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Book ; Online ; E-Book: Glycobiology of the nervous system

Schengrund, Cara-Lynne / Yu, Robert K.

(Advances in Neurobiology ; v.29)

2023

Author's details	edited by Cara-Lynne Schengrund and Robert K. Yu
Series title	Advances in Neurobiology ; v.29
Keywords	Glycoconjugates ; Neurobiology
Subject code	572.567
Language	English
Size	1 online resource (506 pages)
Edition	Second edition.
Publisher	Springer
Publishing place	Cham, Switzerland
Document type	Book ; Online ; E-Book
Note	Includes index.
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
ISBN	3-031-12390-5 ; 9783031123894 ; 978-3-031-12390-0 ; 3031123891
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Book: Glycobiology of the Nervous System

Yu, Robert K. / Schengrund, Cara-Lynne

(Advances in Neurobiology)

2022

Author's details	Cara-Lynne Schengrund, PhD, is Professor Emeritus, Department of Biochemistry and Molecular Biology, Penn State University, Hershey, Pennsylvania§ § Robert K. Yu, PhD, Med ScD, was Professor, Department of Neuroscience and Regenerative Medicine, and GRA Eminent Scholar in Molecular and Cellular Neurobiology, Medical College of Georgia at Augusta University, Augusta, Georgia§ § §
Series title	Advances in Neurobiology
Keywords	N-andO-linkedglycoproteins ; glycoconjugates ; Glycolipids ; Neuroscience ; lectins ; nervecelldifferentiation ; N- and O-linked glycoproteins ; glycobiology ; glycolipids ; nerve cell differentiation ; neuroscience
Language	English
Size	516 p.
Edition	2
Publisher	Springer International Publishing
Document type	Book
Note	PDA Manuell_16
Format	160 x 241 x 34
ISBN	9783031123894 ; 3031123891
Database	PDA

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Book: Glycobiology of the nervous system

Yu, Robert K. / Schengrund, Cara-Lynne

(Advances in neurobiology ; 9)

2014

Author's details	Robert K. Yu ; Cara-Lynne Schengrund ed
Series title	Advances in neurobiology ; 9
Collection
Keywords	Glycomics ; Nervous system/Microbiology ; Glycoconjugates ; Neurobiology
Subject code	612.8
Language	English
Size	XVII, 584 S. : Ill., graph. Darst., 24 cm
Publisher	Springer
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
Note	Includes bibliographical references
HBZ-ID	HT018453265
ISBN	978-1-4939-1153-0 ; 9781493911547 ; 1-4939-1153-8 ; 1493911546
Database	Catalogue ZB MED Medicine, Health

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2014 A 4247	available for loan (reading room)	Lesesaal EG

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Article: Ganglioside Microdomains on Cellular and Intracellular Membranes Regulate Neuronal Cell Fate Determination.

Itokazu, Yutaka / Yu, Robert K

Advances in neurobiology

2022 Volume 29, Page(s) 281–304

Abstract: Gangliosides are sialylated glycosphingolipids (GSLs) with essential but enigmatic functions in brain activities and neural stem cell (NSC) maintenance. Our group has pioneered research on the importance of gangliosides for growth factor receptor ... ...

