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Article ; Online: A Method to Detect Cytochrome c Oxidase Activity and Mitochondrial Proteins in Oligodendrocytes.

Campbell, Graham R / Mahad, Don J

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1936, Page(s) 333–342

Abstract: Cytochrome c oxidase or mitochondrial respiratory chain complex IV is where over 90% of oxygen is consumed. The relationship between complex IV activity and mitochondrial proteins, which provides a guide to understanding the mechanisms in primary ... ...

Abstract	Cytochrome c oxidase or mitochondrial respiratory chain complex IV is where over 90% of oxygen is consumed. The relationship between complex IV activity and mitochondrial proteins, which provides a guide to understanding the mechanisms in primary mitochondrial disorders, has been determined by histochemistry (complex IV activity) and immunohistochemistry in serial sections. In the central nervous system (CNS), mitochondrial activity and immunoreactivity have been determined in populations of cells in serial sections as capturing cells in more than one section is difficult. In this report, we describe a method to determine complex IV activity in relation to mitochondrial proteins at a single-cell level in the CNS. We performed complex IV histochemistry and immunohistochemistry consecutively in snap-frozen sections. Although the product of complex IV histochemistry reduces the sensitivity of standard immunohistochemistry (secondary antibody and ABC method), the biotin-free Menapath polymer detection system enables mitochondrial proteins to be detected following complex IV histochemistry. The co-occurring chromogens may then be separately visualized and analyzed using multispectral imaging. Our technique is applicable for exploring mitochondrial defects within single cells, including oligodendrocytes, in a variety of CNS disorders and animal models of those diseases.
MeSH term(s)	Animals ; Central Nervous System/metabolism ; Electron Transport Complex IV/analysis ; Humans ; Immunohistochemistry ; Mitochondrial Proteins/analysis ; Oligodendroglia/metabolism ; Rats ; Single-Cell Analysis/methods
Chemical Substances	Mitochondrial Proteins ; Electron Transport Complex IV (EC 1.9.3.1)
Language	English
Publishing date	2019-02-28
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9072-6_19
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Article ; Online: The 'best' basic science paper on multiple sclerosis in 2012.

Mahad, Don

Multiple sclerosis (Houndmills, Basingstoke, England)

2013 Volume 19, Issue 9, Page(s) 1128–1129

MeSH term(s)	Animals ; Humans ; Multiple Sclerosis/immunology ; Multiple Sclerosis/physiopathology
Language	English
Publishing date	2013-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1290669-4
ISSN	1477-0970 ; 1352-4585
ISSN (online)	1477-0970
ISSN	1352-4585
DOI	10.1177/1352458513486520
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Article ; Online: Neurodegeneration in Progressive Multiple Sclerosis.

Campbell, Graham / Mahad, Don

Cold Spring Harbor perspectives in medicine

2018 Volume 8, Issue 10

Abstract: The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating molecular changes within neuronal cell bodies. All of these molecular changes to ... ...

Abstract	The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating molecular changes within neuronal cell bodies. All of these molecular changes to intrinsic neurons converge on mitochondria, and the most reproduced change relates to mitochondrial respiratory chain complex deficiency. This compromise in the capacity to generate ATP in the neuronal cell body is coupled with an increased demand for energy by the demyelinated axon, which is particularly relevant to the long tracts such as corticospinal tracts with long projection axons. Recent work in our laboratory and that of our collaborators indicate limited reflection of the molecular changes that are intrinsic neurons in the experimental disease models. The mitochondrial changes within neuronal compartments are an under-recognized aspect of progressive MS and likely to offer novel targets for the improvement of neuronal function as well as neuroprotection.
MeSH term(s)	Humans ; Multiple Sclerosis/complications ; Neurodegenerative Diseases/etiology
Language	English
Publishing date	2018-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a028985
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Article ; Online: Mitochondrial dysfunction and axon degeneration in progressive multiple sclerosis.

Campbell, Graham / Mahad, Don J

FEBS letters

2018 Volume 592, Issue 7, Page(s) 1113–1121

Abstract: The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating that molecular changes converge on mitochondria within neuronal cell bodies. The ... ...

Abstract	The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating that molecular changes converge on mitochondria within neuronal cell bodies. The most reproducible change relates to mitochondrial respiratory chain complex deficiency, which compromises the capacity of neurons to generate ATP. The resulting energy failure state is coupled with an increase in demand for energy by the demyelinated axon, being particularly relevant to the long tracts such as corticospinal tracts with long projection axons. Recent work in our laboratory and that of our collaborators indicates the limited reflection of the mitochondria changes within neurons in experimental disease models. The mitochondrial changes within neuronal compartments are likely to offer novel targets for the improvement in neuronal function in patients with progressive MS.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Axons/metabolism ; Axons/pathology ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/metabolism ; Mitochondrial Diseases/pathology ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2018-03-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.13013
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Article: Mitochondrial dysfunction and axon degeneration in progressive multiple sclerosis

Campbell, Graham / Mahad, Don J.

