Oligodendroglia and neurotrophic factors in neurodegeneration

Bankston, Andrew N.; Mandler, Mariana D.; Feng, Yue

doi:10.1007/s12264-013-1321-3

Cited by 58 publications

(46 citation statements)

References 132 publications

(157 reference statements)

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“…Strong evidence for an essential contribution of dysmyelination/demyelination to neurodegeneration is derived from studies on multiple sclerosis (MS), one of the best-characterized demyelinating disorders of the CNS [66]. Although the initial MS pathology is tightly linked to autoimmune processes followed by focal demyelination, it is important to note that axonal damage and loss of neuronal integrity represent the structural correlates for the progression of functional deficits in MS patients [67, 68].…”

Section: Oligodendroglial and Myelin Dysfunction: A Link To Neurodegementioning

confidence: 99%

Oligodendroglia and Myelin in Neurodegenerative Diseases: More Than Just Bystanders?

2015

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Oligodendrocytes, the myelinating cells of the central nervous system, mediate rapid action potential conduction and provide trophic support for axonal as well as neuronal maintenance. Their progenitor cell population is widely distributed in the adult brain and represents a permanent cellular reservoir for oligodendrocyte replacement and myelin plasticity. The recognition of oligodendrocytes, their progeny, and myelin as contributing factors for the pathogenesis and the progression of neurodegenerative disease has recently evolved shaping our understanding of these disorders. In the present review, we aim to highlight studies on oligodendrocytes and their progenitors in neurodegenerative diseases. We dissect oligodendroglial biology and illustrate evolutionary aspects in regard to their importance for neuronal functionality and maintenance of neuronal circuitries. After covering recent studies on oligodendroglia in different neurodegenerative diseases mainly in view of their function as myelinating cells, we focus on the alpha-synucleinopathy multiple system atrophy, a prototypical disorder with a well-defined oligodendroglial pathology.

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Section: Oligodendroglial and Myelin Dysfunction: A Link To Neurodegementioning

confidence: 99%

Oligodendroglia and Myelin in Neurodegenerative Diseases: More Than Just Bystanders?

2015

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“…The myelin enzyme CNPase was discovered over 50 years ago, and its strong expression profile and peculiar CNPase is possibly one player of many in the axonal support systems provided by myelinating glia [90] .…”

Section: Summary and Open Questionsmentioning

confidence: 99%

The myelin membrane-associated enzyme 2′,3′-cyclic nucleotide 3′-phosphodiesterase: on a highway to structure and function

Raasakka

Kursula

2014

Neurosci. Bull.

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The membrane-anchored myelin enzyme 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNPase) was discovered in the early 1960s and has since then troubled scientists with its peculiar catalytic activity and high expression levels in the central nervous system. Despite decades of research, the actual physiological relevance of CNPase has only recently begun to unravel. In addition to a role in myelination, CNPase is also involved in local adenosine production in traumatic brain injury and possibly has a regulatory function in mitochondrial membrane permeabilization. Although research focusing on the CNPase phosphodiesterase activity has been helpful, several open questions concerning the protein function in vivo remain unanswered. This review is focused on past research on CNPase, especially in the fields of structural biology and enzymology, and outlines the current understanding regarding the biochemical and physiological signifi cance of CNPase, providing ideas and directions for future research.Keywords: 2′,3′-cyclic nucleotide 3′-phosphodiesterase; calmodulin; central nervous system; cytoskeleton; myelin proteins; RNA ·Review· IntroductionMyelin is a specialized multilamellar structure, which is wrapped around neuronal axons by oligodendrocytes in the central nervous system (CNS) and by Schwann cells in the peripheral nervous system (PNS). The membrane sheets of myelin are densely packed, resulting in the extrusion of cytosolic elements and in the formation of a lipid-rich, insulating sheath that enables the acceleration of nerve impulses. A mature myelin sheath can be morphologically divided into compact and non-compact myelin, of which the latter has a higher cytosolic content and further contains several subcompartments, such as the abaxonal and adaxonal layers, as well as the paranodal loops [1,2] .Myelin contains a set of unique proteins that generally display strict localization to either compact or non-compact myelin, which is thought to be at least partially driven by size exclusion [3,4] . The myelin environment being low in aqueous content and harboring negatively charged, tightly packed membrane interfaces, myelin proteins typically exhibit attributes such as strong hydrophobicity, peripheral membrane association, transmembrane domains, and a high positive net charge, as well as intrinsic disorder [5] .Several myelin proteins have delicately regulated expression levels and functions. Past research using cell culture and animal models have outlined the importance of various proteins in demyelination -a situation where myelin undergoes morphological changes and loss [6] .Demyelination causes neurological disorders, including multiple sclerosis (MS), Charcot-Marie-Tooth disease, and leukodystrophies, such as Pelizaeus-Merzbacher disease [7][8][9][10] .2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNPase)is one of the most abundant proteins in CNS myelin and a possible auto-antigen in MS [4,11] . The high expression levels of CNPase, together with its rather unusual enzymatic after the initial di...

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“…OL impairment has become an increasingly recognized pathophysiological feature of numerous neurological disorders originally believed to result from neuronal defects alone, including Alzheimer disease and schizophrenia (1)(2)(3)(4). Moreover, key components of cell signaling pathways traditionally thought to control neuronal development and function have now been found expressed and playing critical roles in OLs as well.…”

mentioning

confidence: 99%

p39, the Primary Activator for Cyclin-dependent Kinase 5 (Cdk5) in Oligodendroglia, Is Essential for Oligodendroglia Differentiation and Myelin Repair

Bankston

Zhang

et al. 2013

Journal of Biological Chemistry

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Background: Cyclin-dependent kinase 5 (Cdk5) is crucial for brain development. Results: In contrast to neurons that utilize p35 as the primary Cdk5 activator, oligodendroglia employ p39-dependent Cdk5 activation to advance differentiation and myelin repair. Conclusion: p39 is the primary Cdk5 activator in oligodendroglia, essential for oligodendroglia development. Significance: Our study revealed distinct mechanisms controlling Cdk5 activity in neurons and oligodendroglia.

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Oligodendroglia and neurotrophic factors in neurodegeneration

Cited by 58 publications

References 132 publications

Oligodendroglia and Myelin in Neurodegenerative Diseases: More Than Just Bystanders?

Oligodendroglia and Myelin in Neurodegenerative Diseases: More Than Just Bystanders?

The myelin membrane-associated enzyme 2′,3′-cyclic nucleotide 3′-phosphodiesterase: on a highway to structure and function

p39, the Primary Activator for Cyclin-dependent Kinase 5 (Cdk5) in Oligodendroglia, Is Essential for Oligodendroglia Differentiation and Myelin Repair

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