This article reviews normative changes in cognition that are observed across the adult life span and considers how specific disabilities may interact with aging processes to increase functional decline in later life. Disabling conditions that directly affect the brain are contrasted with those that do not. The goal is twofold: to create a framework for thinking about how cognitive changes, aging, and disability may interact to help explain individual differences in coping, and to promote the inclusion of cognition in a comprehensive approach to assessment and care.
Cognitive impairment is the primary determinant of disability in late life and, at all ages, cognitive function is the foundation of an individual’s capacity to meet the challenges of disabling conditions. This article reviews normative changes in cognition that are observed across the adult life span and considers how specific disabilities may interact with aging processes to increase functional decline in later life. Disabling conditions that directly affect the brain are contrasted with those that do not; specific exemplars are used to illustrate these points. The author considers that, whereas some cognitive aging processes may impair the capacity of disabled persons to cope with their lives, others may enhance it. The goal of the approach taken here is twofold: to create a framework for thinking about how cognitive changes, aging, and disability may interact to help explain individual differences in coping, and to promote the inclusion of cognition in a comprehensive approach to assessment and care.
What is cognition?
“Cognition” refers to a broad range of largely invisible activities performed by the human brain. Perceiving, thinking, knowing, reasoning, remembering, analyzing, planning, paying attention, generating and synthesizing ideas, creating, judging, being aware, having insight—all these and more—are aspects of cognition. The following is a working definition: cognition includes any and all process by which a person becomes aware of his or her situation, needs, goals, and required actions, and uses this information to implement problem-solving strategies for optimal living. Motivation, usually considered a quality of affect rather than of thought, would, by this definition, be an aspect of cognition and is included as such here.
How does cognition change with age?
Recent critical reviews of cognitive aging distinguish between processes showing gradual declines across the life span and those that remain stable until advanced age. Basic mechanisms common to many cognitive processes, including perceptual and thinking speed, numerical ability, working memory, and encoding and retrieval of new information, appear to show small but continuous, more or less linear declines across the entire adult life span from the early 20s through the 80s, though the magnitude and precise trajectory of these normal changes is debated. Most functions that depend on stable knowledge stores and well-practiced tasks remain stable into old age, and some improve with age, including wisdom—the superior judgment and insight born of life experience and resulting strategic efficiencies. When cognitive decline departs from its relatively linear path to follow an accelerated pattern of loss, the influence of disease processes must be suspected and makes distinctions between pathology and normal aging very difficult to disentangle. The pathologies that account for much of the accelerated cognitive decline that may be observed in elderly people include both systemic diseases with cerebral effects, such as cardiovascular disease and diabetes, and diseases manifested primarily by their cognitive signs and symptoms, such as Alzheimer’s disease. Though studies of brain integrity (eg, those based on neuroimaging technologies, such as structural and functional MRI, positron emission tomography and single-photon emission computed tomography, and MR spectroscopy) provide additional insight into normal versus pathologic aging, it is likely that these distinctions will remain somewhat blurred.
How does cognition change with age?
Recent critical reviews of cognitive aging distinguish between processes showing gradual declines across the life span and those that remain stable until advanced age. Basic mechanisms common to many cognitive processes, including perceptual and thinking speed, numerical ability, working memory, and encoding and retrieval of new information, appear to show small but continuous, more or less linear declines across the entire adult life span from the early 20s through the 80s, though the magnitude and precise trajectory of these normal changes is debated. Most functions that depend on stable knowledge stores and well-practiced tasks remain stable into old age, and some improve with age, including wisdom—the superior judgment and insight born of life experience and resulting strategic efficiencies. When cognitive decline departs from its relatively linear path to follow an accelerated pattern of loss, the influence of disease processes must be suspected and makes distinctions between pathology and normal aging very difficult to disentangle. The pathologies that account for much of the accelerated cognitive decline that may be observed in elderly people include both systemic diseases with cerebral effects, such as cardiovascular disease and diabetes, and diseases manifested primarily by their cognitive signs and symptoms, such as Alzheimer’s disease. Though studies of brain integrity (eg, those based on neuroimaging technologies, such as structural and functional MRI, positron emission tomography and single-photon emission computed tomography, and MR spectroscopy) provide additional insight into normal versus pathologic aging, it is likely that these distinctions will remain somewhat blurred.
