHz. The biological effects of GSM-EMF in humans affected by neuropathological processes remain seldom investigated. In this study, a 2-h head-only exposure to GSM-1800 MHz was applied to (i) rats undergoing an acute neuroinflammation triggered by a lipopolysaccharide (LPS) treatment, (ii) age-matched healthy rats, or (iii) transgenic hSOD1
MeSH term(s)	Animals ; Cerebral Cortex/metabolism ; Cerebral Cortex/radiation effects ; Electromagnetic Fields ; Encephalitis/chemically induced ; Encephalitis/metabolism ; Female ; Gene Expression/radiation effects ; Lipopolysaccharides/administration & dosage ; Male ; Radiometry ; Rats, Sprague-Dawley ; Sequence Analysis, RNA ; Transcriptome/radiation effects
Chemical Substances	Lipopolysaccharides
Keywords	covid19
Language	English
Publishing date	2020-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2036826-4
ISSN	1476-3524 ; 1029-8428
ISSN (online)	1476-3524
ISSN	1029-8428
DOI	10.1007/s12640-020-00191-3
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Zs.A 5749: Show issues

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Article ; Online: The Amyotrophic Lateral Sclerosis M114T PFN1 Mutation Deregulates Alternative Autophagy Pathways and Mitochondrial Homeostasis.

Teyssou, Elisa / Chartier, Laura / Roussel, Delphine / Perera, Nirma D / Nemazanyy, Ivan / Langui, Dominique / Albert, Mélanie / Larmonier, Thierry / Saker, Safaa / Salachas, François / Pradat, Pierre-François / Meininger, Vincent / Ravassard, Philippe / Côté, Francine / Lobsiger, Christian S / Boillée, Séverine / Turner, Bradley J / Seilhean, Danielle / Millecamps, Stéphanie

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: Mutations in profilin 1 (PFN1) have been identified in rare familial cases of Amyotrophic Lateral Sclerosis (ALS). PFN1 is involved in multiple pathways that could intervene in ALS pathology. However, the specific pathogenic role of PFN1 mutations in ALS ...

Abstract	Mutations in profilin 1 (PFN1) have been identified in rare familial cases of Amyotrophic Lateral Sclerosis (ALS). PFN1 is involved in multiple pathways that could intervene in ALS pathology. However, the specific pathogenic role of PFN1 mutations in ALS is still not fully understood. We hypothesized that PFN1 could play a role in regulating autophagy pathways and that PFN1 mutations could disrupt this function. We used patient cells (lymphoblasts) or tissue (post-mortem) carrying PFN1 mutations (M114T and E117G), and designed experimental models expressing wild-type or mutant PFN1 (cell lines and novel PFN1 mice established by lentiviral transgenesis) to study the effects of PFN1 mutations on autophagic pathway markers. We observed no accumulation of PFN1 in the spinal cord of one E117G mutation carrier. Moreover, in patient lymphoblasts and transfected cell lines, the M114T mutant PFN1 protein was unstable and deregulated the RAB9-mediated alternative autophagy pathway involved in the clearance of damaged mitochondria. In vivo, motor neurons expressing M114T mutant PFN1 showed mitochondrial abnormalities. Our results demonstrate that the M114T PFN1 mutation is more deleterious than the E117G variant in patient cells and experimental models and suggest a role for the RAB9-dependent autophagic pathway in ALS.
MeSH term(s)	Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Autophagy/genetics ; Homeostasis ; Humans ; Mice ; Mitochondria/metabolism ; Mutation ; Profilins/genetics ; Profilins/metabolism ; rab GTP-Binding Proteins/metabolism
Chemical Substances	PFN1 protein, human ; Pfn1 protein, mouse ; Profilins ; RAB9A protein, human (EC 3.6.1.-) ; rab9 protein, mouse (EC 3.6.1.-) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-05-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105694
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Article ; Online: Main path and byways: non-vesicular glutamate release by system xc(-) as an important modifier of glutamatergic neurotransmission.

Massie, Ann / Boillée, Séverine / Hewett, Sandra / Knackstedt, Lori / Lewerenz, Jan

Journal of neurochemistry

2015 Volume 135, Issue 6, Page(s) 1062–1079

Abstract: System xc(-) is a cystine/glutamate antiporter that exchanges extracellular cystine for intracellular glutamate. Cystine is intracellularly reduced to cysteine, a building block of GSH. As such, system xc(-) can regulate the antioxidant capacity of cells. ...

