Cognitive Reserve

Theory and Applications

Yaakov Stern

• Publisher: Psychology Press
• Year: 2013
• ISBN:
  9781134954452
• Edition: 1
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

Cognitive reserve has emerged as a powerful concept for interpreting individual differences in susceptibility to, and recovery from, brain injury or pathology. Underlying cognitive reserve is the idea that individual differences in how cognitive tasks are mediated in the brain allow some people to cope with pathology to a greater degree than others. Cognitive Reserve: Theory and Applications describes in depth the source of these individual differences.

This volume provides a comprehensive review of theory, research and clinical application of the cognitive reserve. Chapters explore the theoretical underpinnings of cognitive reserve, and evidence for its existence. Various approaches for studying this concept are addressed, including epidemiologic, cognitive experimental, and neuroimaging. Possible genetic and physiologic underpinnings of cognitive reserve are presented. Application of this concept to a wide range of situations, including child development, aging, Alzheimer's disease, stroke, HIV, and head injury is discussed. The result is an up-to-date, global treatment of cognitive reserve that will be of interest to someone new to the concept or the experienced investigator.

1	The concept of cognitive reserve: A catalyst for research
	Yaakov Stern

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. Two interrelated concepts have been proposed. Brain reserve is an example of what might be called a passive model of reserve, where reserve derives from brain size or neuronal count. The model is passive because reserve is defined in terms of the amount of brain damage that can be sustained before reaching a threshold for clinical expression. In contrast, the cognitive reserve (CR) model suggests that the brain actively attempts to cope with brain damage by using pre-existing cognitive processing approaches or by enlisting compensatory approaches. Individuals with more CR would therefore be more successful at coping with the same amount of brain damage. As will become clear throughout this volume, these models are by no means mutually exclusive.

The threshold model, critically reviewed by Satz (1993), and suggested by many others, is a well articulated model of how reserve may operate. The threshold model revolves around the construct of “brain reserve capacity” (BRC). This is a hypothetical construct, but concrete examples of brain reserve capacity might include brain size or synapse count. The model recognizes that there are individual differences in BRC. It also presupposes that there is a critical threshold of BRC such that specific clinical or functional deficits emerge once BRC is depleted past this threshold. This formulation begins to account for the disjunction between the extent of pathology and the extent of clinical change. If two patients have different amounts of BRC, a lesion of a particular size may exceed the threshold of brain damage sufficient to produce a clinical deficit in one patient but not the other. Thus more BRC can be considered a protective factor, while less BRC would impart vulnerability.

In contrast, the CR model suggests that the brain actively attempts to compensate for the challenge represented by brain damage (Stern, 2002). The active models of reserve focuses more on the mode in which tasks are processed as opposed to differences in underlying physiologic differences. Thus neural reserve could take the form of using brain networks or cognitive paradigms that are more efficient or flexible, and thus less susceptible to disruption. This type of reserve is a normal process used by healthy individuals when coping with task demands, as well as by individuals with brain damage. In contrast, neural compensation refers to adopting new, compensatory brain networks or paradigms because pathology has impacted those that are normally used in no affected individuals. Together, these two types of neural mechanisms could underlie CR.

Individual variability in CR can stem from innate or genetic differences or from life experiences, such as education, occupational experience or leisure activities. These factors could also contribute to brain reserve.

The concept of cognitive reserve provides a ready explanation for why many studies have demonstrated that higher levels of educational and occupational attainment, or of intelligence, and are good predictors of which individuals can sustain greater brain damage before demonstrating functional deficit. Rather than positing that these individuals’ brains are grossly anatomically different than those with less reserve (e.g. they have more synapses), the cognitive reserve hypothesis posits that they process tasks in a more efficient manner.

The concept of reserve is not just applicable to the emergence of a clinical condition such as Alzheimer’s disease. It is equally applicable to the rate of change in clinical function as a result of gradual changes in disease pathology. Similarly, it applies to issues of recovery of function, for example recovery following traumatic brain injury. More generally, reserve is operative whenever there is a balance between some brain change, for example that due to a disease or normal aging, and a person’s current level of functioning. A straightforward example of this is in Alzheimer’s disease, where both imaging and post-mortem studies have suggested that in individuals with the same amount of brain pathology, those with higher levels of reserve show less severe clinical dementia. Thus an individual’s level of function at any point in time is a function of the underlying brain substrate and their ability to make use of this substrate, with the latter influenced by the level of cognitive reserve.

