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Article ; Online: Cell-autonomous immune dysfunction driven by disrupted autophagy in

Banerjee, Poulomi / Mehta, Arpan R / Nirujogi, Raja S / Cooper, James / James, Owen G / Nanda, Jyoti / Longden, James / Burr, Karen / McDade, Karina / Salzinger, Andrea / Paza, Evdokia / Newton, Judith / Story, David / Pal, Suvankar / Smith, Colin / Alessi, Dario R / Selvaraj, Bhuvaneish T / Priller, Josef / Chandran, Siddharthan

Science advances

2023 Volume 9, Issue 16, Page(s) eabq0651

Abstract: Although microglial activation is widely found in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), the underlying mechanism(s) are poorly understood. Here, using human-induced pluripotent stem cell-derived microglia-like cells ( ... ...

Abstract	Although microglial activation is widely found in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), the underlying mechanism(s) are poorly understood. Here, using human-induced pluripotent stem cell-derived microglia-like cells (hiPSC-MG) harboring the most common ALS/FTD mutation (
MeSH term(s)	Humans ; Amyotrophic Lateral Sclerosis/genetics ; Frontotemporal Dementia/genetics ; Induced Pluripotent Stem Cells/metabolism ; C9orf72 Protein/genetics ; C9orf72 Protein/metabolism ; Microglia/metabolism ; Autophagy/genetics
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2023-04-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abq0651
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Article ; Online: The ciliary gene INPP5E confers dorsal telencephalic identity to human cortical organoids by negatively regulating Sonic hedgehog signaling.

Schembs, Leah / Willems, Ariane / Hasenpusch-Theil, Kerstin / Cooper, James D / Whiting, Katie / Burr, Karen / Bøstrand, Sunniva M K / Selvaraj, Bhuvaneish T / Chandran, Siddharthan / Theil, Thomas

Cell reports

2022 Volume 39, Issue 7, Page(s) 110811

Abstract: Defects in primary cilia, cellular antennas that control multiple intracellular signaling pathways, underlie several neurodevelopmental disorders, but it remains unknown how cilia control essential steps in human brain formation. Here, we show that cilia ...

Abstract	Defects in primary cilia, cellular antennas that control multiple intracellular signaling pathways, underlie several neurodevelopmental disorders, but it remains unknown how cilia control essential steps in human brain formation. Here, we show that cilia are present on the apical surface of radial glial cells in human fetal forebrain. Interfering with cilia signaling in human organoids by mutating the INPP5E gene leads to the formation of ventral telencephalic cell types instead of cortical progenitors and neurons. INPP5E mutant organoids also show increased Sonic hedgehog (SHH) signaling, and cyclopamine treatment partially rescues this ventralization. In addition, ciliary expression of SMO, GLI2, GPR161, and several intraflagellar transport (IFT) proteins is increased. Overall, these findings establish the importance of primary cilia for dorsal and ventral patterning in human corticogenesis, indicate a tissue-specific role of INPP5E as a negative regulator of SHH signaling, and have implications for the emerging roles of cilia in the pathogenesis of neurodevelopmental disorders.
MeSH term(s)	Cilia/enzymology ; Cilia/genetics ; Cilia/metabolism ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Humans ; Organoids/metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Telencephalon/enzymology ; Telencephalon/metabolism
Chemical Substances	Hedgehog Proteins ; Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; phosphoinositide 5-phosphatase (EC 3.1.3.36)
Language	English
Publishing date	2022-05-10
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.2022.110811
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Article ; Online: Reducing voltage-dependent potassium channel Kv3.4 levels ameliorates synapse loss in a mouse model of Alzheimer's disease.

Yeap, Jie / Sathyaprakash, Chaitra / Toombs, Jamie / Tulloch, Jane / Scutariu, Cristina / Rose, Jamie / Burr, Karen / Davies, Caitlin / Colom-Cadena, Marti / Chandran, Siddharthan / Large, Charles H / Rowan, Matthew J M / Gunthorpe, Martin J / Spires-Jones, Tara L

Brain and neuroscience advances

2022 Volume 6, Page(s) 23982128221086464

Abstract: Synapse loss is associated with cognitive decline in Alzheimer's disease, and owing to their plastic nature, synapses are an ideal target for therapeutic intervention. Oligomeric amyloid beta around amyloid plaques is known to contribute to synapse loss ... ...

Abstract	Synapse loss is associated with cognitive decline in Alzheimer's disease, and owing to their plastic nature, synapses are an ideal target for therapeutic intervention. Oligomeric amyloid beta around amyloid plaques is known to contribute to synapse loss in mouse models and is associated with synapse loss in human Alzheimer's disease brain tissue, but the mechanisms leading from Aβ to synapse loss remain unclear. Recent data suggest that the fast-activating and -inactivating voltage-gated potassium channel subtype 3.4 (Kv3.4) may play a role in Aβ-mediated neurotoxicity. Here, we tested whether this channel could also be involved in Aβ synaptotoxicity. Using adeno-associated virus and clustered regularly interspaced short palindromic repeats technology, we reduced Kv3.4 expression in neurons of the somatosensory cortex of APP/PS1 mice. These mice express human familial Alzheimer's disease-associated mutations in amyloid precursor protein and presenilin-1 and develop amyloid plaques and plaque-associated synapse loss similar to that observed in Alzheimer's disease brain. We observe that reducing Kv3.4 levels ameliorates dendritic spine loss and changes spine morphology compared to control virus. In support of translational relevance, Kv3.4 protein was observed in human Alzheimer's disease and control brain and is associated with synapses in human induced pluripotent stem cell-derived cortical neurons. We also noted morphological changes in induced pluripotent stem cell neurones challenged with human Alzheimer's disease-derived brain homogenate containing Aβ but, in this in vitro model, total mRNA levels of Kv3.4 were found to be reduced, perhaps as an early compensatory mechanism for Aβ-induced damage. Overall, our results suggest that approaches to reduce Kv3.4 expression and/or function in the Alzheimer's disease brain could be protective against Aβ-induced synaptic alterations.
Language	English
Publishing date	2022-03-24
Publishing country	United States
Document type	Journal Article
ISSN	2398-2128
ISSN (online)	2398-2128
DOI	10.1177/23982128221086464
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Article ; Online: Generation of pure monocultures of human microglia-like cells from induced pluripotent stem cells.

Banerjee, Poulomi / Paza, Evdokia / Perkins, Emma M / James, Owen G / Kenkhuis, Boyd / Lloyd, Amy F / Burr, Karen / Story, David / Yusuf, Dilmurat / He, Xin / Backofen, Rolf / Dando, Owen / Chandran, Siddharthan / Priller, Josef

Stem cell research

2020 Volume 49, Page(s) 102046

Abstract: Microglia are resident tissue macrophages of the central nervous system (CNS) that arise from erythromyeloid progenitors during embryonic development. They play essential roles in CNS development, homeostasis and response to disease. Since microglia are ... ...

Abstract	Microglia are resident tissue macrophages of the central nervous system (CNS) that arise from erythromyeloid progenitors during embryonic development. They play essential roles in CNS development, homeostasis and response to disease. Since microglia are difficult to procure from the human brain, several protocols have been developed to generate microglia-like cells from human induced pluripotent stem cells (hiPSCs). However, some concerns remain over the purity and quality of in vitro generated microglia. Here, we describe a new protocol that does not require co-culture with neural cells and yields cultures of 100% P2Y
MeSH term(s)	Animals ; Brain ; Humans ; Induced Pluripotent Stem Cells ; Membrane Glycoproteins ; Mice ; Microglia ; Neurons ; Receptors, Immunologic
Chemical Substances	Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human ; Trem2 protein, mouse
Language	English
Publishing date	2020-10-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1876-7753
ISSN (online)	1876-7753
DOI	10.1016/j.scr.2020.102046
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Article: Dysregulation in Subcellular Localization of Myelin Basic Protein mRNA Does Not Result in Altered Myelination in Amyotrophic Lateral Sclerosis.

Barton, Samantha K / Gregory, Jenna M / Selvaraj, Bhuvaneish T / McDade, Karina / Henstridge, Christopher M / Spires-Jones, Tara L / James, Owen G / Mehta, Arpan R / Story, David / Burr, Karen / Magnani, Dario / Isaacs, Adrian M / Smith, Colin / Chandran, Siddharthan

Frontiers in neuroscience

2021 Volume 15, Page(s) 705306

Abstract: Pathological hallmarks of amyotrophic lateral sclerosis (ALS), including protein misfolding, are well established in oligodendrocytes. More recently, an RNA trafficking deficit of key myelin proteins has been suggested in oligodendrocytes in ALS but the ... ...

Abstract	Pathological hallmarks of amyotrophic lateral sclerosis (ALS), including protein misfolding, are well established in oligodendrocytes. More recently, an RNA trafficking deficit of key myelin proteins has been suggested in oligodendrocytes in ALS but the extent to which this affects myelination and the relative contribution of this to disease pathogenesis is unclear. ALS autopsy research findings showing demyelination contrasts with the routine clinical-pathological workup of ALS cases where it is rare to see white matter abnormalities other than simple Wallerian degeneration secondary to widespread neuronal loss. To begin to address this apparent variance, we undertook a comprehensive evaluation of myelination at an RNA, protein and structural level using human pathological material from sporadic ALS patients, genetic ALS patients (harboring
Language	English
Publishing date	2021-09-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2021.705306
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Article ; Online: Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction.

