LIVIVO - Search results -

Search results

Result 1 - 10 of total 95

Search options

Article ; Online: Presynaptic perspective: Axonal transport defects in neurodevelopmental disorders.

Xiong, Gui-Jing / Sheng, Zu-Hang

2024 Volume 223, Issue 6

Abstract: Disruption of synapse assembly and maturation leads to a broad spectrum of neurodevelopmental disorders. Presynaptic proteins are largely synthesized in the soma, where they are packaged into precursor vesicles and transported into distal axons to ensure ...

Abstract	Disruption of synapse assembly and maturation leads to a broad spectrum of neurodevelopmental disorders. Presynaptic proteins are largely synthesized in the soma, where they are packaged into precursor vesicles and transported into distal axons to ensure precise assembly and maintenance of presynapses. Due to their morphological features, neurons face challenges in the delivery of presynaptic cargos to nascent boutons. Thus, targeted axonal transport is vital to build functional synapses. A growing number of mutations in genes encoding the transport machinery have been linked to neurodevelopmental disorders. Emerging lines of evidence have started to uncover presynaptic mechanisms underlying axonal transport defects, thus broadening the view of neurodevelopmental disorders beyond postsynaptic mechanisms. In this review, we discuss presynaptic perspectives of neurodevelopmental disorders by focusing on impaired axonal transport and disturbed assembly and maintenance of presynapses. We also discuss potential strategies for restoring axonal transport as an early therapeutic intervention.
MeSH term(s)	Humans ; Axonal Transport ; Axons ; Cell Body ; Mutation ; Neurodevelopmental Disorders/genetics ; Presynaptic Terminals
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202401145
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ub I Zs.190: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Oligodendrocyte-derived transcellular signaling regulates axonal energy metabolism.

Li, Sunan / Sheng, Zu-Hang

Current opinion in neurobiology

2023 Volume 80, Page(s) 102722

Abstract: The unique morphology and functionality of central nervous system (CNS) neurons necessitate specialized mechanisms to maintain energy metabolism throughout long axons and extensive terminals. Oligodendrocytes (OLs) enwrap CNS axons with myelin sheaths in ...

Abstract	The unique morphology and functionality of central nervous system (CNS) neurons necessitate specialized mechanisms to maintain energy metabolism throughout long axons and extensive terminals. Oligodendrocytes (OLs) enwrap CNS axons with myelin sheaths in a multilamellar fashion. Apart from their well-established function in action potential propagation, OLs also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes consisting of proteins, lipids, and RNAs. OL-derived metabolic support is crucial for the maintenance of axonal integrity; its dysfunction has emerged as an important player in neurological disorders that are associated with axonal energy deficits and degeneration. In this review, we discuss recent advances in how these transcellular signaling pathways maintain axonal energy metabolism in health and neurological disorders.
MeSH term(s)	Axons/physiology ; Oligodendroglia ; Myelin Sheath/metabolism ; Central Nervous System/physiology ; Energy Metabolism/physiology
Language	English
Publishing date	2023-04-05
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2023.102722
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3260: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Microfluidic devices as model platforms of CNS injury-ischemia to study axonal regeneration by regulating mitochondrial transport and bioenergetic metabolism.

Huang, Ning / Sheng, Zu-Hang

Cell regeneration (London, England)

2022 Volume 11, Issue 1, Page(s) 33

Abstract: Central nervous system (CNS) neurons typically fail to regenerate their axons after injury leading to neurological impairment. Axonal regeneration is a highly energy-demanding cellular program that requires local mitochondria to supply most energy within ...

