prof. dr. Ezio Giacobini, dr. med.
Geneva University Hospitals, department of international medicine, rehabilitation and geriatrics.
UNIVERSITY OF GENEVA, GENEVA , SWITZERLAND
M. D. 1953 (Turin, Italy); certified M. D. 1960 (Italy); certified M. D. 2003 (Switzerland);
PhD. 1959 (Cellular Neuropharmacology (Karolinska Institute, Stockholm, Sweden); Honorary M.D. 2000 (University of Kuopio, Finland); Staff physician and clinical investigator in Psychiatry (1953-1971).Since July 1995 is a professor associated with the Dept. of Internal Medicine, Rehabilitation and Geriatrics, University of Geneva Medical School in Geneva, Switzerland and an Adjunct Professor of Pharmacology, Psychiatry and Neurology at the Southern Illinois School of Medicine, Springfield, IL, USA. From Janury 1982 until June 1995 he was a Professor and Chairman of the Dept. of Pharmacology and Scientific Director of the NIA (NIH) Alzheimer Center at Southern Illinois University School of Medicine, Springfield IL, USA. Before January 1982, he was Professor of Biobehavioral Science at the University of Connecticut, Storrs, CT and head of the laboratory of neuro-psychopharmacology.His major research interest is in the pre-clinical and clinical development of drug therapy for Alzheimer’s disease. Together with R. Becker he has developed, preclinically and clinically, two new cholinesterase inhibitors (metrifonate and pentastigmine ) and participated in the clinical development of E20-20 ( donepezil) , rivastigmine and phenserine. His present research is in the area of a-beta oligomers , their origin, localization and relation to Alzheimer pathology. He organized 20 International Meetings on Advances in Alzheimer Therapy (AAT) .The next one will be in Torino in march 2018.
He received the LIFE TIME ACHIEVEMENT AWARD IN ALZHEIMER’S DESEASE RESEARCH from the Alzheimer Association (USA) at the 8th Int. Conference on Alzheimer’s Disease in Stockholm, July 2002.
Farmakološko zdravljenje Alzheimerjeve bolezni v letu 2027
Given the average duration of clinical trials ( Phase I to Phase III) of 9-10 years at an average cost of 5-7 billion $ ( SCOTT,2013) is not too early to consider today the possibility of a pharmacological treatment for 2027.The cause of the disease still escape us and the major investment made so far in developing anti-abeta interventions have not given clinically relevant results, therefore, we are limited to design therapies based on results derived from molecular imaging (PET).
This approach moved from traditional neruropathological criteria into a phenotype-targeted therapy which may or may not be casually related.
The multistate transition model (C.Jack et al.2016, 2017) utilizes transition rates to estimate the frequency of each state based on long- term follow up of cognitively unimpaired individuals from 50 to 90 years.
The most recent one (C.Jack, 2017) combines three different measurement in vivo: a-beta aggregation, tauopathy and neurodegeneration, evaluated with repeated PET tested in the same subject.
Subtyping based on these criteria makes it possible to design a differentiated therapy targeting specific pathologies in the individual patient.
This approach emphasizes the critical need to continue our research in order to find the cause of the disease the best therapy within the next ten years.