What Is Cognitive Reserve? Theory and Research Application of the Reserve Concept

The idea of reserve against brain damage stems from the repeated observation that there does not appear to be a direct relationship between the degree of brain pathology or brain damage and the clinical manifestation of that damage. This paper attempts to develop a coherent theoretical account of reserve. One convenient subdivision of reserve models revolves around whether they envision reserve as a passive process, such as in brain reserve or threshold, or see the brain as actively attempting to cope with or compensate for pathology, as in cognitive reserve. Cognitive reserve may be based on more efficient utilization of brain networks or of enhanced ability to recruit alternate brain networks as needed. A distinction is suggested between reserve, the ability to optimize or maximize normal performance, and compensation, an attempt to maximize performance in the face of brain damage by using brain structures. or networks not engaged when the brain is not damaged. Epidemiologic and imaging data that help to develop and support the concept of reserve are presented

An Approach to Studying the Neural Correlates of Reserve

The goal of this paper is to review my current understanding of the concepts of cognitive reserve (CR), brain reserve and brain maintenance, and to describe our group's approach to using imaging to study their neural basis. I present a working model for utilizing data regarding brain integrity, clinical status, cognitive activation and CR proxies to develop analyses that can explore the neural basis of cognitive reserve and brain maintenance. The basic model assumes that the effect of brain changes on cognition is mediated by task-related activation. We treat CR as a moderator to understand how task-related activation might vary as a function of CR, or how CR might operate independently of these differences in task-related activation. My hope is that this presentation will spark discussion across groups that study these concepts, allowing us to come to some common agreement on definitions, methodology and approaches

Cognitive Reserve

The concept of reserve has been proposed to account for the disjunction between the degree of brain damage and its clinical outcome. This paper attempts to produce a coherent theoretical account the reserve in general and of cognitive reserve in particular. It reviews epidemiologic data supporting the concept of cognitive reserve, with a particular focus of its implications for aging and dementia. It then focuses on methodologic issues that are important when attempting to elucidate the neural underpinnings of cognitive reserve using imaging studies, and reviews some of our group's work in order to demonstrate these issues

Cognitive Reserve and Alzheimer Disease

Epidemiologic evidence suggests that individuals with higher IQ, education, occupational attainment, or participation in leisure activities have a reduced risk of developing Alzheimer disease (AD). The concept of cognitive reserve (CR) posits that individual differences in how tasks are processed provide differential reserve against brain pathology or age-related changes. This may take 2 forms. In neural reserve, preexisting brain networks that are more efficient or have greater capacity may be less susceptible to disruption. In neural compensation, alternate networks may compensate for pathology’s disruption of preexisting networks. Imaging studies have begun to identify the neural substrate of CR. Because CR may modulate the clinical expression of AD pathology, it is an important consideration in studies of ‘‘preclinical’’ AD and treatment studies. There is also the possibility that directly enhancing CR may help forestall the diagnosis of AD

Cognitive Reserve in Ageing and Alzheimer's Disease

The concept of cognitive reserve provides an explanation for differences between individuals in susceptibility to age-related brain changes or pathology related to Alzheimer's disease, whereby some people can tolerate more of these changes than others and maintain function. Epidemiological studies suggest that lifelong experiences, including educational and occupational attainment, and leisure activities in later life, can increase this reserve. For example, the risk of developing Alzheimer's disease is reduced in individuals with higher educational or occupational attainment. Reserve can conveniently be divided into two types: brain reserve, which refers to differences in the brain structure that may increase tolerance to pathology, and cognitive reserve, which refers to differences between individuals in how tasks are performed that might enable some people to be more resilient to brain changes than others. Greater understanding of the concept of cognitive reserve could lead to interventions to slow cognitive ageing or reduce the risk of dementia

Inter- and Intraindividual Variability in Recognition Memory: Effects of Aging and Estrogen Use