Abstract	Central nervous system (CNS) neurons typically fail to regenerate their axons after injury leading to neurological impairment. Axonal regeneration is a highly energy-demanding cellular program that requires local mitochondria to supply most energy within injured axons. Recent emerging lines of evidence have started to reveal that injury-triggered acute mitochondrial damage and local energy crisis contribute to the intrinsic energetic restriction that accounts for axon regeneration failure in the CNS. Characterizing and reprogramming bioenergetic signaling and mitochondrial maintenance after axon injury-ischemia is fundamental for developing therapeutic strategies that can restore local energy metabolism and thus facilitate axon regeneration. Therefore, establishing reliable and reproducible neuronal model platforms is critical for assessing axonal energetic metabolism and regeneration capacity after injury-ischemia. In this focused methodology article, we discuss recent advances in applying cutting-edge microfluidic chamber devices in combination with state-of-the-art live-neuron imaging tools to monitor axonal regeneration, mitochondrial transport, bioenergetic metabolism, and local protein synthesis in response to injury-ischemic stress in mature CNS neurons.
Language	English
Publishing date	2022-10-03
Publishing country	China
Document type	Journal Article
ZDB-ID	2682438-3
ISSN	2045-9769
ISSN	2045-9769
DOI	10.1186/s13619-022-00138-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Neurobiology: A pathogenic tug of war.

Cheng, Xiu-Tang / Sheng, Zu-Hang

Current biology : CB

2021 Volume 31, Issue 10, Page(s) R491–R493

Abstract: Pathogenic mutations in the kinase LRRK2 have been implicated in Parkinson's disease. A new study shows that hyperactivation of this kinase reduces the processivity of autophagosomal retrograde transport in axons through an unproductive 'tug-of-war' ... ...

Abstract	Pathogenic mutations in the kinase LRRK2 have been implicated in Parkinson's disease. A new study shows that hyperactivation of this kinase reduces the processivity of autophagosomal retrograde transport in axons through an unproductive 'tug-of-war' between anterograde and retrograde motors, thus contributing to autophagy dysfunction and axonal degeneration.
MeSH term(s)	Autophagy ; Axons ; Humans ; Mutation ; Neurobiology ; Parkinson Disease/genetics
Language	English
Publishing date	2021-06-23
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2021.03.071
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3208: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Energy matters: presynaptic metabolism and the maintenance of synaptic transmission.

Li, Sunan / Sheng, Zu-Hang

Nature reviews. Neuroscience

2021 Volume 23, Issue 1, Page(s) 4–22

Abstract: Synaptic activity imposes large energy demands that are met by local adenosine triphosphate (ATP) synthesis through glycolysis and mitochondrial oxidative phosphorylation. ATP drives action potentials, supports synapse assembly and remodelling, and fuels ...

Abstract	Synaptic activity imposes large energy demands that are met by local adenosine triphosphate (ATP) synthesis through glycolysis and mitochondrial oxidative phosphorylation. ATP drives action potentials, supports synapse assembly and remodelling, and fuels synaptic vesicle filling and recycling, thus sustaining synaptic transmission. Given their polarized morphological features - including long axons and extensive branching in their terminal regions - neurons face exceptional challenges in maintaining presynaptic energy homeostasis, particularly during intensive synaptic activity. Recent studies have started to uncover the mechanisms and signalling pathways involved in activity-dependent and energy-sensitive regulation of presynaptic energetics, or 'synaptoenergetics'. These conceptual advances have established the energetic regulation of synaptic efficacy and plasticity as an exciting research field that is relevant to a range of neurological disorders associated with bioenergetic failure and synaptic dysfunction.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Energy Metabolism/physiology ; Glycolysis ; Humans ; Receptors, Presynaptic/metabolism ; Synaptic Transmission/physiology ; Synaptic Vesicles
Chemical Substances	Receptors, Presynaptic ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2021-11-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2034150-7
ISSN	1471-0048 ; 1471-0048 ; 1471-003X
ISSN (online)	1471-0048
ISSN	1471-0048 ; 1471-003X
DOI	10.1038/s41583-021-00535-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5473: 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 47: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The Interplay of Axonal Energy Homeostasis and Mitochondrial Trafficking and Anchoring.

Sheng, Zu-Hang

Trends in cell biology

2017 Volume 27, Issue 6, Page(s) 403–416

Abstract: Mitochondria are key cellular power plants essential for neuronal growth, survival, function, and regeneration after injury. Given their unique morphological features, neurons face exceptional challenges in maintaining energy homeostasis at distal ... ...

