Amsterdam, The Netherlands and San Antonio, TX, USA, May 25, 2010 – Rudy J. Castellani, Jr., MD, has been chosen as recipient of the 2010 Alzheimer Award presented by the Journal of Alzheimer's Disease in recognition of his outstanding work, "Reexamining Alzheimer's Disease: Evidence for a Protective Role for Amyloid-β Protein Precursor and Amyloid-β," (J Alzheimers Dis 18, 447-452, 2009) by R.J. Castellani et al.
"My co-authors and I are extremely pleased to have been chosen by a distinguished group of our peers as the recipients of this year's Journal of Alzheimer's Disease award for our work on the neuroprotective role of amyloid-β," said Dr. Castellani.
Each year the 310 Associate Editors of the Journal of Alzheimer's Disease vote to select an outstanding article from the previous year's volume to receive this prestigious award, which is made possible by support from IOS Press and Elan Pharmaceuticals. Dr. Castellani will be presented with the bronze Alzheimer Medal with the likeness of Alois Alzheimer and a cash award.
Dr. Castellani's work focuses on a synthesis of pathogenic hypotheses and their relationship with presumed causative lesions (e.g., amyloid-β) and molecules (amyloid-β, amyloid-β protein precursor). His assessment of the state of knowledge is a somewhat cynical and stinging rebuke (necessarily so in his view) of the major school of thought in Alzheimer's disease pathogenesis, which he describes as reductionist and fundamentally backward. He bases this interpretation on the pathology, and the relationship between pathology and disease that clearly indicates plaques, amyloid-β protein precursor processing, and amyloid-β metabolism, as effect, or "host response," rather than cause.
Dr. Castellani goes on to provide evidence for the beneficial and protective effects of amyloid formation across species, and its role as antioxidant, metal chelator, and oligomer detoxifier.
"Perhaps the most important contribution of this article overall," commented Dr. Castellani, "is the previously unemphasized point that the pathology of chronic diseases in general, and Alzheimer's disease in particular, tends to distract from upstream processes, and instead encourages the characterization and continued pursuit of small molecule cascades that are, at best, epiphenomenal. Until there is a fundamental paradigm shift and blunting of the negative impact of an outright misconception, the discovery of upstream processes that lead to lesions will be hampered."
Rudy J. Castellani, Jr., MD, received his medical degree from Wayne State University in 1990, after which he trained in anatomic pathology at Wayne State University's Detroit Medical Center, followed by a neuropathology fellowship at Case Western Reserve University and University Hospitals of Cleveland, under the mentorship of Drs. Pierluigi Gambetti, MD, Mark Cohen, MD, and Uros Roessmann, MD. Since completing his neuropathology training, Dr. Castellani has held faculty positions at Case Western Reserve University, Michigan State University, and, most recently, the University of Maryland School of Medicine, where he is presently Professor of Pathology and Director of Neuropathology. Dr. Castellani is also the current President of the Maryland Society of Pathologists.
Throughout his career Dr. Castellani has studied the pathology and pathogenesis of neurodegenerative disease, most notably human prion diseases and Alzheimer's disease. His work in recent years has focused on the role of Alzheimer's disease pathological lesions, proteins, and cascades comprising those lesions, upstream events including heavy metal toxicity and oxidative stress, and their relevance in clinical disease.