Abstract	Gangliosides are sialylated glycosphingolipids (GSLs) with essential but enigmatic functions in brain activities and neural stem cell (NSC) maintenance. Our group has pioneered research on the importance of gangliosides for growth factor receptor signaling and epigenetic regulation of NSC activity and differentiation. The primary localization of gangliosides is on cell-surface microdomains and the drastic dose and composition changes during neural differentiation strongly suggest that they are not only important as biomarkers, but also are involved in modulating NSC fate determination. Ganglioside GD3 is the predominant species in NSCs and GD3-synthase knockout (GD3S-KO) revealed reduction of postnatal NSC pools with severe behavioral deficits. Exogenous administration of GD3 significantly restored the NSC pools and enhanced the stemness of NSCs with multipotency and self-renewal. Since morphological changes during neurogenesis require a huge amount of energy, mitochondrial functions are vital for neurogenesis. We discovered that a mitochondrial fission protein, the dynamin-related protein-1 (Drp1), as a novel GD3-binding protein, and GD3 regulates mitochondrial dynamics. Furthermore, we discovered that GM1 ganglioside promotes neuronal differentiation by an epigenetic regulatory mechanism. Nuclear GM1 binds with acetylated histones on the promoters of N-acetylgalactosaminyltransferase (GalNAcT; GM2 synthase) as well as on the NeuroD1 genes in differentiated neurons. In addition, epigenetic activation of the GalNAcT gene was detected as accompanied by an apparent induction of neuronal differentiation in NSCs responding to an exogenous supplement of GM1. GM1 is indeed localized in the nucleus where it can interact with transcriptionally active histones. Interestingly, GM1 could induce epigenetic activation of the tyrosine hydroxylase (TH) gene, with recruitment of nuclear receptor related 1 (Nurr1, also known as NR4A2), a dopaminergic neuron-associated transcription factor, to the TH promoter region. In this way, GM1 epigenetically regulates dopaminergic neuron specific gene expression. GM1 interacts with active chromatin via acetylated histones to recruit transcription factors at the nuclear periphery, resulting in changes in gene expression for neuronal differentiation. The significance is that multifunctional gangliosides modulate lipid microdomains to regulate functions of important molecules on multiple sites: the plasma membrane, mitochondrial membrane, and nuclear membrane. Versatile gangliosides could regulate functional neurons as well as sustain NSC functions via modulating protein and gene activities on ganglioside microdomains.
MeSH term(s)	Humans ; G(M1) Ganglioside/metabolism ; Epigenesis, Genetic ; Histones/genetics ; Histones/metabolism ; Tyrosine 3-Monooxygenase/metabolism ; Gangliosides/genetics ; Gangliosides/metabolism ; Neurons/metabolism ; N-Acetylgalactosaminyltransferases/genetics ; N-Acetylgalactosaminyltransferases/metabolism ; Glycosphingolipids/metabolism ; Intracellular Membranes/metabolism ; Biomarkers/metabolism ; Chromatin/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	G(M1) Ganglioside (37758-47-7) ; Histones ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Gangliosides ; N-Acetylgalactosaminyltransferases (EC 2.4.1.-) ; Glycosphingolipids ; Biomarkers ; Chromatin ; Transcription Factors
Language	English
Publishing date	2022-10-15
Publishing country	United States
Document type	Journal Article
ISSN	2190-5215
ISSN	2190-5215
DOI	10.1007/978-3-031-12390-0_10
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Article: Ganglioside GD3 regulates neural stem cell quiescence and controls postnatal neurogenesis.

Fuchigami, Takahiro / Itokazu, Yutaka / Yu, Robert K

bioRxiv : the preprint server for biology

2023

Abstract: The postnatal neural stem cell (NSC) pool hosts quiescent and activated radial glia-like NSCs contributing to neurogenesis throughout adulthood. However, the underlying regulatory mechanism during the transition from quiescent NSCs to activated NSCs in ... ...

Abstract	The postnatal neural stem cell (NSC) pool hosts quiescent and activated radial glia-like NSCs contributing to neurogenesis throughout adulthood. However, the underlying regulatory mechanism during the transition from quiescent NSCs to activated NSCs in the postnatal NSC niche is not fully understood. Lipid metabolism and lipid composition play important roles in regulating NSC fate determination. Biological lipid membranes define the individual cellular shape and help maintain cellular organization and are highly heterogenous in structure and there exist diverse microdomains (also known as lipid rafts), which are enriched with sugar molecules, such as glycosphingolipids. An often overlooked but key aspect is that the functional activities of proteins and genes are highly dependent upon their molecular environments. We previously reported that ganglioside GD3 is the predominant species in NSCs and that the reduced postnatal NSC pools are observed in global GD3-synthase knockout (GD3S-KO) mouse brains. The specific roles of GD3 in determining the stage and cell-lineage determination of NSCs remain unclear, since global GD3S-KO mice cannot distinguish if GD3 regulates postnatal neurogenesis or developmental impacts. Here we show that inducible GD3 deletion in postnatal radial glia-like NSCs promotes the NSC activation, resulting in the loss of the long-term maintenance of the adult NSC pools. The reduced neurogenesis in the subventricular zone (SVZ) and the dentate gyrus (DG) of GD3S-conditional-knockout mice led to impaired olfactory and memory functions. Thus, our results provide convincing evidence that postnatal GD3 maintains the quiescent state of radial glia-like NSCs in the adult NSC niche.
Language	English
Publishing date	2023-03-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.14.532547
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Article ; Online: Ganglioside GD3 regulates neural stem cell quiescence and controls postnatal neurogenesis.