Abstract	System xc(-) is a cystine/glutamate antiporter that exchanges extracellular cystine for intracellular glutamate. Cystine is intracellularly reduced to cysteine, a building block of GSH. As such, system xc(-) can regulate the antioxidant capacity of cells. Moreover, in several brain regions, system xc(-) is the major source of extracellular glutamate. As such this antiporter is able to fulfill key physiological functions in the CNS, while evidence indicates it also plays a role in certain brain pathologies. Since the transcription of xCT, the specific subunit of system xc(-), is enhanced by the presence of reactive oxygen species and inflammatory cytokines, system xc(-) could be involved in toxic extracellular glutamate release in neurological disorders that are associated with increased oxidative stress and neuroinflammation. System xc(-) has also been reported to contribute to the invasiveness of brain tumors and, as a source of extracellular glutamate, could participate in the induction of peritumoral seizures. Two independent reviews (Pharmacol. Rev. 64, 2012, 780; Antioxid. Redox Signal. 18, 2013, 522), approached from a different perspective, have recently been published on the functions of system xc(-) in the CNS. In this review, we highlight novel achievements and insights covering the regulation of system xc(-) as well as its involvement in emotional behavior, cognition, addiction, neurological disorders and glioblastomas, acquired in the past few years. System xc(-) constitutes an important source of extrasynaptic glutamate in the brain. By modulating the tone of extrasynaptic metabotropic or ionotropic glutamate receptors, it affects excitatory neurotransmission, the threshold for overexcitation and excitotoxicity and, as a consequence, behavior. This review describes the current knowledge of how system xc(-) is regulated and involved in physiological as well as pathophysiological brain functioning.
MeSH term(s)	Animals ; Brain/metabolism ; Brain Neoplasms/metabolism ; Glioblastoma/metabolism ; Glutamic Acid/metabolism ; Humans ; Oxidative Stress/physiology ; Synaptic Transmission/physiology
Chemical Substances	Glutamic Acid (3KX376GY7L)
Language	English
Publishing date	2015-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.13348
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Ui II Zs.170: Show issues

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Article ; Online: Evidence for glutamine synthetase function in mouse spinal cord oligodendrocytes.

Ben Haim, Lucile / Schirmer, Lucas / Zulji, Amel / Sabeur, Khalida / Tiret, Brice / Ribon, Matthieu / Chang, Sandra / Lamers, Wouter H / Boillée, Séverine / Chaumeil, Myriam M / Rowitch, David H

Glia

2021 Volume 69, Issue 12, Page(s) 2812–2827

Abstract: Glutamine synthetase (GS) is a key enzyme that metabolizes glutamate into glutamine. While GS is highly enriched in astrocytes, expression in other glial lineages has been noted. Using a combination of reporter mice and cell type-specific markers, we ... ...

Abstract	Glutamine synthetase (GS) is a key enzyme that metabolizes glutamate into glutamine. While GS is highly enriched in astrocytes, expression in other glial lineages has been noted. Using a combination of reporter mice and cell type-specific markers, we show that GS is expressed in myelinating oligodendrocytes (OL) but not oligodendrocyte progenitor cells of the mouse and human ventral spinal cord. To investigate the role of GS in mature OL, we used a conditional knockout (cKO) approach to selectively delete GS-encoding gene (Glul) in OL, which caused a significant decrease in glutamine levels on mouse spinal cord extracts. GS cKO mice (CNP-cre
MeSH term(s)	Amyotrophic Lateral Sclerosis/pathology ; Animals ; Disease Models, Animal ; Glutamate-Ammonia Ligase/genetics ; Glutamate-Ammonia Ligase/metabolism ; Humans ; Mice ; Mice, Transgenic ; Motor Neurons/pathology ; Oligodendroglia/metabolism ; Spinal Cord/metabolism ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism
Chemical Substances	Superoxide Dismutase (EC 1.15.1.1) ; Glutamate-Ammonia Ligase (EC 6.3.1.2)
Language	English
Publishing date	2021-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24071
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Zs.A 2345: Show issues

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Article ; Online: Deletion of the inflammatory S100-A9/MRP14 protein does not influence survival in hSOD1

Ribon, Matthieu / Leone, Céline / Chiot, Aude / Berriat, Félix / Rampanana, Martine / Cottin, Julie / Bohl, Delphine / Millecamps, Stéphanie / Lobsiger, Christian S / Heneka, Michael T / Boillée, Séverine

Neurobiology of aging

2021 Volume 101, Page(s) 181–186

Abstract: Neuroinflammation is a hallmark of Amyotrophic Lateral Sclerosis (ALS) in ... ...

Abstract	Neuroinflammation is a hallmark of Amyotrophic Lateral Sclerosis (ALS) in hSOD1
MeSH term(s)	Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/mortality ; Animals ; Calgranulin B/genetics ; Calgranulin B/metabolism ; Disease Models, Animal ; Gene Deletion ; Histone-Lysine N-Methyltransferase/metabolism ; Inflammation ; Mice ; Microglia/metabolism ; Superoxide Dismutase-1/metabolism ; Survival
Chemical Substances	Calgranulin B ; S100A9 protein, mouse ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; G9a protein, mouse (EC 2.1.1.43) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2021-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2021.01.015
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Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 10: Show issues

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Article ; Online: Neurofilament accumulations in amyotrophic lateral sclerosis patients' motor neurons impair axonal initial segment integrity.