Brain aging: the substrate of cognitive change
A concise review of the evidence regarding neural changes associated with brain aging provides a useful working model emphasizing two critical systems subserving cognitive processes. The first component involves changes in the frontostriatal system, broadly associated with executive abilities and adaptation to new environmental inputs and changes in one’s physical and mental self, and the second, changes in the medial temporal lobes and the bidirectional relays that link the hippocampus and association cortices. By and large, neurobiological data are generated and interpreted through the one-way glass of a “deficit” model of aging: progressive decay of neural tissues, based on “toxic hits” to vulnerable macromolecules, cumulative oxidative stress, diminished bioreparative mechanisms, subtle disease processes, and disuse, produces impairment in cognitive abilities. The deficit model is the basis for investment in brain aging research aimed at identifying preventive and therapeutic interventions that can delay the onset of a particular disease (eg, Alzheimer’s dementia) or mitigate the decline that results. Findings from basic and clinical neurobiology can be most broadly informative if separated, to the extent possible, from specific disease categories, as progress in research has found overlapping molecular mechanisms across a broad spectrum of clinical diagnostic entities. Such findings support a reorientation of research toward locating factors that retard or accelerate brain aging and account for wide variations among individuals in the rate at which brain systems age. The reader is referred to the excellent review cited earlier for a detailed discussion and citation of extensive data supporting a two-component model of brain aging, sketched below. Note that any disease process or injury that affects these age-vulnerable systems is likely to intensify, and be made more disabling as a result of, the age-related changes described here.
Frontostriatal Systems
The prefrontal cortex is particularly expressive of age-related changes, which, like a number of cognitive abilities, shows a linear decline in volume detectable by the 20s (possibly at first the result of extensive synaptic pruning that occurs during the transition from adolescence to early adulthood). Similar volume changes occur in the striatum, to which the prefrontal cortex is linked by a series of parallel pathways that have been associated with cognitive, affective, and motor functions. Not surprisingly, since these pathways use signature neurotransmitters (most prominently, but not limited to, dopamine) as part of their communication systems, neurochemical changes also occur (eg, reductions in dopamine transmission, affecting frontal activation, movement, and motivation). Volumetric changes in frontostriatal systems have been associated with reduced cognitive flexibility, working memory, suppression of unwanted or irrelevant responses, and strategic encoding of time-linked episodic memories. All of these are elements of cognition that underpin everyday multitasking, behavioral regulation, and adaptive functioning.
Medial Temporal Lobes, Hippocampus, and Associated Neocortical Systems
To a far lesser extent than the frontostriatal systems, the volume of medial temporal lobe structures tends to decline a little across the lifespan, but there are few cognitive correlates of such changes until later midlife (eg, age 60) and beyond, when explicit (declarative) memory performance tends to correlate with hippocampal volumes. However, in the healthy aging hippocampus and elsewhere, dendritic branching still occurs and new neural connections form in response to experience (neural plasticity). Functional imaging techniques have shown reductions in hippocampal and corresponding changes in the pattern of prefrontal activation during specific kinds of cognitive tasks in healthy older persons, suggesting altered pathways for at least some information management tasks. The significance of many of the observed changes for everyday function have not been specifically queried, but likely they relate to the gradual declines and shifts in motivation, overall cognitive and motor activity, and efficiency of learning that have been recognized as part of late life throughout history.
What Accounts for the Decreased Volume of Some Aging Brain Structures?
The clearest answer to this question from existing neurobiological research is that brain cells decrease in size (rather than die out) and that the communication highways between regions, the long, myelinated, white matter tracts, undergo gradual thinning and reduced efficiency. Damage to white matter has been extensively attributed to vascular ischemia associated with reduced small-caliber vessel perfusion and the size of the cerebrovascular bed during aging, and to pathologic changes caused by vascular occlusive disease, hypertension, and other cerebrovascular risk factors, and even a form of vascular disease most often recognized as part of Alzheimer’s disease, known as amyloid angiopathy. Amyloid angiopathy is receiving renewed research interest because of the development of neuroimaging techniques capable of identifying its presence and consequences in living patients. Other mechanisms for both white matter and neuronal cell body and axonal damage are also under investigation.
Individual Differences, Choices, and Training Matter
Despite good evidence for some decline in many cognitive functions, reductions in brain tissue volumes, and changes in tissue composition that occur with apparently normal aging, there are large individual differences that increase after late midlife, with the mechanisms responsible for these differences remaining largely unaccounted for. Among the factors that may account for some individual differences are two that can be potentially modified by choice and are prompting revisions in the deficit model of brain and cognitive aging. The two are aerobic fitness and specific cognitive training. Six months of sustained aerobic fitness training increases the volume of both gray and white matter in older persons, reducing or reversing tissue losses previously thought to be inevitable. Is sustaining the level of activity required to bring fitness to the effective level practical for most older adults? Can its brain effects be realized for average older people, and its benefits be maintained over prolonged periods of time? These questions have yet to be explored.
Specialized cognitive training has also been shown, first in uncontrolled studies and more recently in randomized controlled trials, to improve a variety of cognitive processes, including memory, speed, and reasoning and problem solving, among others. “Strategy training,” based on identification of weaker abilities to be targeted for training and teaching of explicit strategies for improving performance, describes a variety of training models and successful approaches. Most improvements resulting from training paradigms are modality-specific, showing little or no transfer or generalization to other cognitive abilities. Reasoning training, however, has been found to cross modalities more effectively than memory and speed-of-processing training and to be associated with less decline in instrumental activities of daily living over a prolonged (5 year) period of follow-up. The reader is referred to a recent comprehensive review of both mental and physical training approaches to sustaining cognitive abilities in normally aging individuals.
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