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Foreword

Khalid Iqbal
Bengt Winblad
Jesus Avila

ACKNOWLEDGEMENTS

This book comprises selected articles of papers presented at the 10th International Conference on Alzheimer Disease and Related Disorders, which was held in Madrid July 15th–20th, 2006. We gratefully acknowledge the chapter contributors and the Scientific Program Committee, which help select all presentations. The Committee included Drs. Jesus Avila (Local Chair), Monique Breteler, Alistair Burns, Antonino Cattaneo, Fréderic Checler, Jean-Francois Dartigues, Richard Frackowiak, Samuel E. Gandy (Ex Officio), Jürgen Götz, Harald Hampel, Khalid Iqbal (Chairman), Takeshi Iwatsubo, Jose Manuel Martinez Lage (Local Co-Chair), Simon Lovestone, Hilkka Soininen, Beka Solomon, Harald Steiner, Fabrizio Tagliavini, William H. Thies (Ex Officio), Cornelia Van Duijn, Fred van Leuven and Bengt Winblad (Co-Chair).

Khalid Iqbal
Bengt Winblad
Jesus Avila

AWARD RECEPIENTS

The Alzheimer’s Association is honored to present the following awards at the 10th International Conference on Alzheimer’s Disease and Related Disorders (ICAD).

Charles Duyckaerts is the distinguished recipient of the Henry Wisniewski Award. The award commemorates the groundbreaking work of Henry M. Wisniewski, M.D., Ph.D., an ICAD founder and a pioneer in experimental neuropathology whose leadership transformed the New York Institute for Basic Research in Development Disabilities into a major center for research.

Charles Duyckaerts was born in 1951 in Liège, Belgium, where he spent most of his school years. In 1969-1970, he completed high school in Palos Verdes, California, after which he began medical school in Paris. The subject of his M.D. thesis (1981) was the neuropathology of hippocampal amnesia. He completed his medical training in neurology, neuroradiology and neuropathology in Rouen Hospital (1976), Salpêtrière Hospital in Paris (1977-1981), and in the Neurology department of Tunis where he served as a civil servant (1978-1979). After completing training as a general pathologist and defending a Ph.D. thesis on Alzheimer’s disease, he became assistant professor in the Neuropathology department of the Salpêtrière Hospital. He was promoted as full Professor in 1991. During his career he has put forth, with colleagues, one of the first prospective studies on Alzheimer’s disease that allowed correlating the topography, time course and clinical consequences of the lesions. Since 2000, he has been studying intracellular beta-amyloid accumulation in APP transgenic animals and, more recently, the involvement of lipid rafts in beta-amyloid secretion.

Colin Masters’ achievements have provided a path to the current development of therapeutic strategies for Alzheimer’s and other neurodegenerative diseases, affecting the quality of life of millions of people worldwide. From the discoveries of the sequence of the beta-amyloid protein in the brain plaques of Alzheimer’s disease, he and his colleagues have gone on to elucidate the pathways leading to the toxicity and accumulation of beta-amyloid in the aging human brain. These pathways have been of great importance in the development of a variety of drug targets, some directed at the secretases that facilitate the release of beta-amyloid protein from nerve cells, and others directed at the toxicity and aggregation of the beta-amyloid protein itself. Thus, from a state 20 years ago when virtually nothing was understood about the molecular basis of Alzheimer’s disease, the studies of Masters with Konrad Beyreuther (University of Heidelberg) are widely acknowledged as having had a major influence on the direction of a now world-wide research effort. The next 10 years are exceptionally promising with the real prospect of developing new drugs aimed at the beta-amyloid amyloidogenic pathway and applying pre-clinical diagnosis using beta-amyloid as the target. Masters’ work has also opened up new insights into other major neurodegenerative diseases (such as Creutzfeldt-Jakob and Parkinson’s diseases) in which aggregated proteins accumulate, work that has thus provided clues to therapeutic interventions for multiple disease states.

Siegfried Hoyer began studying human medicine at the University of Hamburg, Germany, in 1955 and continued on to the University of Saar-area in Homburg/Saar until 1961. From 1961 to 1968 he studied psychiatry, neurology, neurosurgery and internal medicine at the Universities of Homburg/Saar, Munich and Heidelberg. In 1968, Hoyer established and headed a research group to investigate brain blood flow/metabolism in dementia patients and its control mechanisms in experimental animals (dogs and cats) under normal and defined pathophysiological conditions at the Department of Pathochemistry and General Neurochemistry at the University of Heidelberg. In 1980, Hoyer began to study the effect of age on oxidative and released brain metabolism in rats, and the development of rat models related to different disturbances in oxidative energy brain metabolism and behavior (learning and memory capacities) ending up in the model of inhibited control of cerebral glucose/energy metabolism at the neuronal insulin receptor by streptozotocin. Although he retired in 1998, Hoyer has continued his research, and acted as a coordinator of a cooperation between the Universities of Würzburg, Heidelberg (Germany), Zargeb (Croatia) and Sarajevo (Bosnia-Herzegowina) in the frame of the Stability Pact for South Eastern Europa sponsored by the German Government in 2003.

Brian Anderton’s research career has naturally progressed from an initial interest in the cytoskeleton through the pathological involvement of the neuronal cytoskeleton in neurodegenerative diseases and more recently a broader approach to mechanisms of neurodegeneration. Anderton’s team was among the first to apply new mass spectrometric technology to identify phosphorylation sites in cytoskeletal proteins including abnormally phosphorylated tau from Alzheimer brain (Betts et al., 1997; Cleverley et al., 1998; Derkinderen et al., 2005; Hanger et al., 1998). This has included the identification of a novel phosphotyrosine residue in tau, the phosphorylation of tyrosines in tau and other proteins being a rapid response of neurones to the neurotoxic effects of amyloid beta-peptide, the other main pathogenic protein in Alzheimer’s disease, a discovery that may be mechanistically important in the neurodegenerative process (Derkinderen et al., 2005; Williamson et al., 2002).

During the 31 years spent in Florence teaching Pharmacology to the medical students and in the specialization school of Geriatrics and Gerontology, Psychiatry and Clinical Psychology, Dr. Pepeu was appointed chairman of the Department chairman in 1990-96 and vice-Rector for Research and Foreign Relations in 1998-2000. He has also been the chairman of the Center for Laboratory Animals, the president of the Executive Committee of the Medical Library and of the Editorial Board of Florence University Press, a position that he still holds. Among the Honors received, Dr. Pepeu was elected the President of the Italian Society of Pharmacology in 1995-99 of which he is now an honorary member. In addition, he is an honorary fellow of the British Pharmacological Society.

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