Neuroinflammatory modulators of oligodendrogenesis

Armada‐Moreira, Adam; Ribeiro, Filipa F.; Sebastião, Ana M.; Xapelli, Sara

doi:10.4103/2347-8659.167311

Cited by 19 publications

(15 citation statements)

References 107 publications

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“…While neuronal bHLH transcription factors have long been established (Dennis et al, 2019), glial bHLH transcription factors were only recently discovered (Lu et al, 2000;Takebayashi et al, 2000;Zhou et al, 2000). Specifically, oligodendrocyte precursor cells (OPCs), a subtype of glia and precursors to oligodendrocytes (Armada-Moreira et al, 2015), were found to express the novel bHLH transcription factor family of Olig genes (Meijer et al, 2012). The Olig bHLH transcription factors consist of three members, Olig1, Olig2, and Olig3, where their expression have been implicated in not only oligodendrocyte differentiation but neuronal and glial cell lineages as well (Lu et al, 2000;Takebayashi et al, 2000;Zhou et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Impact of the Olig Family on Neurodevelopmental Disorders

et al. 2021

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The Olig genes encode members of the basic helix-loop-helix (bHLH) family of transcription factors. Olig1, Olig2, and Olig3 are expressed in both the developing and mature central nervous system (CNS) and strictly regulate cellular specification and differentiation. Extensive studies have established functional roles of Olig1 and Olig2 in directing neuronal and glial formation during different stages in development. Recently, Olig2 overexpression was implicated in neurodevelopmental disorders down syndrome (DS) and autism spectrum disorder (ASD) but its influence on cognitive and intellectual defects remains unknown. In this review, we summarize the biological functions of the Olig family and how it uniquely promotes cellular diversity in the CNS. This is followed up with a discussion on how abnormal Olig2 expression impacts brain development and function in DS and ASD. Collectively, the studies described here emphasize vital features of the Olig members and their distinctive potential roles in neurodevelopmental disease states.

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Section: Introductionmentioning

confidence: 99%

Impact of the Olig Family on Neurodevelopmental Disorders

et al. 2021

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“…Oligodendrocytes also associated with spatial tissue vulnerability to all conditions aside ALS ( Figure 3A ). Oligodendrocytes are responsible for the synthesis and maintenance of myelin in the brain ( Armada-Moreira et al, 2015 ). Demyelination produces loss of axonal insulation, leading to neuronal dysfunctions ( Armada-Moreira et al, 2015 ; Mot et al, 2018 ).…”

Section: Resultsmentioning

confidence: 99%

“…Oligodendrocytes are responsible for the synthesis and maintenance of myelin in the brain ( Armada-Moreira et al, 2015 ). Demyelination produces loss of axonal insulation, leading to neuronal dysfunctions ( Armada-Moreira et al, 2015 ; Mot et al, 2018 ). Myelin dysfunction may lead to secondary inflammation and subsequent failure of microglia to clear amyloid-β deposition in AD mice models ( Depp et al, 2023 ).…”

Section: Resultsmentioning

confidence: 99%

Distinctive whole-brain cell types predict tissue damage patterns in thirteen neurodegenerative conditions

Pak,

Adewale,

Bzdok

et al. 2024

eLife

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For over a century, brain research narrative has mainly centered on neuron cells. Accordingly, most whole-brain neurodegenerative studies focus on neuronal dysfunction and their selective vulnerability, while we lack comprehensive analyses of other major cell-types’ contribution. By unifying spatial gene expression, structural MRI, and cell deconvolution, here we describe how the human brain distribution of canonical cell-types extensively predicts tissue damage in eleven neurodegenerative disorders, including early- and late-onset Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, amyotrophic lateral sclerosis, frontotemporal dementia, and tauopathies. We reconstructed comprehensive whole-brain reference maps of cellular abundance for six major cell-types and identified characteristic axes of spatial overlapping with atrophy. Our results support the strong mediating role of non-neuronal cells, primarily microglia and astrocytes, on spatial vulnerability to tissue loss in neurodegeneration, with distinct and shared across-disorders pathomechanisms. These observations provide critical insights into the multicellular pathophysiology underlying spatiotemporal advance in neurodegeneration. Notably, they also emphasize the need to exceed the current neuro-centric view of brain diseases, supporting the imperative for cell-specific therapeutic targets in neurodegeneration. Major cell-types distinctively associate with spatial vulnerability to tissue loss in eleven neurodegenerative disorders.

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“…Oligodendrocytes are responsible for the synthesis and maintenance of myelin in the brain 68 . Demyelination produces loss of axonal insulation leading to neuronal dysfunctions 68, 69 . Myelin dysfunction may lead to secondary inflammation and subsequent failure of microglia to clear amyloid-β deposition in AD mice models 70 .…”

Section: Resultsmentioning

confidence: 99%

“…Oligodendrocytes are responsible for the synthesis and maintenance of myelin in the brain 65 . Demyelination produces loss of axonal insulation leading to neuronal dysfunctions 65, 66 . Oligodendrocytes were shown to be highly genetically associated with PD 67–69 and be particularly vulnerable to the alpha-synuclein accumulation 70, 71 In addition, densities of OPCs showed strong correlations with the atrophy patterns of DLB, EOAD, PS1, and FTLD-TDP43 type C. OPCs regulate neural activity and harbor immune-related and vascular-related functions 72 .…”

Section: Resultsmentioning

confidence: 99%

Distinctive Whole-brain Cell Types Predict Tissue Damage Patterns in Thirteen Neurodegenerative Conditions

Pak

Adewale

Bzdok

et al. 2023

Preprint

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For over a century, brain research narrative has mainly centered on neuron cells. Accordingly, most whole-brain neurodegenerative studies focus on neuronal dysfunction and their selective vulnerability, while we lack comprehensive analyses of other major cell-types' contribution. By unifying spatial gene expression, structural MRI, and cell deconvolution, here we describe how the human brain distribution of canonical cell-types extensively predicts tissue damage in eleven neurodegenerative disorders, including early- and late-onset Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies, amyotrophic lateral sclerosis, frontotemporal dementia, and tauopathies. We reconstructed comprehensive whole-brain reference maps of cellular abundance for six major cell-types and identified characteristic axes of spatial overlapping with atrophy. Our results support the strong mediating role of non-neuronal cells, primarily microglia and astrocytes, on spatial vulnerability to tissue loss in neurodegeneration, with distinct and shared across-disorders pathomechanisms. These observations provide critical insights into the multicellular pathophysiology underlying spatiotemporal advance in neurodegeneration. Notably, they also emphasize the need to exceed the current neuro-centric view of brain diseases, supporting the imperative for cell-specific therapeutic targets in neurodegeneration.

show abstract

Neuroinflammatory modulators of oligodendrogenesis

Cited by 19 publications

References 107 publications

Impact of the Olig Family on Neurodevelopmental Disorders

Impact of the Olig Family on Neurodevelopmental Disorders

Distinctive whole-brain cell types predict tissue damage patterns in thirteen neurodegenerative conditions

Distinctive Whole-brain Cell Types Predict Tissue Damage Patterns in Thirteen Neurodegenerative Conditions

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