John Hardy (1954) received his Bachelor of Science degree from the University of Leeds in 1976 and his PhD from Imperial College London in 1981 for research on dopamine and amino acid neuropharmacology. Following his PhD, Hardy did postdoctoral research at the MRC Neuropathogenesis Unit in Newcastle upon Tyne, England and then further postdoctoral work at the Swedish Brain Bank in Umeå, Sweden where he started to work on Alzheimer’s disease. He became Assistant Professor of Biochemistry at St. Mary’s Hospital, Imperial College London in 1985 and initiated genetic studies of Alzheimer’s disease there. He became Associate Professor in 1989 and then took the Pfeiffer Endowed Chair of Alzheimer’s Research at the University of South Florida, in Tampa in 1992. In 1996, he moved to Mayo Clinic in Jacksonville, Florida, as Consultant and Professor of Neuroscience. He became Chair of Neuroscience in 2000 and moved to National Institute on Aging, Bethesda, Maryland, as Chief of the Laboratory of Neurogenetics in 2001. In 2007, he returned to the UK to take up the Chair of Molecular Biology of Neurological Disease at the Reta Lila Weston Institute of Neurological Studies, University College London.
Honors and Awards
• 1993 Potamkin Prize
• 1995 MetLife Prize
• Lord Brain Memorial medal
• 2014 The Thudichum medal
• 2015 The Robert A. Pritzker Prize for his leadership in Parkinson’s genetics research
• 2016 The Breakthrough Prize
He is a member of EMBO, the Academy of Medical Sciences and the Royal Society.
My research interests are in the genetic analysis of neurodegenerative disease. Historically, my research group has worked on the genetic analysis of Alzheimer’s disease and other dementias. More recently, we have worked on Parkinson’s disease and other movement disorders and, most recently on motor neuron disease. Our early studies were on Mendelian forms of disease and these studies continue, but an increasing focus has been on the genetic analysis of complex traits related to disease. My major findings include leading the group which found APP mutations in early-onset disease: the first cause of this dis-ease, helping lead the groups which found tau mutations in frontotemporal dementia, the group which found the synuclein triplication in early-onset Parkinson’s disease and the group which found c9orf72 mutation in frontotemporal dementia/ALS and most recently leading the group which found trem2 variants as a risk factor for AD.