Genes, Environment and Alzheimer's Disease discusses the role that activities such as exercise can play in cardiovascular health, while also highlighting the fact that the last 10 years have brought great discoveries in the strong environmental component of brain disorders, neurodegeneration, and cognitive decline. It is now clear that brain insult is an environmental risk factor for AD, while on the other hand, lifestyle components such as exercise and level of education may play a protective role, delaying the onset and/or severity of the disease. Evidence from experiments in rodent models of Alzheimer’s disease contributes major insight into the molecular mechanisms by which the environment plays its role in AD. Additionally, there are diseases related to lifestyle that may lead to AD. This volume reviews new discoveries related to all these factors, serving as a translational tool for clinicians and researchers interested in genetic and environmental risk factors for the disease. Provides the first volume to link genetic and environmental risk factors for Alzheimer’s disease and dementia - Aids researchers and clinicians in understanding the basic mechanisms of Alzheimer’s disease and cognitive decline - Brings the basic science and clinical perspectives together in a single volume, facilitating translational possibilities - Includes a range of molecular to behavioral components assembled into a single volume that creates an excellent resource for basic and clinical neuroscientists As the first volume to thoroughly explore the interplay between genetic and environmental risk factors in the induction of cognitive decline and the development of dementia related diseases such as Alzheimer's disease, this book provides the latest information on the science While it has long been common knowledge that activities such as exercise promote cardiovascular health, it is only during the last 10 years that researchers have discovered a strong environmental component in brain disorders, neurodegeneration and cognitive decline. It is now clear that brain insult is an environmental risk factor for AD, while on the other hand lifestyle components such as exercise and level of education may play a protective role, delaying the onset and/or severity of the disease. Evidence from experiments in rodent models of Alzheimer’s disease contributes major insight into the molecular mechanisms by which the environment plays its role in AD. Additionally there are diseases related to lifestyle that may lead to AD. This volume reviews new discoveries related to all these factors, serving as a translational tool for clinicians and researchers interested in genetic and environmental risk factors for the disease. Dr. Orly Lazarov is an Associate Professor of Neuroscience in the Department of Anatomy and Cell Biology at the University of Illinois at Chicago. She received a Ph.D. in Neuroscience from the Weizmann Institute of Science in Israel. She was awarded the Feinberg Graduate School Fellowship of Distinction for Outstanding Achievement in Studies and Research and the Yashinsky Award of Excellence for Distinguished Ph.D. Students. During her postdoctoral training at the University of Chicago she studied molecular and cellular mechanisms underlying Alzheimer’s disease. In 2006 she accepted a tenure track Faculty position as an Assistant Professor at the University of Illinois at Chicago. Dr. Lazarov was the first to show that experience in a complex (enriched) environment ameliorates Alzheimer’s pathology in a rodent model of the disease. Dr. Lazarov’s research is aimed at understanding brain plasticity, particularly, neurogenesis, in relation to learning and memory and cognitive deterioration in Alzheimer’s disease. Dr. Giuseppina Tesco is an Associate Professor (with tenure) at Tufts University. She received her MD and PhD from the University of Florence, Italy. She also completed her residency in Neurology at the University of Florence. In 1995, she was awarded a prestigious Fogarty Postdoctoral Visiting Fellow award to study the role of potassium channels in the learning and memory process and in Alzheimer’s disease at NINDS. In 1997, she joined the Department of Neurology at Massachusetts General Hospital and Harvard Medical School where she became Assistant Professor. In 2009 Dr. Tesco accepted a Faculty position at Tufts University. Her research focuses on Alzheimer’s Disease (AD). She identified a novel mechanism that regulates BACE1 levels and activity via the trafficking molecules GGA1 and GGA3 (golgi-localized gamma-ear-containing ARF binding protein 1-3). She was the first one to demonstrate that BACE1 is normally degraded in the lysosomes and that caspase-mediated cleavage of GGA3 and GGA1 produces BACE1 elevation in murine models of stroke and TBI. The importance of GGAs' control of BACE1 levels was supported by the observation that, in brain tissue from Alzheimer's patients, reductions in GGA1 and 3 were tightly co