Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–6 of 6 results
Advanced filters: Author: "Rickie Patani" Clear advanced filters
  • Intron retention (IR) can increase protein diversity and function, and yet unregulated IR may be detrimental to cellular health. This study shows that aberrant IR occurs in ALS and finds nuclear loss of an RNA-binding protein called SFPQ as a new molecular hallmark in this devastating condition.

    • Raphaelle Luisier
    • Giulia E. Tyzack
    • Rickie Patani
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-15
  • Rickie Patani is Professor of Human Stem Cells and Regenerative Neurology at University College London and The Francis Crick Institute, and is a consultant neurologist at The National Hospital for Neurology, Queen Square, London. He has over a decade of experience using human stem cell models of neurodegeneration, and his research contributions have been recognized by the International Paulo Gontijo Award in Medicine and the International 3Rs prize.

    • Rickie Patani
    Comments & Opinion
    Nature Medicine
    Volume: 26, P: 449
  • A common genetic cause of Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is expansion of the intronic hexanucleotide repeat (GGGGCC)n in C9orf72. Here the authors reveal that the RNA (GGGGCC)n expansion repeat associated with ALS/FTD can generate condensates in the absence of proteins, highlighting the potential relevance of targeting RNA-structures to treat neurodegenerative diseases.

    • Federica Raguseo
    • Yiran Wang
    • Marco Di Antonio
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-15
  • Astrocytes can have protective or detrimental effects on neurons during injury, but the molecular mechanisms that determine these different states are unresolved. Here the authors identify a pathway via neuronal EphB1 that induces neuroprotective signalling in astrocytes through ephrin-B1 mediated STAT3 activation, which is impaired in models of amyotrophic lateral sclerosis.

    • Giulia E. Tyzack
    • Claire E. Hall
    • András Lakatos
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-17