Neuron-Glia Interactions in Neurodevelopmental Disorders

Kim, Yoo Sung; Choi, Juwon; Yoon, Bo-Eun

doi:10.3390/cells9102176

Cited by 83 publications

(70 citation statements)

References 183 publications

(218 reference statements)

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“…This is also evident in Alzheimer’s diseases and leads to cognitive decline in animal models, which may translate to ASD models ( Pellegrini et al, 2020 ; Rivers-Auty et al, 2021 ). Increased cytokine expression and the activation of glial cells have been linked to synapse loss and modification of synaptic function ( Kim et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

Stanton

Malijauskaite

McGourty

et al. 2021

Front. Mol. Neurosci.

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Metal dyshomeostasis plays a significant role in various neurological diseases such as Alzheimer’s disease, Parkinson’s disease, Autism Spectrum Disorders (ASD), and many more. Like studies investigating the proteome, transcriptome, epigenome, microbiome, etc., for years, metallomics studies have focused on data from their domain, i.e., trace metal composition, only. Still, few have considered the links between other “omes,” which may together result in an individual’s specific pathologies. In particular, ASD have been reported to have multitudes of possible causal effects. Metallomics data focusing on metal deficiencies and dyshomeostasis can be linked to functions of metalloenzymes, metal transporters, and transcription factors, thus affecting the proteome and transcriptome. Furthermore, recent studies in ASD have emphasized the gut-brain axis, with alterations in the microbiome being linked to changes in the metabolome and inflammatory processes. However, the microbiome and other “omes” are heavily influenced by the metallome. Thus, here, we will summarize the known implications of a changed metallome for other “omes” in the body in the context of “omics” studies in ASD. We will highlight possible connections and propose a model that may explain the so far independently reported pathologies in ASD.

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Section: Discussionmentioning

confidence: 99%

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

Stanton

Malijauskaite

McGourty

et al. 2021

Front. Mol. Neurosci.

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“…A recent report suggests that a mutation in the eukaryotic translation initiation factor 4E (eIF4E) in microglia produces sex-dependent ASD-like behaviors by modifying synaptic development and function in male mice [ 48 ]. Therefore, neuroinflammation and pro-inflammatory cytokines released by microglia can alter gliotransmission, ion-channel expression, brain plasticity, and oxidative stress that may also lead to behavioral dysfunctions [ 49 ]. Interestingly, oxidative stress has also been implicated in the pathophysiological process of ASD by affecting the myelination process [ 50 , 51 ].…”

Section: Pathophysiological Basis Of Asdmentioning

confidence: 99%

Role of Oligodendrocytes and Myelin in the Pathophysiology of Autism Spectrum Disorder

et al. 2020

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Autism Spectrum Disorder (ASD) is an early neurodevelopmental disorder that involves deficits in interpersonal communication, social interaction, and repetitive behaviors. Although ASD pathophysiology is still uncertain, alterations in the abnormal development of the frontal lobe, limbic areas, and putamen generate an imbalance between inhibition and excitation of neuronal activity. Interestingly, recent findings suggest that a disruption in neuronal connectivity is associated with neural alterations in white matter production and myelination in diverse brain regions of patients with ASD. This review is aimed to summarize the most recent evidence that supports the notion that abnormalities in the oligodendrocyte generation and axonal myelination in specific brain regions are involved in the pathophysiology of ASD. Fundamental molecular mediators of these pathological processes are also examined. Determining the role of alterations in oligodendrogenesis and myelination is a fundamental step to understand the pathophysiology of ASD and identify possible therapeutic targets.

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“…The most frequent type of glial cells are oligodendrocytes (45–75%), followed by astrocytes (19–40%) and microglia (around 10%) [ 63 ]. In recent years, a significant amount of data was collected indicating that glial cells are not passive elements of the white matter but are actively involved in synaptic development and plasticity and in the regulation of neuronal activity through tripartite synapses [ 64 , 65 , 66 , 67 ]. Glial cells could significantly impact the information flow in the cortical circuitry by influencing WMIN (see WMIN function below).…”

Section: Total Neuronal Number Density and Spatial Distribution mentioning

confidence: 99%

White Matter Interstitial Neurons in the Adult Human Brain: 3% of Cortical Neurons in Quest for Recognition

Sedmak

Judaš

2021

Cells

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White matter interstitial neurons (WMIN) are a subset of cortical neurons located in the subcortical white matter. Although they were fist described over 150 years ago, they are still largely unexplored and often considered a small, functionally insignificant neuronal population. WMIN are adult remnants of neurons located in the transient fetal subplate zone (SP). Following development, some of the SP neurons undergo apoptosis, and the remaining neurons are incorporated in the adult white matter as WMIN. In the adult human brain, WMIN are quite a large population of neurons comprising at least 3% of all cortical neurons (between 600 and 1100 million neurons). They include many of the morphological neuronal types that can be found in the overlying cerebral cortex. Furthermore, the phenotypic and molecular diversity of WMIN is similar to that of the overlying cortical neurons, expressing many glutamatergic and GABAergic biomarkers. WMIN are often considered a functionally unimportant subset of neurons. However, upon closer inspection of the scientific literature, it has been shown that WMIN are integrated in the cortical circuitry and that they exhibit diverse electrophysiological properties, send and receive axons from the cortex, and have active synaptic contacts. Based on these data, we are able to enumerate some of the potential WMIN roles, such as the control of the cerebral blood flow, sleep regulation, and the control of information flow through the cerebral cortex. Also, there is a number of studies indicating the involvement of WMIN in the pathophysiology of many brain disorders such as epilepsy, schizophrenia, Alzheimer’s disease, etc. All of these data indicate that WMIN are a large population with an important function in the adult brain. Further investigation of WMIN could provide us with novel data crucial for an improved elucidation of the pathophysiology of many brain disorders. In this review, we provide an overview of the current WMIN literature, with an emphasis on studies conducted on the human brain.

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Neuron-Glia Interactions in Neurodevelopmental Disorders

Cited by 83 publications

References 183 publications

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

Role of Oligodendrocytes and Myelin in the Pathophysiology of Autism Spectrum Disorder

White Matter Interstitial Neurons in the Adult Human Brain: 3% of Cortical Neurons in Quest for Recognition

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