Back to search

Article

Dysregulated expression of inflammasome and extracellular matrix genes in <i>C9orf72</i> -ALS/FTD microglia

2025-02-14

Abstract excerpt

Hexanucleotide repeat expansion (HRE) in the non-coding region of the gene C9orf72 is the most prevalent mutation in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The C9orf72 HRE contributes to neuron degeneration in ALS/FTD through both cell- autonomous mechanisms and non-cell autonomous disease processes involving glial cells such as microglia. The molecular mechanisms underlying the c...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
18408d14-b0e4-56a3-9891-e8466cf3439a
DOI
10.1101/2025.02.13.638162
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
Dysregulated expression of inflammasome and extracellular matrix genes in <i>C9orf72</i> -ALS/FTD microgliaDOI 10.1101/2025.02.13.638162
C9orf72-ALS human iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9Semantic proximity
Cellular and molecular phenotypes of <i>C9orf72</i> ALS/FTD patient derived iPSC-microglia mono-culturesSemantic proximity
Moderate intrinsic phenotypic alterations in C9orf72 ALS/FTD iPSC-microglia despite the presence of C9orf72 pathological featuresSemantic proximity
Hexanucleotide repeat expansions in C9orf72 alter microglial responses and prevent a coordinated glial reaction in ALSSemantic proximity
Cell-autonomous immune dysfunction driven by disrupted autophagy in <i>C9orf72</i> -ALS iPSC-derived microglia contributes to neurodegenerationSemantic proximity
Hexanucleotide repeat expansions in C9orf72 alter microglial responses and prevent a coordinated glial reaction in ALSSemantic proximity
Inflammasome mediated neuronal-microglial crosstalk: a therapeutic substrate for the familial <i>C9orf72</i> variant of the frontotemporal dementia/amyotrophic lateral sclerosisSemantic proximity
Cell-autonomous immune dysfunction driven by disrupted autophagy in C9orf72 -ALS iPSC-derived microglia contributes to neurodegenerationSemantic proximity
Inflammasome mediated neuronal-microglial crosstalk: a therapeutic substrate of the familial C9orf72 variant of frontotemporal dementia/amyotrophic lateral sclerosisSemantic proximity
<i>C9orf72</i> repeat expansion-carrying iPSC-microglia from FTD patients show increased phagocytic activity concomitantly with decreased number of autophagosomal-lysosomal vesiclesSemantic proximity
Mechanisms of Immune Activation by c9orf72-Expansions in Amyotrophic Lateral Sclerosis and Frontotemporal DementiaSemantic proximity
Astrocytes and Microglia as Potential Contributors to the Pathogenesis of C9orf72 Repeat Expansion-Associated FTLD and ALSSemantic proximity
Select a neighboring publication to make it the new centre.