Scientists looking at the aging heart found that age-related changes in the arteries, like arterial stiffening, do increase the risk for cardiovascular diseases. The BLSA is changing our understanding of cardiovascular disease. They can determine what distinguishes two seemingly healthy people: one who will go on to develop a certain health problem, the other who will not.īelow are a few examples of relationships between aging and disease the BLSA has helped explain. Scientists can look back at information collected from participants over time, including data from years before a diagnosis, and attempt to identify the changes that precede and perhaps predict clinical symptoms, the so-called precursors of disease. ![]() Answers to "What is normal aging?" led scientists to the question, "What is the relationship between aging and disease ?"īLSA's longitudinal design supports the pursuit of links between aging and disease. But they also found that the two were probably not independent either. They found, as predicted, that "normal" aging is not synonymous with disease. To study normal aging, BLSA scientists originally attempted to cut out all diseases from their research. What Are the Links Between Aging and Disease? Although, for the most part, people age differently, scientists have identified certain common changes experienced by nearly everyone. The study of normal aging has helped change our understanding of what it means to grow older. The Baltimore Longitudinal Study of Aging (BLSA) looks for answers to the question, "What is normal aging?" This may seem like a simple question, but for scientists, it gets to the heart of something quite complex: how to identify the true effects of aging and how to separate factors such as disease, socioeconomic disadvantage, or lack of educational opportunity from the underlying biological or other mechanisms common to human aging. All rights reserved.What is Normal Aging? Lessons from the BLSA We conclude that it will be difficult to understand AD without understanding why it preferably affects older brains, and that we need a model that accounts for age-related changes in AD-vulnerable regions independently of AD-pathology.Īlzheimer's disease (AD) Amyloid Cerebral cortex Default mode network (DMN) Hippocampus Normal aging.Ĭopyright © 2014 Elsevier Ltd. We suggest that regions characterized by a high degree of life-long plasticity are vulnerable to detrimental effects of normal aging, and that this age-vulnerability renders them more susceptible to additional, pathological AD-related changes. ![]() ![]() Thus, rather than necessarily reflecting early signs of disease, these changes may be part of normal aging, and may inform on why the aging brain is so much more susceptible to AD than is the younger brain. This normalcy-pathology homology is critical to understand, since aging itself is the major risk factor for sporadic AD. Importantly, these regions show high levels of amyloid deposition in AD, and are both structurally and functionally vulnerable early in the disease. We argue that prominent cortical reductions are evident in fronto-temporal regions in elderly even with low probability of AD, including regions overlapping the default mode network. We review recent research on changes of the cerebral cortex and the hippocampus in aging and the borders between normal aging and AD. What can be expected in normal aging, and where does normal aging stop and pathological neurodegeneration begin? With the slow progression of age-related dementias such as Alzheimer's disease (AD), it is difficult to distinguish age-related changes from effects of undetected disease.
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