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Potential of activated microglia as a source of dysregulated extracellular microRNAs contributing to neurodegeneration in amyotrophic lateral sclerosis

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posted on 2023-06-07, 06:53 authored by Eleni ChristoforidouEleni Christoforidou, Greig JoilinGreig Joilin, Majid HafezparastMajid Hafezparast
Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron degeneration in adults, and several mechanisms underlying the disease pathology have been proposed. It has been shown that glia communicate with other cells by releasing extracellular vesicles containing proteins and nucleic acids, including microRNAs (miRNAs), which play a role in the post-transcriptional regulation of gene expression. Dysregulation of miRNAs is commonly observed in ALS patients, together with inflammation and an altered microglial phenotype. However, the role of miRNA-containing vesicles in microglia-to-neuron communication in the context of ALS has not been explored in depth. This review summarises the evidence for the presence of inflammation, pro-inflammatory microglia and dysregulated miRNAs in ALS, then explores how microglia may potentially be responsible for this miRNA dysregulation. The possibility of pro-inflammatory ALS microglia releasing miRNAs which may then enter neuronal cells to contribute to degeneration is also explored. Based on the literature reviewed here, microglia are a likely source of dysregulated miRNAs and potential mediators of neurodegenerative processes. Therefore, dysregulated miRNAs may be promising candidates for the development of therapeutic strategies.

Funding

Confirming a set of newly identified non-coding RNA biomarkers for amyotrophic lateral sclerosis and investigating their functional relevance to the disease.; G2429; MNDA-MOTOR NEURONE DISEASE ASSOCIATION; Hafezparast/Apr18/861-791

Identification of non-coding RNA biomarkers from serum and cerebrospinal fluid for use as biomarkers in amyotrophic lateral sclerosis patients; G1722; MNDA-MOTOR NEURONE DISEASE ASSOCIATION; HAFEZPARAST/APR15/836-791

History

Publication status

  • Published

File Version

  • Published version

Journal

Journal of Neuroinflammation

ISSN

1742-2094

Publisher

BioMed Central

Issue

a135

Volume

17

Page range

1-15

Department affiliated with

  • Neuroscience Publications

Research groups affiliated with

  • Sussex Neuroscience Publications

Full text available

  • Yes

Peer reviewed?

  • Yes

Legacy Posted Date

2020-04-29

First Open Access (FOA) Date

2020-04-29

First Compliant Deposit (FCD) Date

2020-04-28

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