Chronic oligodendrocyte injury in central nervous system pathologies

Molina-González, Irene; Miron, Véronique E.; Antel, Jack P.

doi:10.1038/s42003-022-04248-1

Cited by 13 publications

(9 citation statements)

References 198 publications

(179 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In mature myelinated CNS cultures, ZIKV infection damages myelinated fibers (Cumberworth et al, 2017; Schultz, Barrie, et al, 2021). Of note, oligodendrocyte cell death might lead to secondary autoimmune demyelination (Molina‐Gonzalez et al, 2022), and these observations are critical for understanding the effects of ZIKV in the mature CNS.…”

Section: Glial Cells As Targets Of Zikv Infectionmentioning

confidence: 99%

The role of glial cells in Zika virus‐induced neurodegeneration

Quincozes‐Santos

Bobermin

Costa

et al. 2023

Glia

View full text Add to dashboard Cite

Zika virus (ZIKV) is a strongly neurotropic flavivirus whose infection has been associated with microcephaly in neonates. However, clinical and experimental evidence indicate that ZIKV also affects the adult nervous system. In this regard, in vitro and in vivo studies have shown the ability of ZIKV to infect glial cells. In the central nervous system (CNS), glial cells are represented by astrocytes, microglia, and oligodendrocytes. In contrast, the peripheral nervous system (PNS) constitutes a highly heterogeneous group of cells (Schwann cells, satellite glial cells, and enteric glial cells) spread through the body. These cells are critical in both physiological and pathological conditions; as such, ZIKV-induced glial dysfunctions can be associated with the development and progression of neurological complications, including those related to the adult and aging brain. This review will address the effects of ZIKV infection on CNS and PNS glial cells, focusing on cellular and molecular mechanisms, including changes in the inflammatory response, oxidative stress, mitochondrial dysfunction, Ca 2+ and glutamate homeostasis, neural metabolism, and neuron-glia communication. Of note, preventive and therapeutic strategies that focus on glial cells may emerge to delay and/or prevent the development of ZIKV-induced neurodegeneration and its consequences.André Quincozes-Santos and Larissa Daniele Bobermin contributed equally to this work.

show abstract

Section: Glial Cells As Targets Of Zikv Infectionmentioning

confidence: 99%

The role of glial cells in Zika virus‐induced neurodegeneration

Quincozes‐Santos

Bobermin

Costa

et al. 2023

Glia

View full text Add to dashboard Cite

show abstract

“…It is known that metabolic stress, glutamate and inflammatory mediators play a central role here ( Philips et al, 2013 ; Masaki et al, 2020 ; Molina-Gonzalez et al, 2022 ; Jahan-Abad et al, 2023 ) and since some evidence suggests that axonal damage may be present before demyelination ( Dutta and Trapp, 2007 ; Simkins et al, 2021 ), neurons may be affected first but this is yet to be probed.…”

Section: Discussionmentioning

confidence: 99%

“…Even though RBPs dysfunction has been found in OLs in both pathologies ( Lu et al, 2016 ; Masaki et al, 2020 ; Jahan-Abad et al, 2023 ), cells are affected very differently; in MS, active demyelinating lesions ( Figure 2J ) suggest the preservation of OLs because numbers are comparable to the ones in normal-appearing white matter, on the other hand, chronic lesions show significant cell loss ( Prineas and Parratt, 2012 ; Heß et al, 2020 ). In acute lesions, OLs retract their processes from axons but their somas remain intact, suggesting a stage of sub-lethal injury ( Molina-Gonzalez et al, 2022 ).…”

Section: Different Features In Pathophysiologymentioning

confidence: 99%

RNA-binding proteins as a common ground for neurodegeneration and inflammation in amyotrophic lateral sclerosis and multiple sclerosis

Acosta-Galeana

Hernández-Martínez

Reyes-Cruz

et al. 2023

Front. Mol. Neurosci.

View full text Add to dashboard Cite

The neurodegenerative and inflammatory illnesses of amyotrophic lateral sclerosis and multiple sclerosis were once thought to be completely distinct entities that did not share any remarkable features, but new research is beginning to reveal more information about their similarities and differences. Here, we review some of the pathophysiological features of both diseases and their experimental models: RNA-binding proteins, energy balance, protein transportation, and protein degradation at the molecular level. We make a thorough analysis on TDP-43 and hnRNP A1 dysfunction, as a possible common ground in both pathologies, establishing a potential link between neurodegeneration and pathological immunity. Furthermore, we highlight the putative variations that diverge from a common ground in an atemporal course that proposes three phases for all relevant molecular events.

show abstract

“… 4 , 5 In vivo and in vitro studies in animals indicate that myelination capacity decreases with age, reflecting intrinsic properties of the oligodendroglia (OL) lineage cells (differentiation and migration) 6 and the influence of positive and negative signals received from the local environment. 7 …”

Section: Introductionmentioning

confidence: 99%

Age-dependent effects of metformin on human oligodendrocyte lineage cell ensheathment capacity

Mohammadnia,

Cui,

Weng

et al. 2024

Brain Communications

View full text Add to dashboard Cite

Metformin restores myelination potential of aged rat A2B5+ oligodendrocyte progenitor cells and may enhance recovery in children with post-radiation brain injury. Human late progenitor cells (O4 + A2B5+) have superior capacity to ensheath nanofibers compared to mature oligodendrocytes, with cells from pediatric sources exceeding adults. In this study we assessed effects of metformin on ensheathment capacity of human adult and pediatric progenitors and mature oligodendrocytes and relate differences to transcriptional changes. A2B5+ progenitors and mature cells, derived from surgical tissues by immune-magnetic separation, were assessed for ensheathment capacity in nanofiber plates over 2 weeks. Metformin (10 µM every other day) was added to selected cultures. RNA was extracted from treated and control cultures after 2 days. For all ages, ensheathment by progenitors exceeded mature oligodendrocytes. Metformin enhanced ensheathment by adult donor cells but reduced ensheathment by pediatric cells. Metformin marginally increased cell death in pediatric progenitors. Metformin induced changes in gene expression distinct for each cell type. Adult progenitors showed up-regulation of pathways involved in process outgrowth and promoting lipid biosynthesis. Pediatric progenitors showed a relatively greater proportion of down- versus up-regulated pathways, these involved cell morphology, development, and synaptic transmission. Metformin induced AMPK activation in all cell types; AMPK inhibitor BML-275 reduced functional metformin effects only with adult cells. Our results indicate age and differentiation stage related differences of human oligodendroglia lineage cells in response to metformin. Clinical trials for demyelinating conditions will indicate how these differences translate in vivo.

show abstract

Chronic oligodendrocyte injury in central nervous system pathologies

Cited by 13 publications

References 198 publications

The role of glial cells in Zika virus‐induced neurodegeneration

The role of glial cells in Zika virus‐induced neurodegeneration

RNA-binding proteins as a common ground for neurodegeneration and inflammation in amyotrophic lateral sclerosis and multiple sclerosis

Age-dependent effects of metformin on human oligodendrocyte lineage cell ensheathment capacity

Contact Info

Product

Resources

About