Abstract	Mitochondria are key cellular power plants essential for neuronal growth, survival, function, and regeneration after injury. Given their unique morphological features, neurons face exceptional challenges in maintaining energy homeostasis at distal synapses and growth cones where energy is in high demand. Efficient regulation of mitochondrial trafficking and anchoring is critical for neurons to meet altered energy requirements. Mitochondrial dysfunction and impaired transport have been implicated in several major neurological disorders. Thus, research into energy-mediated regulation of mitochondrial recruitment and redistribution is an important emerging frontier. In this review, I discuss new insights into the mechanisms regulating mitochondrial trafficking and anchoring, and provide an updated overview of how mitochondrial motility maintains energy homeostasis in axons, thus contributing to neuronal growth, regeneration, and synaptic function.
MeSH term(s)	Animals ; Axons/metabolism ; Energy Metabolism ; Homeostasis ; Humans ; Mitochondria/metabolism ; Protein Transport ; Synapses/metabolism
Language	English
Publishing date	2017-02-20
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2017.01.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.MG 25: Show issues
Zs.MO 113: Show issues
Zs.A 3410: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.

Cheng, Xiu-Tang / Huang, Ning / Sheng, Zu-Hang

Neuron

2022 Volume 110, Issue 12, Page(s) 1899–1923

Abstract: Mitochondria generate ATP essential for neuronal growth, function, and regeneration. Due to their polarized structures, neurons face exceptional challenges to deliver mitochondria to and maintain energy homeostasis throughout long axons and terminal ... ...

Abstract	Mitochondria generate ATP essential for neuronal growth, function, and regeneration. Due to their polarized structures, neurons face exceptional challenges to deliver mitochondria to and maintain energy homeostasis throughout long axons and terminal branches where energy is in high demand. Chronic mitochondrial dysfunction accompanied by bioenergetic failure is a pathological hallmark of major neurodegenerative diseases. Brain injury triggers acute mitochondrial damage and a local energy crisis that accelerates neuron death. Thus, mitochondrial maintenance defects and axonal energy deficits emerge as central problems in neurodegenerative disorders and brain injury. Recent studies have started to uncover the intrinsic mechanisms that neurons adopt to maintain (or reprogram) axonal mitochondrial density and integrity, and their bioenergetic capacity, upon sensing energy stress. In this review, we discuss recent advances in how neurons maintain a healthy pool of axonal mitochondria, as well as potential therapeutic strategies that target bioenergetic restoration to power neuronal survival, function, and regeneration.
MeSH term(s)	Axons/metabolism ; Brain Injuries/metabolism ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; Neurodegenerative Diseases/metabolism ; Regeneration
Language	English
Publishing date	2022-04-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2022.03.015
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2496: 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 92: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Neuronal endolysosomal transport and lysosomal functionality in maintaining axonostasis.

Roney, Joseph C / Cheng, Xiu-Tang / Sheng, Zu-Hang

The Journal of cell biology

2022 Volume 221, Issue 3

Abstract: Lysosomes serve as degradation hubs for the turnover of endocytic and autophagic cargos, which is essential for neuron function and survival. Deficits in lysosome function result in progressive neurodegeneration in most lysosomal storage disorders and ... ...

Abstract	Lysosomes serve as degradation hubs for the turnover of endocytic and autophagic cargos, which is essential for neuron function and survival. Deficits in lysosome function result in progressive neurodegeneration in most lysosomal storage disorders and contribute to the pathogenesis of aging-related neurodegenerative diseases. Given their size and highly polarized morphology, neurons face exceptional challenges in maintaining cellular homeostasis in regions far removed from the cell body where mature lysosomes are enriched. Neurons therefore require coordinated bidirectional intracellular transport to sustain efficient clearance capacity in distal axonal regions. Emerging lines of evidence have started to uncover mechanisms and signaling pathways regulating endolysosome transport and maturation to maintain axonal homeostasis, or "axonostasis," that is relevant to a range of neurologic disorders. In this review, we discuss recent advances in how axonal endolysosomal trafficking, distribution, and lysosomal functionality support neuronal health and become disrupted in several neurodegenerative diseases.
MeSH term(s)	Animals ; Autophagy ; Axons/metabolism ; Biological Transport ; Endosomes/metabolism ; Humans ; Lysosomes/metabolism ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology
Language	English
Publishing date	2022-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202111077
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ub I Zs.190: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Developmental regulation of microtubule-based trafficking and anchoring of axonal mitochondria in health and diseases.

