UK DRI scientists pay tribute to Professor Peter Davies

Our community is deeply saddened to hear that Professor Peter Davies has passed away after a long battle with cancer. 

Peter spent more than forty years searching for a cure for Alzheimer’s disease and his early work was seminal in the development of the cholinesterase inhibitor class of drugs for the condition. He was best known – and internationally recognised – for his studies of pathology relating to the protein tau, and for progress he made towards developing a way of using monoclonal antibodies to tau as a potential treatment.

UK DRI colleagues have been sharing tributes and memories of working with Peter.

Prof Bart De Strooper, UK DRI Director, said: 

“With Peter, the field loses one of its pioneers and a charismatic and inspiring leader. Personally, it feels like losing a friend. His work was fundamental to the acetylcholine hypothesis and the first drugs for Alzheimer’s disease. In later years he focused on tau pathology in Alzheimer’s disease, his monoclonal antibodies being the gold standard to detect abnormal conformations of tau. We had many friendly and interesting discussions about presenilin. Despite me being in the amyloid wing of the debates in the field, he liked my work and his comments were, for me – a young scientist at the time – very encouraging and helpful. Peter was a great scientist, a wise man and a good friend. We will miss him dearly.”

Prof John Hardy, Group Leader at UK DRI at UCL, commented: 

“I suspect I have known Peter Davies longer than anyone else in Alzheimer’s research. I was a first year undergraduate at Leeds University in 1974 and doing a lab practical on phage infection of bacteria. Peter was the PhD student doing the practical demonstration. He was, himself, doing a PhD project on lipoprotein lipase in fat cells. I will remember him sat on the window sill of the laboratory, smoking a cigarette, and certainly showing little interest in helpless male undergraduates like me!

Biochemistry at Leeds was fun. The department in Leeds had two halves: an old, large Victorian terraced house (9 Hyde Terrace) and then, about 100 yards away on the new campus, modern (1960s!) concrete tower block labs. Halfway between them was the Faversham pub in whose beer gardens most unofficial tutorials were held. Peter was often there and was always the centre of a laughing crowd of students and lecturers.  

His 1976 paper, Favies and Maloney (PMID: 63862), together with contemporaneous papers from Bowen and the Perrys, started the road to cholinergic therapies – quite an achievement! And then he moved to the US where he spent the rest of his career. When I moved to the US in 1992, I met him and immediately remembered him from my Leeds days. And he was still fun. He could always be guaranteed to take a contrarian view just to provoke a discussion, and he loved an argument – which were never personal. I always knew that if Peter was at a meeting, there would be some fun. 

We ended up on opposite sides of the “baptist” vs ”tauist” debate. I would remind him that he said (in 1986) we should believe that genetics will tell us how the disease starts (PMID: 2951608), and then really tried to ignore the genetics findings on amyloid precursor protein.

And he would say to me, ‘how may failed drug trials will it take before you change your views?’

I will miss him. Meetings will be tamer. The bars afterwards will be quieter (though he was teetotal in later life). And the science will be just a little less fun.”

Prof Karen Duff, Centre Director, UK DRI at UCL, commented: 

“I got to know Peter in the mid 90s when I was looking for an expert to lend credibility to my newest mouse, the htau mouse. I had grown up believing that amyloid beta was the most important part of Alzheimer’s but had been struck by how little was known of the ‘other’ Alzheimer’s pathology. I was determined to make a mouse model of Alzheimer’s tauopathy, using a large PAC genomic construct to make all six isoforms of wildtype tau (it was years before the frontotemporal dementia mutations were identified), and I spent over a year doing the complex molecular biology required. Having made the mouse I was terrified of publishing it without the seal of approval of a card-carrying tauologist as several of the amyloid mice had been retracted from top journals due to either fraudulent or artifactual pathology claims. 

Peter came to my rescue. He was patient and tolerant in teaching me the ways of tau, especially how to avoid misinterpreting artifacts. I spent many hours in his office at the Albert Einstein College of Medicine in New York, which always started with photos of his daughter and grandchildren and ended with us having to move to avoid the inevitable water leak dripping from the ceiling that he seemed content to live with for years. He always sent me off with a pocket full of his antibodies which truly revolutionalised the field.

My fondest memories are of our discussions about how amyloid beta might fit into the equation, which, no matter how it was presented, he dismissed outright with a charming smile. 

During my early days as a tauologist, the ‘tau session’ was always the last session of any conference and the smattering of tau mouse models were always presented at the end of the end. There were usually only (the same) five people in the audience but Peter was always there to help, nodding and adding supportive comments. Of course, things are very different now, in large part due to Peter. Peter was an insightful, skilled and rigorous researcher, an enabling and encouraging mentor, and a vocal challenger of the status quo. He will be much missed.”

Article published: 2 September 2020