Brain Changes in Older Adults at Very Low Risk for Alzheimer's Disease
Research Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, 0317 Oslo, Norway, Multimodal Imaging Laboratory and Department of Neurosciences, University of California, San Diego, California 92093, and Department of Radiology, University of California, San Diego, California 92103. The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
(Impact Factor: 6.34).
05/2013; 33(19):8237-42. DOI: 10.1523/JNEUROSCI.5506-12.2013
Alzheimer's disease (AD) has a slow onset, so it is challenging to distinguish brain changes in healthy elderly persons from incipient AD. One-year brain changes with a distinct frontotemporal pattern have been shown in older adults. However, it is not clear to what extent these changes may have been affected by undetected, early AD. To address this, we estimated 1-year atrophy by magnetic resonance imaging (MRI) in 132 healthy elderly persons who had remained free of diagnosed mild cognitive impairment or AD for at least 3 years. We found significant volumetric reductions throughout the brain. The sample was further divided into low-risk groups based on clinical, biomarker, genetic, or cognitive criteria. Although sample sizes varied, significant reductions were observed in all groups, with rates and topographical distribution of atrophy comparable to that of the full sample. Volume reductions were especially pronounced in the default mode network, closely matching the previously described frontotemporal pattern of changes in healthy aging. Atrophy in the hippocampus predicted change in memory, with no additional default mode network contributions. In conclusion, reductions in regional brain volumes can be detected over the course of 1 year even in older adults who are unlikely to be in a presymptomatic stage of AD.
Available from: Juan Li
- "The MTL also shows accelerated volume loss during aging (Raz et al., 2004; Fjell et al., 2013) and is known to be the initial site of histopathological changes in Alzheimer's disease (Greicius et al., 2004). Evidence from a recent longitudinal study suggests that in older adults free of dementia, the MTL shows the greatest volumetric reductions, followed by the prefrontal cortex (Fjell et al., 2013). Further, the structural and functional changes in the MTL have been linked to cognitive decline in older adults (Persson et al., 2012). "
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ABSTRACT: The prefrontal cortex and medial temporal lobe are particularly vulnerable to the effects of aging. The disconnection between them is suggested to be an important cause of cognitive decline in normal aging. Here, using multimodal intervention training, we investigated the functional plasticity in resting-state connectivity of these two regions in older adults. The multimodal intervention, comprised of cognitive training, Tai Chi exercise, and group counseling, was conducted to explore the regional connectivity changes in the default-mode network, as well as changes in prefrontal-based voxel-wise connectivity in the whole brain. Results showed that the intervention selectively affected resting-state functional connectivity between the medial prefrontal cortex and medial temporal lobe. Moreover, the strength of resting-state functional connectivity between these regions correlated with individual cognitive performance. Our results suggest that multimodal intervention could postpone the effects of aging and improve the function of the regions that are most heavily influenced by aging, as well as play an important role in preserving the brain and cognition during old age.
Frontiers in Aging Neuroscience 03/2014; 6:39. DOI:10.3389/fnagi.2014.00039 · 4.00 Impact Factor
Available from: Lucas J Carr
- "Please cite this article in press as: Voss, M. W., et al., Revenge of the " sit " II: Does lifestyle impact neuronal and cognitive health through distinct mechanisms associated with sedentary behavior and physical activity?, Mental Health and Physical Activity (2014), http://dx.doi.org/10.1016/ j.mhpa.2014.01.001 significance as described above, the hippocampus is especially vulnerable to structural decline during normal aging (Fjell et al., 2013). "
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ABSTRACT: It is generally understood that regular moderate to vigorous physical activity (MVPA) promotes good health from head to toe. Evidence also supports the notion that too much sitting can increase all-cause mortality and risk of chronic diseases such as diabetes. Moreover, there is evidence that daily MVPA may not offset negative effects of sedentary behavior on systemic risk factors. We extend the discussion to brain structure and function and argue that while MVPA is recognized as a protective behavior against age-related dementia, sedentary behavior may also be an important contributor to brain health and even counteract the benefits of MVPA due to overlapping or interacting mechanistic pathways. Thus, the goals of this review are (1) to outline evidence linking both PA and sedentary behavior to neurobiological systems that are known to influence behavioral outcomes such as cognitive aging and (2) to propose productive areas of future research.
Mental Health and Physical Activity 03/2014; 7(1). DOI:10.1016/j.mhpa.2014.01.001
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ABSTRACT: We present an overview of recent concepts in mechanisms underlying cognitive decline associated with brain aging and neurodegeneration from the perspective of MRI.
Recent findings challenge the established link between neuroimaging biomarkers of neurodegeneration and age-related or disease-related cognitive decline. Amyloid burden, white matter hyperintensities and local patterns of brain atrophy seem to have differential impact on cognition, particularly on episodic and working memory - the most vulnerable domains in 'normal aging' and Alzheimer's disease. Studies suggesting that imaging biomarkers of neurodegeneration are independent of amyloid-β give rise to new hypothesis regarding the pathological cascade in Alzheimer's disease. Findings in patients with autosomal-dominant Alzheimer's disease confirm the notion of differential temporal trajectory of amyloid deposition and brain atrophy to add another layer of complexity on the basic mechanisms of cognitive aging and neurodegeneration. Finally, the concept of cognitive reserve in 'supernormal aging' is questioned by evidence for the preservation of neurochemical, structural and functional brain integrity in old age rather than recruitment of 'reserves' for maintaining cognitive abilities.
Recent advances in clinical neuroscience, brain imaging and genetics challenge pathophysiological hypothesis of neurodegeneration and cognitive aging dominating the field in the last decade and call for reconsidering the choice of therapeutic window for early intervention.
Current opinion in neurology 10/2013; 26(6). DOI:10.1097/WCO.0000000000000029 · 5.31 Impact Factor
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