Cheng, Xiu-Tang / Sheng, Zu-Hang

Developmental neurobiology

2020 Volume 81, Issue 3, Page(s) 284–299

Abstract: Mitochondria are cellular power plants that supply most of the ATP required in the brain to power neuronal growth, function, and regeneration. Given their extremely polarized structures and extended long axons, neurons face an exceptional challenge to ... ...

Abstract	Mitochondria are cellular power plants that supply most of the ATP required in the brain to power neuronal growth, function, and regeneration. Given their extremely polarized structures and extended long axons, neurons face an exceptional challenge to maintain energy homeostasis in distal axons, synapses, and growth cones. Anchored mitochondria serve as local energy sources; therefore, the regulation of mitochondrial trafficking and anchoring ensures that these metabolically active areas are adequately supplied with ATP. Chronic mitochondrial dysfunction is a hallmark feature of major aging-related neurodegenerative diseases, and thus, anchored mitochondria in aging neurons need to be removed when they become dysfunctional. Investigations into the regulation of microtubule (MT)-based trafficking and anchoring of axonal mitochondria under physiological and pathological circumstances represent an important emerging area. In this short review article, we provide an updated overview of recent in vitro and in vivo studies showing (1) how mitochondria are transported and positioned in axons and synapses during neuronal developmental and maturation stages, and (2) how altered mitochondrial motility and axonal energy deficits in aging nervous systems link to neurodegeneration and regeneration in a disease or injury setting. We also highlight a major role of syntaphilin as a key MT-based regulator of axonal mitochondrial trafficking and anchoring in mature neurons.
MeSH term(s)	Axons/metabolism ; Microtubules ; Mitochondria/pathology ; Neurons/metabolism ; Synapses/metabolism
Language	English
Publishing date	2020-05-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2256184-5
ISSN	1932-846X ; 1097-4695 ; 1932-8451 ; 0022-3034
ISSN (online)	1932-846X ; 1097-4695
ISSN	1932-8451 ; 0022-3034
DOI	10.1002/dneu.22748
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 853: 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)

Order via subito

Details ▾

Article ; Online: Mechanisms for the maintenance and regulation of axonal energy supply.

Chamberlain, Kelly Anne / Sheng, Zu-Hang

Journal of neuroscience research

2019 Volume 97, Issue 8, Page(s) 897–913

Abstract: The unique polarization and high-energy demand of neurons necessitates specialized mechanisms to maintain energy homeostasis throughout the cell, particularly in the distal axon. Mitochondria play a key role in meeting axonal energy demand by generating ... ...

Abstract	The unique polarization and high-energy demand of neurons necessitates specialized mechanisms to maintain energy homeostasis throughout the cell, particularly in the distal axon. Mitochondria play a key role in meeting axonal energy demand by generating adenosine triphosphate through oxidative phosphorylation. Recent evidence demonstrates how axonal mitochondrial trafficking and anchoring are coordinated to sense and respond to altered energy requirements. If and when these mechanisms are impacted in pathological conditions, such as injury and neurodegenerative disease, is an emerging research frontier. Recent evidence also suggests that axonal energy demand may be supplemented by local glial cells, including astrocytes and oligodendrocytes. In this review, we provide an updated discussion of how oxidative phosphorylation, aerobic glycolysis, and oligodendrocyte-derived metabolic support contribute to the maintenance of axonal energy homeostasis.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Astrocytes/pathology ; Axons/metabolism ; Axons/pathology ; Brain/metabolism ; Brain/pathology ; Energy Metabolism/physiology ; Homeostasis/physiology ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Oligodendroglia/metabolism ; Oligodendroglia/pathology ; Protein Transport/physiology
Language	English
Publishing date	2019-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/jnr.24411
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1232: 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)

Order via subito

Details ▾

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito