My husband, John Dobbs, who has died aged 81, brought about transformative shifts in the approach to chronic brain disease. A lateral thinker with a rare breadth and depth of knowledge, his influence on work relating to the drivers and mediators of Parkinson’s disease was gamechanging.
In 2000, he established the Host Microbiome Interaction: Clinical Pharmacology and Therapeutics (HMI:CPT) group at the Institute of Pharmaceutical Science, King’s College London, holding honorary consultantships in gastroenterology at King’s College hospital and the Maudsley hospital. He jointly led, with myself and André Charlett, a statistician and modeller, the “gut-brain axis clinic” research until his last research clinic in December 2025.
Born in Neath to Dylys (nee Bevan) and Selwyn, a tinplate operator, John attended Neath grammar school and was proud of his Welsh heritage. He and I met in 1965 at Manchester University medical school where, in 1967, he graduated (surgical prize). In the same year we married. He held a diploma in child health (1969) and a doctor of medicine degree (vascular pharmacology, 1982). He trained in clinical pharmacology at University College hospital and St George’s hospital medical school, London (1974-81), and he and I jointly set up the Therapeutics in the Elderly programme at the Medical Research Council’s Clinical Research Centre at Northwick Park hospital, north-west London, in 1984. At this point we moved from Stalybridge, Greater Manchester, to Berkhamsted, Hertfordshire.
John was a listener, a quiet strategist and an astute diplomat, drawing inspiration from study participants. His core concepts were that brain inflammation in Parkinson’s disease is mediated by (treatable) entire-body inflammatory processes; major drivers are gut microbes and infectious agents; and the severity of the disease is determined by environmental exposures and their mediators, modified by human genetics. This suggested that causes of the disease should be sought outside the brain, with a view to targeted intervention.
John showed that age-related changes in walking may represent a tendency towards Parkinsonism; demonstrated premature inflammatory ageing in Parkinson’s disease; described the various disease manifestations by deficiencies in substances derived from microbes in stool, and the presence or absence of disease by inflammation in the gut and blood; and showed that the stomach bacterium Helicobacter can be a driver of Parkinson’s disease.
He also monitored the impact on the disease of treating inflammation in the colon; investigated the role of specific infectious agents in the excess mortality from Parkinson’s disease in livestock farmers; and designed the ongoing layered analysis of major microbial groupings as a determinant of disease features and to reveal opportunities for clinical intervention. He leaves the legacy of an escalating research programme, in the John Dobbs HMI:CPT.
John was well travelled – particularly to Kashmir, Ladakh, Bhutan, Tibet and Myanmar – and had a passion for diverse cultures and ancient sites.
He was much loved, kind and perceptive, with a wicked sense of humour. As one colleague put it: “Beneath that hairy exterior lies a heart of gold.”