FEBS letters. 2018 Apr., v. 592, no. 7

2018

Abstract: The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating that molecular changes converge on mitochondria within neuronal cell bodies. The ... ...

Abstract	The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating that molecular changes converge on mitochondria within neuronal cell bodies. The most reproducible change relates to mitochondrial respiratory chain complex deficiency, which compromises the capacity of neurons to generate ATP. The resulting energy failure state is coupled with an increase in demand for energy by the demyelinated axon, being particularly relevant to the long tracts such as corticospinal tracts with long projection axons. Recent work in our laboratory and that of our collaborators indicates the limited reflection of the mitochondria changes within neurons in experimental disease models. The mitochondrial changes within neuronal compartments are likely to offer novel targets for the improvement in neuronal function in patients with progressive MS.
Keywords	axons ; electron transport chain ; energy ; mitochondria ; sclerosis
Language	English
Dates of publication	2018-04
Size	p. 1113-1121.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.13013
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Targeting mitochondria to protect axons in progressive MS.

Campbell, Graham / Licht-Mayer, Simon / Mahad, Don

Neuroscience letters

2019 Volume 710, Page(s) 134258

Abstract: Inflammatory demyelinating processes target the neuron, particularly axons and synapses, in multiple sclerosis (MS). There is a gathering body of evidence indicating molecular changes which converge on mitochondria within neurons in progressive forms of ... ...

Abstract	Inflammatory demyelinating processes target the neuron, particularly axons and synapses, in multiple sclerosis (MS). There is a gathering body of evidence indicating molecular changes which converge on mitochondria within neurons in progressive forms of MS. The most reproducible changes are the increase in mitochondrial content within demyelinated axons and mitochondrial respiratory chain complex deficiency in neurons, which compromises the capacity to generate ATP. The resulting lack of ATP and the likely energy failure state and its coupling with an increase in demand for energy by the demyelinated axon, are particularly relevant to the long tracts such as corticospinal tracts with long projection axons. Recent work in our laboratory and that of our collaborators indicate the limited reflection of the mitochondrial changes within neurons in the experimental disease models. Enhancing the energy producing capacity of neurons to meet the increased energy demand of demyelinated axons is likely to be a novel neuroprotective strategy in progressive MS.
MeSH term(s)	Animals ; Axons/pathology ; Axons/physiology ; Demyelinating Diseases/metabolism ; Humans ; Mitochondria/pathology ; Mitochondria/physiology ; Mitochondrial Diseases/metabolism ; Multiple Sclerosis/physiopathology ; Nerve Degeneration/etiology ; Nerve Degeneration/pathology ; Neurons/physiology
Language	English
Publishing date	2019-05-10
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2019.05.012
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Article ; Online: Metabolic support of axons by oligodendrocytes: Implications for multiple sclerosis.

Campbell, Graham R / Mahad, Don J

Multiple sclerosis and related disorders

2014 Volume 3, Issue 1, Page(s) 28–30

Language	English
Publishing date	2014-01
Publishing country	Netherlands
Document type	Journal Article
ISSN	2211-0356
ISSN (online)	2211-0356
DOI	10.1016/j.msard.2013.06.008
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Article ; Online: Test-retest reliability and minimal detectable change of ankle kinematics and spatiotemporal parameters in MS population.

Andreopoulou, Georgia / Mahad, Don J / Mercer, Thomas H / van der Linden, Marietta L

Gait & posture

2019 Volume 74, Page(s) 218–222

Abstract: Background: Many people with multiple sclerosis (pwMS) experience walking impairments often including foot drop, evident as either reduced dorsiflexion at initial contact and/or at the swing phase of the gait cycle. To measure even subtle differences in ...

Abstract	Background: Many people with multiple sclerosis (pwMS) experience walking impairments often including foot drop, evident as either reduced dorsiflexion at initial contact and/or at the swing phase of the gait cycle. To measure even subtle differences in ankle kinematics, 3D gait analysis is considered a 'gold' standard. However, the psychometric properties of ankle kinematics in the MS population have not yet been examined. Objective: The aim of the study was to examine test-retest relative and absolute reliability of sagittal ankle kinematics and spatiotemporal parameters in two groups of pwMS with different levels of walking impairment. Methods: Two groups of pwMS underwent 3D gait analysis on two occasions 7-14 days apart. Group A consisted of 21 (14 female) people with Expanded Disability Status Scale (EDSS) 1-3.5 and group B consisted of 28 participants (14 female) with EDSS 4-6. The Intraclass Correlation Coefficient (ICC Results: Both groups presented 'excellent' ICC values (>0.75) for DF in swing, IC and step length of most and least affected limbs, walking speed and cadence, with GPS for both limbs exhibiting 'fair' to 'good' ICCs (0.489-0.698). The MDC Conclusion: The present results suggest that ankle kinematic and spatiotemporal parameters derived from 3D gait analysis are reliable outcome measures to be used in the MS population. Further, this study provides indices of reliability that can be applied to both clinical decision making and in the design of studies aimed at treating foot drop in people with MS.
MeSH term(s)	Adult ; Ankle Joint/physiopathology ; Biomechanical Phenomena ; Female ; Gait/physiology ; Gait Disorders, Neurologic/physiopathology ; Humans ; Male ; Middle Aged ; Multiple Sclerosis/physiopathology ; Reproducibility of Results ; Walking
Language	English
Publishing date	2019-09-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1162323-8
ISSN	1879-2219 ; 0966-6362
ISSN (online)	1879-2219
ISSN	0966-6362
DOI	10.1016/j.gaitpost.2019.09.015
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Article ; Online: Mitochondrial changes associated with demyelination: consequences for axonal integrity.