A consistent set of variables have been linked with the concept of cognitive reserve, including IQ, educational and occupational attainment, and enriching activities such as leisure activities. These variables have often been shown to operate independently and additively. This speaks to a conception of CR as a malleable entity, whose level at any point in time is dependent on the summation of life experience and exposures up to that time. This also raises the possibility of enhancing cognitive reserve, and thus improving people’s ability to maintain their capacities in the face of insult to brain function.

This volume

This volume assembles a body of work which defines, explores and utilizes the concept of cognitive reserve. I have attempted to gather together a diverse set of research approaches ranging from genetics to neurogenesis, and from neuroepidemiology to neuroimaging.

The volume began as a special issue of the Journal of Clinical and Experimental Neuropsychology. For this volume, the authors of those articles were invited to revise and expand their original contributions. This has allowed the majority of the authors to bring the research findings reported previously into a larger theoretical context, and to more thoroughly review and discuss the applicability of the concept of CR to their research domain. In addition, I have invited five additional investigators to contribute chapters to this volume. The intention was to expand to an even greater degree the diversity of domains in which the CR concept is discussed and applied.

Lee (Chapter 2) reviews the genetic basis for cognitive performance and how this might interact with the concept of cognitive reserve. Since a potentially substantial proportion of variability in cognitive abilities can be genetically determined, this is a fitting place to begin the special issue. This is followed by Richards et al. (Chapter 3), who set the stage for a comprehensive consideration of the factors across the lifespan that can contribute to cognitive reserve. They also describe a prospective study that elegantly demonstrates that cognitive reserve is malleable, and that both genetic (childhood IQ) and experiential components contribute to it.

The next four chapters thoughtfully apply the concept of cognitive reserve to conditions and situations that that have received relatively little attention in this context. Dennis et al. (Chapter 4) explore cognitive reserve in the setting of childhood development and brain injury, while Bigler (Chapter 5) explores the implications of CR for recovery from traumatic brain injury. This chapter nicely demonstrates the interplay between supposed brain size, supposedly a passive indicator of reserve, and more active forms of cognitive reserve. Boyle et al. (Chapter 6) consider two situations where the implications of CR can be directly studied: electroconvulsive therapy and coronary artery bypass grafting surgery. Finally, Bieliauskas and Antonucci (Chapter 7) review the implications of CR on the estimation of disease progression, particularly in the context of clinical trials.

The next four chapters evaluate the potential influence on cognitive reserve of lifetime activities, including physical activity, general lifestyle activities, cognitively stimulating activities, and leisure. These activities are explored in relation to outcomes including late life cognition or cognitive decline, as well as the onset of dementia. Dik et al. (Chapter 8) present data from a large cohort of prospectively followed elders regarding the association between early life physical activity and cognition in aging. Wilson et al. (Chapter 9) review their epidemiologic research, focusing on lifetime participation in cognitively stimulating activities. Small et al. (Chapter 10) review the implication of lifestyle activities for cognitive change in aging. Finally, Scarmeas (Chapter 11) reviews my group’s and others’ studies evaluating the relationship between elders’ engagement in leisure activities and two outcomes: cognitive decline in normal aging, and the incidence or severity of Alzheimer’s disease.

The following series of chapters incorporate a series of proxies for cognitive reserve, and apply them in three different settings. Reinhard et al. (Chapter 12) followed a cohort of HIV positive individuals, using onset of AIDS, dementia and mortality as outcomes and Shipley IQ as the proxy for cognitive reserve. Manly et al. (Chapter 13) demonstrate that literacy may be an important measure of cognitive reserve in the context of cognitive decline and incident dementia in aging. Finally, Mortimer et al. (Chapter 14) report data from the Nun Study, using the diagnosis of dementia as an outcome. They used education as a proxy measure for reserve, and also looked at head size, which has been associated with reserve against dementia in several studies.

Three chapters review functional imaging studies intended to elucidate the neural substrates of cognitive reserve. In Chapter 15 I attempt to develop a theoretical framework for studying the neural correlates of cognitive reserve, and then describe four studies that incorporate these ideas. Grady (Chapter 16) reviews her ground-breaking work on compensatory brain activity in older adults or AD patients. Then, Friedman (Chapter 17) provides a thoughtful review of event-related potential data that shed light on the concept of compensation.

Finally Kozorovitskiy and Gould (Chapter 18) provide an insightful review on the topic of adult neurogenesis and its potential for being a compensatory mechanism for brain damage. Theoretical treatments of cognitive reserve and compensation have traditionally emphasized mechanisms for coping with brain damage. These approaches typically view the brain as a resource that can be depleted or damaged, and do not incorporate recent information about neurogenesis in the mature brain. This review points to the future, where compensation may not simply be adaptation of alternate brain networks, but regeneration of underlying brain circuitry.

The diversity of the subject matter in this volume highlights the utility and flexibility of the concept of cognitive reserve for understanding how the brain copes with challenge and pathology. Hopefully, the present volume will encourage further exploration of this concept in diverse research domains.

Acknowledgements

This work was supported by NIA grant AG 14671.

References

Satz, P. (1993). Brain reserve capacity on symptom onset after brain injury: A formulation and review of evidence for threshold theory. Neuropsychology, 7, 273–295.

Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society, 8, 448–460.

2	Understanding cognitive reserve through genetics and genetic epidemiology
	Joseph H. Lee

The basis for cognitive reserve (CR) arose from the observation that the severity of neuropathological manisfestations of Alzheimer’s disease (AD) did not always correlate well with severity of AD (Katzman et al., 1988). This observation led several investigators to propose the concept of CR (Katzman, 1993; Satz, 1993; Stern, Alexander, Prohovnik, & Mayeux, 1992; Stern et al., 1994). They argue that individuals develop cognitive reserve in the presence of favorable environments such as high educational level or by genetic predisposition, or both, and that CR increases the threshold for neuropsychological responses to brain insult. Those with a greater brain reserve capacity have a higher threshold for brain insult before clinical deficit appears. The concept of CR is evolving to include broader phenomena. Others have argued that more efficient circuitry is less likely to be disrupted and more resilient in the event of brain insult (Grady et al., 1996; Grasby et al., 1994). Stern (2002) applies CR to any situation where there is variation in response to brain injury, suggesting that CR can be applied to individuals who are healthy as well as those who are suffering from neurodegeneration.

A multitude of factors may contribute to the variable responses to brain insults observed in individuals. Both genetic and environmental factors are likely to affect the responses to injury. Gene dosage and timing will influence the responses to the insult. Similarly, the strength and timing of environmental factors will bring about variations among individuals. Factors present early in life may influence cognitive reserve and be as important as factors present later. To ...

Table of contents

• Cover
• Half Title
• Full Title
• Copyright
• Dedication
• Contents
• List of figures
• List of tables
• About the editor
• List of contributors
• From the series editor
• 1 The concept of cognitive reserve: A catalyst for research
• 2 Understanding cognitive reserve through genetics and genetic epidemiology
• 3 Lifetime antecedents of cognitive reserve
• 4 Brain reserve capacity, cognitive reserve capacity, and age-based functional plasticity after congenital and acquired brain injury in children
• 5 Traumatic brain injury and cognitive reserve
• 6 Electroconvulsive therapy and coronary artery bypass grafting surgery: Pseudoexperimental paradigms for studying cognitive reserve
• 7 The impact of cognitive reserve on neuropsychological measures in clinical trials
• 8 Association between early life physical activity and late-life cognition: Evidence for cognitive reserve
• 9 Assessment of lifetime participation in cognitively stimulating activities
• 10 Lifestyle activities and late-life changes in cognitive performance
• 11 Lifestyle patterns and cognitive reserve
• 12 Brain reserve: HIV morbidity and mortality
• 13 Literacy and cognitive decline among ethnically diverse elders
• 14 Brain reserve and risk of dementia: Findings from the Nun Study
• 15 Imaging cognitive reserve
• 16 Cognitive reserve in healthy aging and Alzheimer disease: Evidence for compensatory reorganization of brain networks
• 17 A neurocognitive overview of aging phenomena based on the event-related brain potential (ERP)
• 18 Adult neurogenesis and regeneration in the brain
• Author index
• Subject index