Fuchigami, Takahiro / Itokazu, Yutaka / Yu, Robert K

Glia

2023 Volume 72, Issue 1, Page(s) 167–183

Abstract	The postnatal neural stem cell (NSC) pool hosts quiescent and activated radial glia-like NSCs contributing to neurogenesis throughout adulthood. However, the underlying regulatory mechanism during the transition from quiescent NSCs to activated NSCs in the postnatal NSC niche is not fully understood. Lipid metabolism and lipid composition play important roles in regulating NSC fate determination. Biological lipid membranes define the individual cellular shape and help maintain cellular organization and are highly heterogeneous in structure and there exist diverse microdomains (also known as lipid rafts), which are enriched with sugar molecules, such as glycosphingolipids. An often overlooked but key aspect is that the functional activities of proteins and genes are highly dependent on their molecular environments. We previously reported that ganglioside GD3 is the predominant species in NSCs and that the reduced postnatal NSC pools are observed in global GD3-synthase knockout (GD3S-KO) mouse brains. The specific roles of GD3 in determining the stage and cell-lineage determination of NSCs remain unclear, since global GD3S-KO mice cannot distinguish if GD3 regulates postnatal neurogenesis or developmental impacts. Here, we show that inducible GD3 deletion in postnatal radial glia-like NSCs promotes NSC activation, resulting in the loss of the long-term maintenance of the adult NSC pools. The reduced neurogenesis in the subventricular zone (SVZ) and the dentate gyrus (DG) of GD3S-conditional-knockout mice led to the impaired olfactory and memory functions. Thus, our results provide convincing evidence that postnatal GD3 maintains the quiescent state of radial glia-like NSCs in the adult NSC niche.
MeSH term(s)	Mice ; Animals ; Neural Stem Cells/metabolism ; Neurogenesis/physiology ; Gangliosides/genetics ; Gangliosides/metabolism ; Cell Differentiation ; Mice, Knockout
Chemical Substances	ganglioside, GD3 (62010-37-1) ; Gangliosides
Language	English
Publishing date	2023-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24468
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Article ; Online: Brief Report: Atypical Temporal Sensitivity in Coarticulation in Autism: Evidence from Sibilant-Vowel Interaction in Cantonese.

Yu, Alan C L / McAllister, Robert / Mularoni, Nicholas / To, Carol K S

Journal of autism and developmental disorders

2024

Abstract: Purpose: Atypicalities in the prosodic aspects of speech are commonly considered in clinical assessments of autism. While there is an increasing number of studies using objective measures to assess prosodic deficits, such studies have primarily focused ... ...

Abstract	Purpose: Atypicalities in the prosodic aspects of speech are commonly considered in clinical assessments of autism. While there is an increasing number of studies using objective measures to assess prosodic deficits, such studies have primarily focused on the intonational and rhythmic aspects of prosody. Little is known about prosodic deficits that are reflected at the segmental level, despite the strong connection between prosody and segmental realization. This study examines the nature of sibilant-vowel coarticulation among male adult native speakers of Cantonese with autism and those without. Methods: Fifteen Cantonese-speaking autistic (ASD) adults (mean age = 25 years) and 23 neuro-typical (NT) adults (mean age = 20 years) participated. Each participant read aloud 42 syllables with a sibilant onset in carrier phrase. Spectral means and variance, skewness and kurtosis were measured, and regressed by vocalic rounding (rounded vs. unrounded), cohort (ASD vs. NT), sibilant duration, and articulation rate. Results: While neurotypical participants exhibit sibilant-vowel coarticulation that are sensitive to variation in sibilant duration, autistic participants show no sensitivity to segmental temporal changes. Conclusion: These findings point to the potential for atypicalities in prosody-segment interaction as an important characteristic of autistic speech.
Language	English
Publishing date	2024-03-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	391999-7
ISSN	1573-3432 ; 0162-3257
ISSN (online)	1573-3432
ISSN	0162-3257
DOI	10.1007/s10803-024-06258-w
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Article ; Online: Restoration of Adult Neurogenesis by Intranasal Administration of Gangliosides GD3 and GM1 in The Olfactory Bulb of A53T Alpha-Synuclein-Expressing Parkinson's-Disease Model Mice.

Fuchigami, Takahiro / Itokazu, Yutaka / Morgan, John C / Yu, Robert K

Molecular neurobiology

2023 Volume 60, Issue 6, Page(s) 3329–3344

Abstract: Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting the body and mind of millions of people in the world. As PD progresses, bradykinesia, rigidity, and tremor worsen. These motor symptoms are associated with the ... ...

Abstract	Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting the body and mind of millions of people in the world. As PD progresses, bradykinesia, rigidity, and tremor worsen. These motor symptoms are associated with the neurodegeneration of dopaminergic neurons in the substantia nigra. PD is also associated with non-motor symptoms, including loss of smell (hyposmia), sleep disturbances, depression, anxiety, and cognitive impairment. This broad spectrum of non-motor symptoms is in part due to olfactory and hippocampal dysfunctions. These non-motor functions are suggested to be linked with adult neurogenesis. We have reported that ganglioside GD3 is required to maintain the neural stem cell (NSC) pool in the subventricular zone (SVZ) of the lateral ventricles and the subgranular layer of the dentate gyrus (DG) in the hippocampus. In this study, we used nasal infusion of GD3 to restore impaired neurogenesis in A53T alpha-synuclein-expressing mice (A53T mice). Intriguingly, intranasal GD3 administration rescued the number of bromodeoxyuridine + (BrdU +)/Sox2 + NSCs in the SVZ. Furthermore, the administration of gangliosides GD3 and GM1 increases doublecortin (DCX)-expressing immature neurons in the olfactory bulb, and nasal ganglioside administration recovered the neuronal populations in the periglomerular layer of A53T mice. Given the relevance of decreased ganglioside on olfactory impairment, we discovered that GD3 has an essential role in olfactory functions. Our results demonstrated that intranasal GD3 infusion restored the self-renewal ability of the NSCs, and intranasal GM1 infusion promoted neurogenesis in the adult brain. Using a combination of GD3 and GM1 has the potential to slow down disease progression and rescue dysfunctional neurons in neurodegenerative brains.
MeSH term(s)	Mice ; Animals ; alpha-Synuclein/metabolism ; Parkinson Disease ; G(M1) Ganglioside ; Olfactory Bulb/metabolism ; Administration, Intranasal ; Gangliosides ; Neurogenesis/physiology ; Dopaminergic Neurons/metabolism
Chemical Substances	alpha-Synuclein ; ganglioside, GD3 (62010-37-1) ; G(M1) Ganglioside (37758-47-7) ; Gangliosides
Language	English
Publishing date	2023-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03282-2
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Zs.A 2411: Show issues

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Article ; Online: Correction of the hypomorphic

Yu, Wenxi / Mulligan, Megan K / Williams, Robert W / Meisler, Miriam H

HGG advances

2021 Volume 3, Issue 1, Page(s) 100064

Abstract: ... De ... ...

Abstract	De novo
Language	English
Publishing date	2021-10-08
Publishing country	United States
Document type	Journal Article
ISSN	2666-2477
ISSN (online)	2666-2477
DOI	10.1016/j.xhgg.2021.100064
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Article: Functional Impairment of the Nervous System with Glycolipid Deficiencies.

Itokazu, Yutaka / Fuchigami, Takahiro / Yu, Robert K

Advances in neurobiology

2022 Volume 29, Page(s) 419–448

Abstract: Patients with nervous system disorders suffer from impaired cognitive, sensory and motor functions that greatly inconvenience their daily life and usually burdens their family and society. It is difficult to achieve functional recovery for the damaged ... ...

Abstract	Patients with nervous system disorders suffer from impaired cognitive, sensory and motor functions that greatly inconvenience their daily life and usually burdens their family and society. It is difficult to achieve functional recovery for the damaged central nervous system (CNS) because of its limited ability to regenerate. Glycosphingolipids (GSLs) are abundant in the CNS and are known to play essential roles in cell-cell recognition, adhesion, signal transduction, and cellular migration, that are crucial in all phases of neurogenesis. Despite intense investigation of CNS regeneration, the roles of GSLs in neural regeneration remain unclear. Here we focus on the respective potentials of glycolipids to promote regeneration and repair of the CNS. Mice lacking glucosylceramide, lactosylceramide or gangliosides show lethal phenotypes. More importantly, patients with ganglioside deficiencies exhibit severe clinical phenotypes. Further, neurodegenerative diseases and mental health disorders are associated with altered GSL expression. Accumulating studies demonstrate that GSLs not only delimit physical regions but also play central roles in the maintenance of the biological functions of neurons and glia. We anticipate that the ability of GSLs to modulate behavior of a variety of molecules will enable them to ameliorate biochemical and neurobiological defects in patients. The use of GSLs to treat such defects in the human CNS will be a paradigm-shift in approach since GSL-replacement therapy has not yet been achieved in this manner clinically.
MeSH term(s)	Animals ; Humans ; Mice ; Glycolipids ; Lactosylceramides ; Glucosylceramides ; Gangliosides/chemistry ; Gangliosides/metabolism ; Neurons/metabolism
Chemical Substances	Glycolipids ; Lactosylceramides ; Glucosylceramides ; Gangliosides
Language	English
Publishing date	2022-10-18
Publishing country	United States
Document type	Journal Article
ISSN	2190-5215
ISSN	2190-5215
DOI	10.1007/978-3-031-12390-0_14
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