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Gemma L. Fryatt

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Articles by Gemma L. Fryatt

RNA sequencing significantly improves HYDIN diagnosis and defines the effects of common deletions in primary ciliary dyskinesia

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By Carolina Jaramillo Oquendo, Janice Coles, Lee Baker, David Bunyan, N. Thomas, James Thompson, Gemma L. Fryatt, Sajida Khan, David Hunt, John Holloway, Jane Lucas, Diana Baralle, Woolf Walker, Claire Jackson
| Nature Verified
Abstract Primary Ciliary Dyskinesia (PCD) is a rare genetic disorder affecting ~1:7500 individuals characterised by recurrent chronic respiratory infections, bronchiectasis, laterality defects, and infertility. While at least 60 PCD-causing genes are reported, approximately 30% of patients remain without a confirmed molecular diagnosis. PCD caused by biallelic HYDIN variants is difficult to diagnose due to a 98% homologous pseudogene (HYDIN2).
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Replicative senescence dictates the emergence of disease-associated microglia and contributes to Aβ pathology

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By Bystrykh L.V, Yanling Hu, Gemma L. Fryatt, Mohammadmersad Ghorbani
| Cell Reports Verified
Highlights • In Alzheimer’s-like pathology, a fraction of microglia undergo replicative senescence • Disease-associated microglia (DAM) display several features of senescence • Prevention of proliferation impairs the development of microglial senescence and DAMs • Prevention of microglial senescence leads to reduced amyloidosis and synaptic damage Summary The sustained proliferation of microglia is a key hallmark of Alzheimer’s disease (AD), accelerating its progression.
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