Traditionally, studies of cognitive aging have focused on comparing the average performance of younger and older adults, whereas variability around the mean has been attributed to task-irrelevant noise. The present study examined the hypothesis that variability in memory performance increases with age and that estrogen helps temper age-related increases in variability. Postmenopausal estrogen users, estrogen and progestin (est + prog) users, and nonusers, as well as younger women, completed 16 blocks of an item-source memory task. Older women showed greater variability than younger women on measures of dispersion and consistency. Estrogen users, but not est + prog users, performed more consistently than nonusers. Overall, age-related increases in variability differed with the type of variability measured, and estrogen use, but not est + prog use, appeared to reduce age-related increases in at least 1 form of variability

Cognitive Reserve: Implications for Diagnosis and Prevention of Alzheimer's Disease

Epidemiologic evidence suggests that higher occupational attainment and education, as well as increased participation in intellectual, social, and physical aspects of daily life, are associated with slower cognitive decline in healthy elderly and may reduce the risk of incident Alzheimer's disease (AD). There is also evidence from structural and functional imaging studies that patients with such life experiences can tolerate more AD pathology before showing signs of clinical dementia. It has been hypothesized that such aspects of life experience may result in functionally more efficient cognitive networks and, therefore, provide a cognitive reserve that delays the onset of clinical manifestations of dementia. In this article, we review some of the relevant literature of the noted associations between markers of cognitive reserve and AD and discuss the possible mechanisms that may explain these associations

Imaging Studies and APOE Genotype in Persons at Risk for Alzheimer's Disease

Many studies have investigated APOE-related differences in cerebral structure, blood flow, metabolism, and activation in an attempt to detect early brain changes in subjects at risk for Alzheimer's disease (AD). Structural magnetic resonance imaging studies have produced conflicting results, with some failing to detect APOE-related differences and others suggesting that epsilon4 carriers have more pronounced atrophy, particularly at medial temporal structures. All functional imaging studies done during rest in middle-aged and elderly subjects have found decreased cerebral metabolism for epsilon4 carriers (mostly in areas that usually are affected by AD), and some have reported faster cerebral metabolic reductions over time. Areas with decreased resting cerebral perfusion and metabolism, in addition to other areas with increased perfusion, have been reported in young epsilon4 carriers. Imaging studies done during the performance of various cognitive tasks in middle-aged and elderly subjects, and a single study in young subjects, have produced mixed results with regionally nonspecific increased, decreased, or nondifferential APOE-related activations depending on the cognitive task used. APOE-related findings in imaging studies of nondemented subjects may be the result of incipient AD pathologic changes or of genetic heterogeneity in brain structure and function

Exploring the Neural Basis of Cognitive Reserve in Aging

The concept of reserve arose from the mismatch between the extent of brain changes or pathology and the clinical manifestations of these brain changes. The cognitive reserve hypothesis posits that individual differences in the flexibility and adaptability of brain networks underlying cognitive function may allow some people to cope better with brain changes than others. Although there is ample epidemiologic evidence for cognitive reserve, the neural substrate of reserve is still a topic of ongoing research. Here we review some representative studies from our group that exemplify possibilities for the neural substrate of reserve including neural reserve, neural compensation, and generalized cognitive reserve networks. We also present a schematic overview of our ongoing research in this area. This article is part of a Special Issue entitled: Imaging Brain Aging and Neurodegenerative disease

Efficiency, Capacity, Compensation, Maintenance, Plasticity: Emerging Concepts in Cognitive Reserve

Cognitive reserve (CR) is a concept meant to account for the frequent discrepancy between an individual's measured level of brain pathology and her expected cognitive performance. It is particularly important within the context of aging and dementia, but has wider applicability to all forms of brain damage. As such, it has intimate links to related compensatory and neuroprotective concepts, as well as to the related notion of brain reserve. In this article, we introduce the concept of cognitive reserve and explicate its potential cognitive and neural implementation. We conclude that cognitive reserve is compatible and complementary with many related concepts, but that each much draw sharper conceptual boundaries in order to truly explain preserved cognitive function in the face of aging or brain damage