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Barbara Tedesco on Muck Rack

Barbara Tedesco

As seen in: Nature, Corriere Del Veneto, Corriere Della Sera
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Articles

VCP modulation ameliorates pathological features in C9orf72 models

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By Veronica Ferrari, Barbara Tedesco, Marta Cozzi, Paola Pramaggiore, Maria Cristina Gagliani, Elena Casarotto, Ali Mohamed, Maria Brodnanova, Carmelo Milioto, Margherita Piccolella, Mariarita Galbiati, Valeria Crippa, Katia Cortese, Paola Rusmini, Riccardo M. Cristofani, Angelo Poletti, Rocio Magdalena, Laura Cornaggia, Marta Chierichetti, Alessandro Provenzani
| Nature Verified
Abstract Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases linked by similar pathological mechanisms, which, in some familial forms, may be associated with the same genetic alterations. Among them, the most common is the C9ORF72 (C9) mutation. The C9 mutation consists in an aberrant expansion of the hexanucleotide repeat (G4C2)n that leads to the production and accumulation of toxic dipeptide repeat proteins (DPRs).
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Impairment of lysosomal quality control in Huntington disease - Cell Death & Disease

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By Paola Rusmini, Marta Valenza, Veronica Ferrari, Barbara Tedesco, Marta Cozzi, Ali Mohamed, Paola Pramaggiore, Maria Brodnanova, Margherita Piccolella, Riccardo M. Cristofani, Mariarita Galbiati, Valeria Crippa
| Nature Verified
Abstract Huntington disease (HD) is a neurodegenerative disease caused by a polyglutamine expansion (polyQ) in the Huntingtin protein (muHTT), which makes it prone to misfolding and aggregation. muHTT aggregates sequester a wide variety of proteins essential for cell homeostasis, including chaperones and transcription factors, and their depletion may contribute to HD pathogenesis.
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Novel HSPB8 mutations in severe early-onset myopathy with involvement of respiratory and cardiac muscles cause proteostasis defects in cell models - European Journal of Human Genetics

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By Barbara Tedesco, Jiayan Tan, Ana Töpf, Vincent Timmerman, Volker Straub, Angelo Poletti, Goknur Selen Kocak, Veronica Marchesi
| Nature Verified
Abstract Heat shock protein family B (small) member 8 (HSPB8) promotes chaperone-assisted selective autophagy (CASA), which assures proteostasis in muscles and neurons. HSPB8 frameshift mutations found in neuromyopathies are translated on the same frame, generating the same C-terminal extension, which causes HSPB8 aggregation and proteostasis defects.
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