Perkins, Emma M / Burr, Karen / Banerjee, Poulomi / Mehta, Arpan R / Dando, Owen / Selvaraj, Bhuvaneish T / Suminaite, Daumante / Nanda, Jyoti / Henstridge, Christopher M / Gillingwater, Thomas H / Hardingham, Giles E / Wyllie, David J A / Chandran, Siddharthan / Livesey, Matthew R

Molecular neurodegeneration

2021 Volume 16, Issue 1, Page(s) 13

Abstract: Background: Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat ... ...

Abstract	Background: Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat expansion (C9ORF72 Methods: To address this we have generated cortical neurons from patient-derived iPSCs harbouring C9ORF72 Results: We find that C9ORF72 Conclusion: These findings suggest synaptic pathophysiology is widespread in ALS-FTD and has an early and fundamental role in driving altered network function that is thought to contribute to neurodegenerative processes in these patients. The overall importance is the identification of previously unidentified defects in pre and postsynaptic compartments affecting synaptic plasticity, synaptic vesicle stores, and network propagation, which directly impact upon cortical function.
MeSH term(s)	Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; C9orf72 Protein/genetics ; C9orf72 Protein/metabolism ; DNA Repeat Expansion/genetics ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology ; Motor Neurons/metabolism ; Mutation/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2021-03-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-021-00433-8
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Article ; Online: Mitochondrial bioenergetic deficits in C9orf72 amyotrophic lateral sclerosis motor neurons cause dysfunctional axonal homeostasis.

Mehta, Arpan R / Gregory, Jenna M / Dando, Owen / Carter, Roderick N / Burr, Karen / Nanda, Jyoti / Story, David / McDade, Karina / Smith, Colin / Morton, Nicholas M / Mahad, Don J / Hardingham, Giles E / Chandran, Siddharthan / Selvaraj, Bhuvaneish T

Acta neuropathologica

2021 Volume 141, Issue 2, Page(s) 257–279

Abstract: Axonal dysfunction is a common phenotype in neurodegenerative disorders, including in amyotrophic lateral sclerosis (ALS), where the key pathological cell-type, the motor neuron (MN), has an axon extending up to a metre long. The maintenance of axonal ... ...

Abstract	Axonal dysfunction is a common phenotype in neurodegenerative disorders, including in amyotrophic lateral sclerosis (ALS), where the key pathological cell-type, the motor neuron (MN), has an axon extending up to a metre long. The maintenance of axonal function is a highly energy-demanding process, raising the question of whether MN cellular energetics is perturbed in ALS, and whether its recovery promotes axonal rescue. To address this, we undertook cellular and molecular interrogation of multiple patient-derived induced pluripotent stem cell lines and patient autopsy samples harbouring the most common ALS causing mutation, C9orf72. Using paired mutant and isogenic expansion-corrected controls, we show that C9orf72 MNs have shorter axons, impaired fast axonal transport of mitochondrial cargo, and altered mitochondrial bioenergetic function. RNAseq revealed reduced gene expression of mitochondrially encoded electron transport chain transcripts, with neuropathological analysis of C9orf72-ALS post-mortem tissue importantly confirming selective dysregulation of the mitochondrially encoded transcripts in ventral horn spinal MNs, but not in corresponding dorsal horn sensory neurons, with findings reflected at the protein level. Mitochondrial DNA copy number was unaltered, both in vitro and in human post-mortem tissue. Genetic manipulation of mitochondrial biogenesis in C9orf72 MNs corrected the bioenergetic deficit and also rescued the axonal length and transport phenotypes. Collectively, our data show that loss of mitochondrial function is a key mediator of axonal dysfunction in C9orf72-ALS, and that boosting MN bioenergetics is sufficient to restore axonal homeostasis, opening new potential therapeutic strategies for ALS that target mitochondrial function.
MeSH term(s)	Adult ; Aged ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Axons/metabolism ; C9orf72 Protein/genetics ; Electron Transport/genetics ; Energy Metabolism/genetics ; Female ; Gene Dosage ; Gene Expression Regulation ; Homeostasis ; Humans ; Induced Pluripotent Stem Cells ; Male ; Middle Aged ; Mitochondria/metabolism ; Motor Neurons/metabolism ; Posterior Horn Cells/pathology
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human
Language	English
Publishing date	2021-01-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-020-02252-5
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Article ; Online: iPSC-derived myelinoids to study myelin biology of humans.

