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Cognition and plasticity throughout the human lifespan
More about this project can be found at www.walhovd.com/neuro Background
Throughout life, our mental capacities and brains are under continuous alteration, regardless of health, sickness or injuries. Some changes are part of positive development, others are debilitating. We know too little about the mechanisms underlying different types of change in brain and cognition, and whether, and how, we ourselves can initiate, enhance or slow them.
This project seeks to uncover markers and mechanisms underlying changes in brain and cognitive behavior throughout the lifespan. The goal is to detail the nature of age changes in brain anatomy, activity and cognitive processes, such as attention and memory. This is done both within healthy individuals from 7 to 90 years of age, as well as in kids with biomedical risk factors and elderly with memory problems (mild cognitive impairment and Alzheimer disease). A related project focuses on how cognitive training can affect cognitive abilities and brain structure and function (LINK). The project integrates a broad specter of methods – structural MRI (brain morphometry, diffusion tensor imaging [DTI]), functional MRI (fMRI), electrophysiology (EEG/ ERP), in addition to standardized and experimental cognitive and neuropsychological tests. In addition, genetic testing, PET scans, and CSF biomarkers are measured in related projects on mild cognitive impairment and Alzheimer disease. Depending on further funding, the project is planned to be longitudinal with several follow-up examinations of the participants. Main research questions
(1) What is the nature of maturational and degenerative age changes?
A tough riddle in the neuroscience of lifespan changes is the seemingly contradictory interpretation of brain changes as maturational when observed in children, and degenerative when observed in aging. For instance, reduction of the volume of cerebral gray matter is rather linear from early to higher age (7 to 90 yrs). In childhood, this is referred to as pruning, contributing to improved cognitive functions. However, at some point in life, the effect of thinning becomes adverse, resulting in reduced cognitive abilities. In the absence of clear breaking points, it is difficult to decide when volumetric reductions no longer reflect positive or maturational, but rather degenerative, brain changes. Thus, we need to turn to detailed neuroanatomical, neurophysiological and cognitive measures to understand which changes in brain characteristics are beneficial or detrimental for cognitive capacity. Further, we believe it is important to regard the changes in the brain and cognitive system as processes that go on continuously across the entire human lifespan. The development of the human CNS does not stop at age 20, and important insights may be gained by tracking specific cognitive functions and their neurobiological foundation from childhood to old age. The present study seeks to meet both these needs. Special focus is given to executive functions and episodic memory, since these are abilities that develop late and undergoes profound age-changes. (2) Which patterns of age changes in neural activity signify successful compensation for neural age changes and which signify inefficient processing?
Individual differences and the concept of reserve in aging point to the possibility of compensating for neural age changes by using different brain areas in old than in young age. The big story in the cognitive neuroscience of aging is the recent discovery of what appears to be functional reorganization and compensation in the aging brain. This allows for a new research tradition, which stands in contrast to a heavier focus on brain underactivations and atrophy in aging. There is, however, a need to better integrate multiple methodological levels, where patterns of activation (in ERP and fMRI attention and memory paradigms) can be systematically related to structural neuroanatomy (brain morphometry and DTI) as well as cognitive behavioral performance both in healthy persons and in patients with age-related memory complaints. In the present study, we seek a fuller picture of which patterns of changed or more widely distributed activation are beneficial to cognitive performance and not. This will hopefully increase our understanding of how the brain works throughout the lifespan, and what changes signify negative or pathological changes. People
Center for the study of Human Cognition, UiO: Kristine B Walhovd, Anders M Fjell, Ylva Østby, Christian K. Tamnes, Lars T Westlye, Inge Amlien Ullevål University Hospital: Øyvind Sundseth Rikshospitalet University Hospital: Atle Bjørnerud, Paulina Due-Tønnesen Harvard Medical School: Bruce Fischl, Doug Greve, David Salat University of California, San Diego: Anders M Dale, Don Hagler Schwartz Center for Computational Neuroscience, San Diego: Scott Makeig, Arnoldo Delorme |