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 6, Page(s) 150

Abstract: Amyotrophic lateral sclerosis (ALS) is the most common motor neuron (MN) disease in adults with no curative treatment. Neurofilament (NF) level in patient' fluids have recently emerged as the prime biomarker of ALS disease progression, while NF ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is the most common motor neuron (MN) disease in adults with no curative treatment. Neurofilament (NF) level in patient' fluids have recently emerged as the prime biomarker of ALS disease progression, while NF accumulation in MNs of patients is the oldest and one of the best pathological hallmarks. However, the way NF accumulations could lead to MN degeneration remains unknown. To assess NF accumulations and study the impact on MNs, we compared MNs derived from induced pluripotent stem cells (iPSC) of patients carrying mutations in C9orf72, SOD1 and TARDBP genes, the three main ALS genetic causes. We show that in all mutant MNs, light NF (NF-L) chains rapidly accumulate in MN soma, while the phosphorylated heavy/medium NF (pNF-M/H) chains pile up in axonal proximal regions of only C9orf72 and SOD1 MNs. Excitability abnormalities were also only observed in these latter MNs. We demonstrate that the integrity of the MN axonal initial segment (AIS), the region of action potential initiation and responsible for maintaining axonal integrity, is impaired in the presence of pNF-M/H accumulations in C9orf72 and SOD1 MNs. We establish a strong correlation between these pNF-M/H accumulations, an AIS distal shift, increased axonal calibers and modified repartition of sodium channels. The results expand our understanding of how NF accumulation could dysregulate components of the axonal cytoskeleton and disrupt MN homeostasis. With recent cumulative evidence that AIS alterations are implicated in different brain diseases, preserving AIS integrity could have important therapeutic implications for ALS.
MeSH term(s)	Humans ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/pathology ; Intermediate Filaments ; Superoxide Dismutase-1/genetics ; C9orf72 Protein/genetics ; Motor Neurons/pathology
Chemical Substances	Superoxide Dismutase-1 (EC 1.15.1.1) ; C9orf72 Protein
Language	English
Publishing date	2023-05-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04797-6
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Zs.A 195: Show issues

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Article ; Online: Ultrasound-Induced Blood-Spinal Cord Barrier Opening in Rabbits.

Montero, Anne-Sophie / Bielle, Franck / Goldwirt, Lauriane / Lalot, Adrien / Bouchoux, Guillaume / Canney, Michael / Belin, Florine / Beccaria, Kevin / Pradat, Pierre-François / Salachas, François / Boillée, Severine / Lobsiger, Christian / Lafon, Cyril / Chapelon, Jean-Yves / Carpentier, Alexandre

Ultrasound in medicine & biology

2019 Volume 45, Issue 9, Page(s) 2417–2426

Abstract: The blood-spinal cord barrier (BSCB) considerably limits the delivery and efficacy of treatments for spinal cord diseases. The blood-brain barrier can be safely opened with low-intensity pulsed ultrasound when microbubbles are simultaneously administered ...

Abstract	The blood-spinal cord barrier (BSCB) considerably limits the delivery and efficacy of treatments for spinal cord diseases. The blood-brain barrier can be safely opened with low-intensity pulsed ultrasound when microbubbles are simultaneously administered intravenously. This technique was tested on the BSCB in a rabbit model in this work. Twenty-three segments of spinal cord were sonicated with a 1-MHz unfocused pulsed ultrasound device and compared with non-sonicated segments. BSCB disruption was assessed using Evan's blue dye (EBD) extravasation. Tolerance was assessed by histologic analysis. An increased EBD concentration indicating BSCB disruption was clearly observed in sonicated segments compared with controls (p = 0.004). On one animal, which received 10 sonications, repetitive BSCB disruptions revealed no evidence of cumulative toxicity. BSCB can be disrupted using an unfocused pulsed ultrasound device in combination with microbubbles without neurotoxicity even in case of repeated sonications.
MeSH term(s)	Animals ; Contrast Media/pharmacokinetics ; Evans Blue/pharmacokinetics ; Microbubbles ; Models, Animal ; Phospholipids/pharmacokinetics ; Rabbits ; Spinal Cord/metabolism ; Sulfur Hexafluoride/pharmacokinetics ; Ultrasonics/methods
Chemical Substances	Contrast Media ; Phospholipids ; contrast agent BR1 ; Evans Blue (45PG892GO1) ; Sulfur Hexafluoride (WS7LR3I1D6)
Language	English
Publishing date	2019-06-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186150-5
ISSN	1879-291X ; 0301-5629
ISSN (online)	1879-291X
ISSN	0301-5629
DOI	10.1016/j.ultrasmedbio.2019.05.022
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