Many studies report an association of cognitive and social experiential factors and related traits with dementia risk. Further, many clinical-pathologic studies find a poor correspondence between levels of neuropathology and the presence of dementia and level of cognitive impairment. The poor correspondence suggests that other factors contribute to the maintenance or loss of cognitive function, with factors associated with the maintenance of function referred to as neural or cognitive reserve. This has led investigators to examine the associations of cognitive and social experiential factors with neuropathology as a first step in disentangling the complex associations between these experiential risk factors, neuropathology, and cognitive impairment. Despite the consistent associations of a range of cognitive and social lifestyle factors with cognitive decline and dementia risk, the extant clinical-pathologic data find only a single factor from one cohort, linguistic ability, related to AD pathology. Other factors, including education, harm avoidance, and emotional neglect, are associated with cerebrovascular disease. Overall, the associations are weak. Some factors, such as education, social networks, and purpose in life, modify the relation of neuropathology to cognition. Finally, some factors such as cognitive activity appear to bypass known pathologies altogether suggesting a more direct association with biologic indices that promote person-specific differences in reserve and resilience. Future work will first need to replicate findings across more studies to ensure the veracity of the existing data. Second, effort is needed to identify the molecular substrates of neural reserve as potential mediators of the association of lifestyle factors with cognition.
"We specifically examined the observed changes in communication and recreational functioning limitations, given background literature on neuroprotective effects of engagement in social, physical and intellectual activities (e.g. Bennett et al., 2014). Limitation in ability to engage in such activities is therefore a serious concern. "
[Show description][Hide description] DESCRIPTION: Supported living and retirement villages are becoming a significant option for older adults with independence concerns or for forward planning in older age, but evidence as to their psychological benefits for residents is sparse. This study examined the hypothesis that increased accessibility of an active and engaged lifestyle, with increased support, will impact on psychological and independence measures in older adults moving into “extra care” independent living environments.
", 2010 ; Landau et al . , 2012 ) . In contrast to previous evidence arguing for compensatory processes in AD patients , evidence for a direct relationship between lifestyle factors and AD neuropathological processes have mainly been reported in cognitively normal older adults . Although only poorly supported by autopsy studies ( for a review , see Bennett et al . , 2014 ) , this idea has received further support from animal and intervention studies . Thus , researches in animals showed , for example , increased clearance of Aβ and reduced Aβ levels in mice exposed to enriching environments ( Lazarov et al . , 2005 ; Costa et al . , 2007 ) ."
[Show abstract][Hide abstract] ABSTRACT: The large majority of neuroimaging studies in Alzheimer's disease (AD) patients have supported the idea that lifestyle factors may protect against the clinical manifestations of AD rather than influence AD neuropathological processes (the cognitive reserve hypothesis). This evidence argues in favor of the hypothesis that lifestyle factors act as moderators between AD pathology and cognition, i.e., through indirect compensatory mechanisms. In this review, we identify emerging evidence in cognitively normal older adults that relate lifestyle factors to established AD neuroimaging biomarkers. While some of these investigations are in agreement with the compensatory view of cognitive reserve, other studies have revealed new clues on the neural mechanisms underlying beneficial effects of lifestyle factors on the brain. Specifically, they provide novel evidence suggesting direct effects of lifestyle factors on AD neuropathological processes. We propose a tentative theoretical model where lifestyle factors may act via direct neuroprotective and/or indirect compensatory mechanisms. Importantly, we suggest that neuroprotective mechanisms may have a major role during early stages and compensatory mechanisms in later stages of the disease. In the absence of an effective treatment for AD and considering the potential of lifestyle factors in AD prevention, understanding the neural mechanisms underlying lifestyle effects on the brain seems crucial. We hope to provide an integrative view that may help to better understand the complex effects of lifestyle factors on AD neuropathological processes, starting from the preclinical stage.
"This was an intentional component of our sample of subjects, which was designed to eliminate confounded effects of age and level of education on performance and brain activation. However, given that years of formal education is among the first cognitive or social lifestyle factors that may create cognitive reserve in late adulthood (Bennett et al., 2014), the probable high supply of neural resources of older adults in our sample may limit the generalizability of these results to the whole aging population. Consequently, further studies using a more various population are needed to confirm our findings and to generalize the results to the entire aging population. "
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