Key note speakers Cognitive reserve in Alzheimer’s disease
Yaakov Stern
Yaakov Stern
Yaakov Stern is Professor of Neuropsychology and chief of the Cognitive Neuroscience Division of the Department of Neurology at Columbia University College of Physicians and Surgeons. The cognitive reserve hypothesis posits that individual differences in the flexibility and adaptability of brain networks underlying cognitive function may allow some people to cope better with age- or dementia-related brain changes than others. This is in contrast to the complementary concept of brain reserve, where the variability in the anatomic features of the brain itself provides reserve against pathology. Recent evidence also supports the idea that there are individual differences in preserving a healthy brain, a process that has been called brain maintenance. This talk will review the development, epidemiologic and imaging support for these theoretical concepts, and discuss their implications for healthy cognitive aging. It will also review current attempts to come to consensus on operational definitions for these concepts.
Paul J. Lucassen
Paul J. Lucassen
Paul Lucassen is Professor of Brain Plasticity at the Swammerdam Institute of Life Sciences at the University of Amsterdam. The research in his group focuses on structural and functional plasticity in relation to stress and disease. A strong focus is on adult neurogenesis, which refers to the birth of new neurons in an adult brain, and its regulation by environmental factors, like (early life) stress, nutrition, neuro-inflammation, psychoactive compounds and exercise. Moreover, the group aims to understand the role of brain plasticity in cognition, brain reserve and in brain disorders like depression and dementia. Brain plasticity is studied from a molecular, cellular and behavioral perspective in in vitro and rodent models, and also in a translational approach using human postmortem brain tissue and neuro-imaging of patients. In his talk, he will take a preclinical perspective and discuss possible elements underlying cognitive reserve and show how stress during the early life period can have long lasting consequences on later cognition and also on Alzheimer-related features like amyloid processing, plaque load and cognition in mouse models.
Rik Ossenkoppele
Rik Ossenkoppele
Rik Ossenkoppele is a senior researcher at the Alzheimercentrum Amsterdam and Lund University in Sweden. His expertise lies in neuroimaging (PET and MRI), clinical heterogeneity and cognitive reserve in Alzheimer’s disease (AD). Earlier this year, he received the prestigious European Grand Prix for Research on Alzheimer’s disease. During his talk, he will discuss the development of a neuroimaging method to capture cognitive reserve in individuals with AD. Briefly, the method uses neuropsychological test results to predict a patient’s level of gray matter atrophy on structural MRI scans. The difference between someone’s expected and observed level of atrophy is used to quantify cognitive reserve. Dr. Ossenkoppele will demonstrate the application of this neuroimaging method to predict clinical progression in AD patients. In addition, he will talk about biological and lifestyle factors that contribute to cognitive reserve and briefly go into underlying brain mechanisms of reserve.
Michael Ewers
Michael Ewers
Michael Ewers is Professor of Neuroimaging at the Institute for Stroke and Dementia Research, Ludwig Maximilian University (LMU) Munich. His major research interest focusses on the identification of predictors of disease progression and the examination of functional brain mechanisms that underlie reserve in AD. He has published more than 120 articles. The talk will focus on functional connectivity of hubs as a potential neural substrate of reserve in AD. In particular, the inferior frontal junction (BA 6/44) in the left frontal cortex (LFC) is a major hub of the cognitive control network. The cognitive control network regulates the activity of other functional networks and is critical for cognitively challenging task performance. Prof. dr. Ewers will demonstrate that higher LFC hub connectivity moderates the impact of key AD pathology on cognition, such that at higher levels of hub connectivity, cognitive impairment is attenuated. LFC hub connectivity is closely coupled to network efficiency, which may underlie the enhanced resilience in AD.
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