s.purro@prion.ucl.ac.uk • PubMed • |
Research Synopsis
Globally, the numbers of people living with dementia will increase from 50 millions in 2018 to 152 millions in 2050, a 204 % increase. Furthermore, the cost of dementia in the UK is expected to more than double in the next 25 years, from £26 billions to £55 billions in 2040. Currently, there are no treatments for Alzheimer’s disease, one of the more common dementias. Understanding the mechanisms that underlie the pathology of the disease will pave the way for finding new therapies.
We are interested in the process of protein misfolding and aggregation, particularly on amyloid-β and tau. Profiting from all the expertise on prion disease mechanisms in the Institute, we are perfectly posed to study Alzheimer’s disease, a prion-like disease. We use a variety of in vivo mouse models, mouse behavioural tasks, primary cell cultures, highly sensitive immunoassays and protein purification techniques.
At the Alzheimer’s disease group our aim is to better understand how amyloid-β and tau propagate in the brain, which are the characteristics of the seeds and also which are the links between amyloid-β, tau and the prion protein.
Selected Publications
Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone.
Purro SA, Farrow MA, Linehan J, Nazari T, Thomas DX, Chen Z, Mengel D, Saito T, Saido T, Rudge P, Brandner S, Walsh DM, Collinge J. Nature. 2018 Dec;564(7736):415-419.
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy.
Jaunmuktane Z, Mead S, Ellis M, Wadsworth JD, Nicoll AJ, Kenny J, Launchbury F, Linehan J, Richard-Loendt A, Walker AS, Rudge P, Collinge J, Brandner S. Nature. 2015 Sep 10;525(7568):247-50
Reversal of synapse degeneration by restoring Wnt signaling in the adult hippocampus.
Marzo A, Galli S, Lopes D, McLeod F, Podpolny M, Segovia-Roldan M, Ciani L, Purro SA, Cacucci F, Gibb A, Salinas PC. Current Biology 2018, 26:2551-2561
Dysfunction of Wnt signalling and synaptic disassembly in neurodegenerative diseases.
Purro SA, Galli S, Salinas PC. Journal of Molecular Cell Biology 2014, 6:75-80.
mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo
N-W. Hu, A.J. Nicoll, D. Zhang, A.J. Mably, T. O’Malley, S.A. Purro, C. Terry, J. Collinge, D.M. Walsh, M.J. Rowan (2014). Nature Communications, 5:3374.
The secreted Wnt antagonist Dickkopf-1 is required for Amyloid β-mediated synaptic loss.
S.A. Purro, E.M. Dickins, P.C. Salinas (2012). Journal of Neuroscience, 32:3492-8.