To identify the impact of early life factors on neurocognitive lifespan changes and aging. This is crucial to understand the early mechanisms, and to identify what and how residual variance may be affected by late-life factors. Genetic and experiential factors interact throughout life to shape brain and cognition. Hence, aging starts in the womb, and a number of risk factors for poor cognitive function and decline in aging may be similar to those for aberrant development.
We hypothesize that factors affecting brain and cognition in aging will often do so through a life-long accumulation of impact and not be specific to aging, may often represent quantitative rather than qualitative differences between health and decline, and constitute a range of environmental and genetic factors and their interplay. A unique combination of a longitudinal neurocognitive imaging experimental approach and registry data, national and international cross-disciplinary collaboration, yields novel possibilities to uncover determinants of healthy aging of brain and cognition, preventive and intervention measures to reduce cognitive decline.
The aim is to understand how maturation and aging of the brain-networks for reconstructive memory impacts the ability to form and re-experience one’s past. To address this aim, we will study children (4-10 years), adolescents (11-19 years), young adults (20-30 years) and elderly (60-80 years), 100 participants in each group, with repeated cognitive testing and brain scanning with magnetic resonance imaging (MRI). The children will be examined annually, yielding four examinations, while the other participants will be examined bi-annually, yielding two examinations within the project period.
The primary objective is to address the overarching question of why do some people maintain their cognitive abilities in old age while others decline? The secondary objective is to conduct the most intensive study of brain changes in aging to date. The most novel part is that we directly address the possibly interacting role of neuro-inflammation and deposition of amyloid in brain atrophy and cognitive change. It is speculated that these factors are of critical importance both in normal aging and Alzheimer, but this has not been tested in humans. By measuring amyloid and inflammation in the same participants, and relate this to extremely comprehensive longitudinal measures of brain structure, function and cognition, as well as life-style factors and candidate genes, we hope to really move the boarders of our understanding of brain aging. This will put us in a unique position to increase brain health in normal aging as well as in a range of age-related diseases