The Fratta Lab

Motor neuron diseases are incurable and inevitably fatal

 
Our mission is to:
  • Improve basic understanding of these neurodegenerative disorders
  • Develop new therapies to alleviate symptoms and slow disease progression

Our Research

Our ultimate goal is to gain insight into the molecular and cellular mechanisms that underpin motor neuron disorders, and use this understanding to develop new treatments. We utilise a wide range of experimental and computational approaches, ranging from experimental interrogation of iPSC and animal models of disease, to the development of cutting-edge bioinformatic pipelines for hypothesis-free discovery of novel pathological mechanisms.

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We are a diverse, international group of scientists with a wide range of expertise and interests. Our wet- and dry-lab researchers are always looking for ways to work together to tackle the most difficult biological problems.

We have a strongly collaborative approach to our research: in addition to working closely with many other groups at UCL, we have multiple international collaborations with labs across Europe and North America.

Our Team

(Image shows iPSC-derived cortical neurons grown in a two channel microfluidic chamber. Axons have been incubated with cholera toxin (green) to retrogradely label their cell bodies, the RNA binding protein FMRP is labelled in magenta, and the nuclear marker DAPI is in blue.)

We are recruiting!

 

If you would like to work in an exciting research environment and tackle important disease-relevant questions, then we want to hear from you!

Latest news:

  • A decade-long genetic mystery solved

    ​We recently uncovered the molecular mechanism behind one of the most important genetic risk factors for ALS and frontotemporal dementia. By performing in-depth splicing analysis on iPSC-derived neurons with TDP-43 knockdown, we identified a novel cryptic exon which is exacerbated by ALS/FTD-linked genetic variants. The full study is published in Nature.

  • Cryptic splicing - a novel pathogenesis mechanism of HnRNP K mislocalisation

    HnRNP K is an important regulator of splicing, but it is mislocalised in various neurodegenerative disorders. We show that this results in the production of cryptic exons, potentially contributing to disease pathology.

  • FUS-ALS mutants alter FMRP phase separation equilibrium and impair protein translation

    Many neurodegenerative disorders, including ALS, involve the loss of proteostasis. By studying animal and iPSC models of FUS-linked ALS, we found that mutant FUS alters the phase separation properties of FMRP, a key translational regulator, resulting in impaired neuronal protein synthesis.

Our Funders 

Our lab and its members are funded by:

  • The UK Medical Research Council

  • The UK Motor Neurone Disease Association

  • The Rosetrees Trust

  • UCLH NIHR Biomedical Research Centre

  • The Wellcome Trust

  • The UCL Neurogenetic Therapies Programme, funded by the Sigrid Rausing Trust

  • The Crick Institute Translation fund

  • The My Name'5 Doddie Foundation