Professor Rickie Patani is a physician scientist with over a decade of direct experience working on human induced pluripotent stem cell models of neurodegeneration. Rickie obtained his BSc (in cellular and molecular neuroscience) and MBBS from Imperial College London in 2004.
He gained MRCP in 2007 and a PhD in human stem cell neurobiology from Cambridge University in 2011, funded by a Wellcome Trust clinical research fellowship. While completing his higher clinical training in neurology, he was awarded a Wellcome Trust clinician scientist fellowship and started his research group at UCL Queen Square Institute of Neurology in 2013.
Rickie gained MRCP (neurology) in 2015 and was appointed honorary consultant neurologist at the National Hospital for Neurology and Neurosurgery, Queen Square in 2017. Rickie's lab moved to the Francis Crick Institute in 2017, where they continue to work primarily on human induced pluripotent stem cell models of neurodegeneration, with particular focus on the themes of RNA metabolism and cellular autonomy.
In 2018, Rickie was elected fellow of the Royal College of Physicians and secured an MRC senior clinical fellowship. Rickie was promoted to associate professor in 2018 and subsequently full professor in 2019. The Patani Lab have a diverse portfolio of public engagement activities (see the group's twitter account @PataniLab for more information).
The Patani laboratory is based at the Francis Crick Institute (https://www.crick.ac.uk/research/labs/rickie-patani). His research group study diseases of the nervous system, focusing on motor neuron disease (ALS) and dementia. In ALS, patients lose the ability to move, eat, speak and ultimately breathe. ALS is untreatable because we do not understand the underlying cause(s) of disease.
In order to understand disease mechanisms, we use human stem cells generated from real patients. With over a decade of experience using this technology, the Patani Lab can now transform stem cells from patients into human nerve cells and, separately, their support cells (called glia). This approach allows the research team to determine the sequence of disease-related events within particular cell types. The overarching goal of the Patani Lab is to identify precisely what goes wrong, when this begins and in which cell type. They specifically focus on how the following three factors contribute to nerve cell death in ALS:Messages called RNAs, which are made from our DNA blueprintAstrocytes, which are star-shaped cells that normally support nerve cellsAgeing, which is the biggest risk factor for many neurodegenerative diseases including ALS.
The more that is understood about human neurological diseases using this approach, the more progress will be made to therapeutically target underlying disease mechanisms. The Patani Lab ultimately wish to use this new information to benefit patients with untreatable neurological diseases.
Most recent publications
1. Hagemann C, Tyzack GE, Taha DM, Devine H, Greensmith L, Newcombe J, Patani R*, Serio A*, Luisier R*. Automated and unbiased classification of motor neuron phenotypes with single cell resolution in ALS tissue. Under review.
2. Tyzack GE, Neeves J, Klein P, Crerar H, Ziff O, Taha DM, Luisier R*, Luscombe NM*, Patani R*. An aberrant cytoplasmic intron retention programme is a blueprint for ALS- related RBP mislocalization. In revision in Brain.
3. Harley J, Hagemann C, Serio A*, Patani R*. FUS is lost from nuclei and gained in neurites
of motor neurons in a human stem cell model of VCP-related ALS. Brain. In press 2020.
4. Clarke BE, Taha DM, Ziff OJ, Alam A, Thelin EP, Garcia N, Helmy A, Patani R*. ‘Human stem cell-derived astrocytes exhibit region-specific heterogeneity in their secretory profiles’ Brain. In press 2020.
5. Clarke BE, Patani R*. The microglial component of ALS. Brain. In press 2020.
6. Tyzack GE, Manferrari G, Newcombe J, Luscombe NM, Luisier R, Patani R*. Paraspeckle components NONO and PSPC1 are not mislocalized from motor neuron nuclei in sporadic ALS. Brain. 2020 Aug 1;143(8):e66. doi: 10.1093/brain/awaa205.
7. Patani R*. The FUS about SFPQ in FTLD spectrum disorders. Brain. 2020 Aug 1;143(8):2330-2332. doi: 10.1093/brain/awaa207.
8. Clarke BE, Taha DM, Tyzack GE, Patani R*. Regionally encoded functional heterogeneity of astrocytes in health and disease: A perspective. Glia. 2020 Jun 17. doi: 10.1002/glia.23877.
9. Wang Y, Patani R*. Novel therapeutic targets for amyotrophic lateral sclerosis: ribonucleoproteins and cellular autonomy. Expert Opin Ther Targets. 2020 Aug 30:1-14. doi: 10.1080/14728222.2020.1805734. (Corresponding author).
10. Patani R*. Human stem cell models of disease and the prognosis of academic medicine. Nature Medicine. 2020 Apr;26(4):449. doi: 10.1038/s41591-020-0814-7.
11. Smethurst P, Risse E, Tyzack G, Mitchell JS, Taha DM, Chen Y, Newcombe J, Collinge, Sidle K*, Patani R*. Distinct responses of neurons and astrocytes to TDP-43 proteinopathy in amyotrophic lateral sclerosis. Brain. 2020 Feb 1;143(2):430-440. doi: 10.1093/brain/awz419.
12. Pandya VA, Patani R*. Decoding the relationship between ageing and amyotrophic lateral sclerosis: a cellular perspective. Brain. 2019 Dec 18. pii: awz360. doi: 10.1093/brain/awz360. (Corresponding author).