James, Owen G / Selvaraj, Bhuvaneish T / Magnani, Dario / Burr, Karen / Connick, Peter / Barton, Samantha K / Vasistha, Navneet A / Hampton, David W / Story, David / Smigiel, Robert / Ploski, Rafal / Brophy, Peter J / Ffrench-Constant, Charles / Lyons, David A / Chandran, Siddharthan

Developmental cell

2021 Volume 57, Issue 1, Page(s) 146

Language	English
Publishing date	2021-12-31
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2021.12.009
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Zs.A 5742: 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)
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Article ; Online: iPSC-derived myelinoids to study myelin biology of humans.

Developmental cell

2021 Volume 56, Issue 9, Page(s) 1346–1358.e6

Abstract: Myelination is essential for central nervous system (CNS) formation, health, and function. Emerging evidence of oligodendrocyte heterogeneity in health and disease and divergent CNS gene expression profiles between mice and humans supports the ... ...

Abstract	Myelination is essential for central nervous system (CNS) formation, health, and function. Emerging evidence of oligodendrocyte heterogeneity in health and disease and divergent CNS gene expression profiles between mice and humans supports the development of experimentally tractable human myelination systems. Here, we developed human iPSC-derived myelinating organoids ("myelinoids") and quantitative tools to study myelination from oligodendrogenesis through to compact myelin formation and myelinated axon organization. Using patient-derived cells, we modeled a monogenetic disease of myelinated axons (Nfasc155 deficiency), recapitulating impaired paranodal axo-glial junction formation. We also validated the use of myelinoids for pharmacological assessment of myelination-both at the level of individual oligodendrocytes and globally across whole myelinoids-and demonstrated reduced myelination in response to suppressed synaptic vesicle release. Our study provides a platform to investigate human myelin development, disease, and adaptive myelination.
MeSH term(s)	Axons/metabolism ; Axons/ultrastructure ; Humans ; Induced Pluripotent Stem Cells/cytology ; Myelin Sheath/physiology ; Myelin Sheath/ultrastructure ; Nerve Growth Factors/deficiency ; Nerve Growth Factors/metabolism ; Organoids/physiology ; Organoids/ultrastructure ; Tetanus Toxin/pharmacology ; Time Factors
Chemical Substances	Nerve Growth Factors ; Tetanus Toxin
Language	English
Publishing date	2021-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2021.04.006
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Article ; Online: Reprogramming adult Schwann cells to stem cell-like cells by leprosy bacilli promotes dissemination of infection.

Masaki, Toshihiro / Qu, Jinrong / Cholewa-Waclaw, Justyna / Burr, Karen / Raaum, Ryan / Rambukkana, Anura

Cell

2013 Volume 152, Issue 1-2, Page(s) 51–67

Abstract: Differentiated cells possess a remarkable genomic plasticity that can be manipulated to reverse or change developmental commitments. Here, we show that the leprosy bacterium hijacks this property to reprogram adult Schwann cells, its preferred host niche, ...

Abstract	Differentiated cells possess a remarkable genomic plasticity that can be manipulated to reverse or change developmental commitments. Here, we show that the leprosy bacterium hijacks this property to reprogram adult Schwann cells, its preferred host niche, to a stage of progenitor/stem-like cells (pSLC) of mesenchymal trait by downregulating Schwann cell lineage/differentiation-associated genes and upregulating genes mostly of mesoderm development. Reprogramming accompanies epigenetic changes and renders infected cells highly plastic, migratory, and immunomodulatory. We provide evidence that acquisition of these properties by pSLC promotes bacterial spread by two distinct mechanisms: direct differentiation to mesenchymal tissues, including skeletal and smooth muscles, and formation of granuloma-like structures and subsequent release of bacteria-laden macrophages. These findings support a model of host cell reprogramming in which a bacterial pathogen uses the plasticity of its cellular niche for promoting dissemination of infection and provide an unexpected link between cellular reprogramming and host-pathogen interaction.
MeSH term(s)	Animals ; Cell Movement ; Cell Survival ; Epigenesis, Genetic ; Epithelial-Mesenchymal Transition ; Granuloma/microbiology ; Host-Pathogen Interactions ; Humans ; Leprosy/genetics ; Leprosy/microbiology ; Leprosy/pathology ; Macrophages/microbiology ; Macrophages/pathology ; Mice ; Mice, Nude ; Mycobacterium leprae ; Peripheral Nerves/pathology ; Schwann Cells/microbiology ; Schwann Cells/pathology ; Stem Cells/pathology
Language	English
Publishing date	2013-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2012.12.014
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