Campbell, Graham R / Mahad, Don J

Mitochondrion

2012 Volume 12, Issue 2, Page(s) 173–179

Abstract: The loss of myelin sheath (demyelination) renders axons vulnerable to a variety of insults. Axonal degeneration is well recognised in inflammatory demyelinating disorders of the central nervous system (CNS) such as multiple sclerosis (MS) and also ... ...

Abstract	The loss of myelin sheath (demyelination) renders axons vulnerable to a variety of insults. Axonal degeneration is well recognised in inflammatory demyelinating disorders of the central nervous system (CNS) such as multiple sclerosis (MS) and also certain neurodegenerative diseases. Energy required for nerve impulse conduction and maintenance of structural integrity of axons is met by mitochondria. Based on the distribution of ion channels and the Na(+)/K(+) ATPase, the energy requirements of demyelinated and dysmyelinated axons are likely to differ from myelinated axons. In this review we discuss the changes in mitochondrial presence within axons in relation to presence or absence of healthy myelin sheaths and propose the increase in mitochondrial presence following demyelination as an adaptive process. An energy deficit within demyelinated axons is likely to be more detrimental compared to myelinated axons, judging by the neuropathological findings in primary mitochondrial disorders due to mitochondrial and nuclear DNA mutations and the mitochondrial changes that follow demyelination. Agents that enhance and protect mitochondria, as potential therapy, need to be considered and investigated in earnest for demyelinating disorders of the CNS such as MS.
MeSH term(s)	Axons/pathology ; Axons/physiology ; Demyelinating Diseases/pathology ; Humans ; Mitochondria/pathology ; Multiple Sclerosis/pathology
Language	English
Publishing date	2012-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2011.03.007
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Article ; Online: Clonal expansion of mitochondrial DNA deletions and the progression of multiple sclerosis.

Campbell, Graham R / Mahad, Don J

CNS & neurological disorders drug targets

2012 Volume 11, Issue 5, Page(s) 589–597

Abstract: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Mechanisms of disease progression in MS are poorly understood but are thought to relate to both focal pathology as well as diffuse inflammation in the white ... ...

Abstract	Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Mechanisms of disease progression in MS are poorly understood but are thought to relate to both focal pathology as well as diffuse inflammation in the white and grey matter. Evidence points to neurodegeneration combined with a loss of cellular function in the remaining tissue as an important factor to the progression of MS. Mitochondria are implicated to play a role in the pathogenesis of MS with evidence of loss of mitochondrial respiratory chain activity, down regulation of both nuclear DNA and mitochondrial DNA (mtDNA) encoded transcripts as well as oxidative damage to, and deletions of, the mitochondrial DNA (mtDNA). The double stranded circle of mtDNA (16.6 kb) encompasses genes encoding key subunits within the mitochondrial respiratory chain required for the production of ATP as well as transfer RNA and ribosomal RNA molecules within the cell. The stability of mtDNA is essential for a healthy CNS as highlighted by the patients with primary mitochondrial disease. In this review, we focus on the potential role of mtDNA mutations, in particular somatic mtDNA deletions, in the pathogenesis of the progressive stage of MS. We propose clonal expansion of somatic mtDNA deletions as a potential molecular link between early inflammatory events and a delayed cellular energy failure, dysfunction and degeneration. The high level of somatic mtDNA deletions within single cells in MS is likely to cause cellular dysfunction as well as increase the susceptibility of the CNS tissue to additional stress.
MeSH term(s)	Animals ; Cell Respiration ; Clone Cells ; DNA, Mitochondrial/genetics ; Disease Progression ; Electron Transport ; Gene Deletion ; Humans ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Multiple Sclerosis/physiopathology ; Nerve Degeneration/etiology ; Neurons/metabolism ; Neurons/pathology
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2012-03-16
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2228394-8
ISSN	1996-3181 ; 1871-5273
ISSN (online)	1996-3181
ISSN	1871-5273
DOI	10.2174/187152712801661194
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