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Inflammasome mediated neuronal-microglial crosstalk: a therapeutic substrate for the familial <i>C9orf72</i> variant of the frontotemporal dementia/amyotrophic lateral sclerosis

2022-01-28

Abstract excerpt

Intronic G 4 C 2 hexanucleotide repeat expansions (HRE) of C9orf72 are the most common cause of familial variants of frontotemporal dementia/amyotrophic lateral sclerosis (FTD/ALS). G 4 C 2 HREs in C9orf72 undergo non-canonical repeat-associated translation, producing dipeptide repeat (DPR) proteins, with various deleterious impacts on cellular homeostasis. While five different DPRs are produced, poly(glycin...

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Literature Corpus work
29a51660-75f0-5a81-adbb-e76af8104345
DOI
10.1101/2022.01.27.478078
Open publication

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Inflammasome mediated neuronal-microglial crosstalk: a therapeutic substrate for the familial <i>C9orf72</i> variant of the frontotemporal dementia/amyotrophic lateral sclerosisDOI 10.1101/2022.01.27.478078
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