Suzanne M. de la Monte, M.D., M.P.H, received her AB from Cornell University and MD from Cornell University Medical College. After graduating from medical school, she worked as a research staff fellow at the NIH for 2 years, and then started a residency in Pathology at the Johns Hopkins Medical Institutions. During her 4th year of residency training, she simultaneously completed a masters degree in public health with concentration in international health and tropical medicine. Dr. de la Monte then went to the Massachusetts General Hospital to obtain 2 years of subspecialty training in neuropathology where she was principally mentored by the late E. P. Richardson, Jr., M.D. Dr. de la Monte's research in Alzheimer's disease began with her Alzheimer's disease research center (ADRC) fellowship. Her initial studies led to the characterization of patterns of cerebral atrophy in several neurodegenerative diseases, including Alzheimer's disease. However, during her fellowship, she established the MGH-ADRC brain bank and set up a system of cataloging the cases with particular attention toward future retrieval of unexpected correlative data. This proved to be critical to the execution of the study for which she was awarded the Alzheimer Medal. Very quickly after beginning her research in AD, she developed a keen interest in the molecular and cellular mechanisms of cell loss and sprouting, and decided to pursue basic science research to understand disease assuming no prior bias, and just approaching the problem in ways that are done for any other system. This approach led to the characterization of pancreatic thread protein expression in brains with Alzheimer's disease, the discovery of a novel family of genes termed neuronal thread proteins, two of which are aberrantly expressed early in the course of AD, and more recently, the role of free radical injury, ischemia, and nitric oxide as factors contributing to the progression of AD neurodegeneration. Her hypothesis is that the protean clinical and pathological features of AD are largely due to co-existent injury caused by any number of variables including cerebrovascular disease, hypoxic/ischemic injury, free radical injury, and ethanol neurotoxicity. After having spent approximately 13 years at the MGH as a clinical and molecular neuropathologist, Dr. de la Monte joined her research team at Brown University School of Medicine and the Rhode Island Hospital and has been there for approximately 1 year.

Importance of published article

Stemming from her observation that the pathology of AD was quite heterogeneous, Dr. de la Monte embarked upon a clinicopathological correlative research project to investigate the potential role of cerebrovascular injury as a contributing factor in the development of clinical AD. With the knowledge gained from earning a MPH degree, combined with the well-organized and computerized MGF-ADRC database, Dr. de la Monte was in an excellent position to direct this important project, largely with the assistance of medical students. The study was designed to re-examine the brains of patients with clinical AD who at post-mortem exam had either classical AD or AD+small infarcts or ischemic lesions (AD+CVA). The question was whether the severity of classical AD lesions was less in individuals with AD+CVA relative to those with AD only. The hypothesis was that since cerebrovascular injury causes tissue damage and cell loss, the additive effects of two moderate disease processes could render patients as demented as with severe AD. That hypothesis proved to be correct. The study published by Dr. de la Monte's group, "Cerebrovascular pathology contributes to the heterogeneity of Alzheimer's disease"; Authors: D. Etiene, J. Kraft, N. Ganju, T. Gomez-Isla, B. Hyman, E.T. Hedley-Whyte, J.R. Wands and S. M. de la Monte, demonstrated that AD+CVA accounted for up to 30% of the clinically diagnosed cases of AD in the MGH-ADRC brain bank. Quantitative assessments of AD pathology revealed that brains with AD+CVA had significantly lower densities of neurofibrillary tangles and neuritic plaques, and significantly reduced densities of Aß-amyloid-immunreactive plaques. A completely unexpected finding was that many of the cerebrovascular lesions were distributed in the same structures that are typically damaged by AD neurodegeneration. This could explain why patients who had AD only could not be clinically distinguished from those who had AD+CVA. The authors concluded that cerebrovascular lesions in regions typically destroyed by AD could contribute to the clinical manifestations of AD. The importance of this work is that it provides evidence that environmental and systemic disease processes can regulate the time of onset and progression of clinical AD, and therefore, AD neurodegeneration may be delayed or prevented in a subset of patients by protecting the brain from this type of injury.

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