Protein aggregate formation in oligodendrocytes: tau and the cytoskeleton at the intersection of neuroprotection and neurodegeneration

Richter‐Landsberg, Christiane

doi:10.1515/hsz-2015-0157

Cited by 17 publications

(21 citation statements)

References 76 publications

(103 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A few glial cells colocalize with HSP and ubiquitin thus pinpointing the combined reaction of stress responses and impaired function of the ubiquitin-protesome system (Richter-Landsberg and Bauer, 2004). Further insights linking HDAC6, tau acetylation, tau phosphorylation, stress responses, proteasome and autophagy are exemplified in oligodendroglia cell culture paradigms (Richter-Landsberg, 2016).…”

Section: Tauopathiesmentioning

confidence: 99%

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

View full text Add to dashboard Cite

Oligodendrocytes are in contact with neurons, wrap axons with a myelin sheath that protects their structural integrity, and facilitate nerve conduction. Oligodendrocytes also form a syncytium with astrocytes which interacts with neurons, promoting reciprocal survival mediated by activity and by molecules involved in energy metabolism and trophism. Therefore, oligodendrocytes are key elements in the normal functioning of the central nervous system. Oligodendrocytes are affected following different insults to the central nervous system including ischemia, traumatism, and inflammation. The term oligodendrogliopathy highlights the prominent role of altered oligodendrocytes in the pathogenesis of certain neurological diseases, not only in demyelinating diseases and most leukodystrophies, but also in aging and age-related neurodegenerative diseases with abnormal protein aggregates. Most of these diseases are characterized by the presence of abnormal protein deposits, forming characteristic and specific inclusions in neurons and astrocytes but also in oligodendrocytes, thus signaling their involvement in the disease. Emerging evidence suggests that such deposits in oligodendrocytes are not mere bystanders but rather are associated with functional alterations. Moreover, operative modifications in oligodendrocytes are also detected in the absence of oligodendroglial inclusions in certain diseases. The present review focuses first on general aspects of oligodendrocytes and precursors, and their development and functions, and then introduces and updates alterations and dysfunction of oligodendrocytes in selected neurodegenerative diseases with abnormal protein aggregates such as multiple system atrophy, Lewy body diseases, tauopathies, Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal lobar degeneration with TDP-43 inclusions (TDP-43 proteinopathies), and Creutzfeldt-Jakob´s disease as a prototypical human prionopathy.

show abstract

Section: Tauopathiesmentioning

confidence: 99%

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

View full text Add to dashboard Cite

show abstract

“…With regard to the OLG/OPC growth cone, however, the microtubule‐rich central region has up to now received extremely little attention. The reader is referred to previously published review articles that discuss the increasingly recognized relevance of the microtubule‐rich central region to motile growth cone behaviors in neurons (Cammarata, Bearce, & Lowery, ; Kahn & Baas, ), as well as to those that address more general roles of the microtubule cytoskeleton in OLG lineage cells (Bauer et al, ; Richter‐Landsberg, , , ). This review focuses on the actin cytoskeletal aspects of the OLG/OPC growth cone by providing an overview of its role in driving dynamic morphological changes at the different stages of the OLG lineage.…”

Section: Introductionmentioning

confidence: 99%

The oligodendrocyte growth cone and its actin cytoskeleton: A fundamental element for progenitor cell migration and CNS myelination

Thomason

Escalante

Osterhout

et al. 2019

Glia

View full text Add to dashboard Cite

Cells of the oligodendrocyte (OLG) lineage engage in highly motile behaviors that are crucial for effective central nervous system (CNS) myelination. These behaviors include the guided migration of OLG progenitor cells (OPCs), the surveying of local environments by cellular processes extending from differentiating and premyelinating OLGs, and during the process of active myelin wrapping, the forward movement of the leading edge of the myelin sheath's inner tongue along the axon.Almost all of these motile behaviors are driven by actin cytoskeletal dynamics initiated within a lamellipodial structure that is located at the tip of cellular OLG/OPC processes and is structurally as well as functionally similar to the neuronal growth cone. Accordingly, coordinated stoichiometries of actin filament (F-actin) assembly and disassembly at these OLG/OPC growth cones have been implicated in directing process outgrowth and guidance, and the initiation of myelination. Nonetheless, the functional importance of the OLG/OPC growth cone still remains to be fully understood, and, as a unique aspect of actin cytoskeletal dynamics, F-actin depolymerization and disassembly start to predominate at the transition from myelination initiation to myelin wrapping. This review provides an overview of the current knowledge about OLG/OPC growth cones, and it proposes a model in which actin cytoskeletal dynamics in OLG/OPC growth cones are a main driver for morphological transformations and motile behaviors. Remarkably, these activities, at least at the later stages of OLG maturation, may be regulated independently from the transcriptional gene expression changes typically associated with CNS myelination. K E Y W O R D Sactin cytoskeleton, growth cone, migration, myelination, oligodendrocyte

show abstract

“…Moreover, in cultured oligodendrocytes, inhibition of ubiquitin-dependent pathway enzymes and the proteasome were both shown to result in tau aggregation. 92 …”

Section: Potential Mechanisms Of Glial Tau Toxicitymentioning

confidence: 99%

Glial Tau Pathology in Tauopathies: Functional Consequences

2015

View full text Add to dashboard Cite

Tauopathies are a class of neurodegenerative diseases characterized by the presence of hyperphosphorylated and aggregated tau pathology in neuronal and glial cells. Though the ratio of neuronal and glial tau aggregates varies across diseases, glial tau aggregates can populate the same degenerating brain regions as neuronal tau aggregates. While much is known about the deleterious consequences of tau pathology in neurons, the relative contribution of glial tau pathology to these diseases is less clear. Recent studies using a number of model systems implicate glial tau pathology in contributing to tauopathy pathogenesis. This review aims to highlight the functional consequences of tau overexpression in glial cells and explore the potential contribution of glial tau pathology in the pathogenesis of neurodegenerative tauopathies.

show abstract

Protein aggregate formation in oligodendrocytes: tau and the cytoskeleton at the intersection of neuroprotection and neurodegeneration

Cited by 17 publications

References 76 publications

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

The oligodendrocyte growth cone and its actin cytoskeleton: A fundamental element for progenitor cell migration and CNS myelination

Glial Tau Pathology in Tauopathies: Functional Consequences

Contact Info

Product

Resources

About