The field of gerontology – the scientific study of aging – emerged as a major scientific discipline in the

20th century (e.g., Birren, 1964). Research on intelligence and intellectual development played a major
role in shaping the field of psychological gerontology (e.g., Botwinick, 1977). This chapter reviews what
is known and not yet known about adult intellectual development after decades of research on the
topic. Most of the information we have available concerns aspects of what Sternberg (1985) has defined
as academic intelligence (based on traditional psychometric tests of human abilities).

This chapter focuses on what is known about these types of human abilities and their correlates,
although I also briefly treat other aspects of intellect, such as practical intelligence and tacit knowledge.

Descriptive Research on Adult Age Differences

Early studies of psychometric intelligence prior to 1940 determined that there were large differences in
performance on general tests of intellectual aptitude (see Salthouse, 1982 for an excellent summary and
review). Wechsler (1939) characterized the performance tests on the Wechsler Adult Intelligence Scale
(WAIS) as “don’t-hold” tests because of the lower performance on those subscales (e.g., WAIS Block
Design) by older adults in his cross-sectional norming studies of the test. Conversely, Wechsler found
that tests like WAIS vocabulary were typically shown to have much smaller age differences, causing
them to be characterized as “hold” tests. This basic idea, that one class of intellectual ability tests
manifests age decline whereas others do not, has been widely replicated and studied across a variety of
intelligence tests, and today represents a virtual “truism” about aging and intelligence. These findings
mirrored outcomes of studies using other tests to evaluate age differences in human abilities, studies
that spanned much of the 20th century (Salthouse, 1982). The concept of contrasting maintenance of
knowledge and verbal abilities, relative to other types of human abilities, has therefore figured
prominently in theoretical treatment of how aging affects intelligence. Cattell (1971) developed the
theory of fluid and crystallized intelligence, arguing that this basic pattern reflected two prototypic
classes of intellectual abilities. Fluid intelligence was seen as the fundamental ability to think, reason,
and process information, and prone to adult age decline as a function of biological aging processes (Horn
& Cattell, 1967; Horn & Hofer, 1992). Crystallized intelligence, on the other hand was seen as
determined by investment of fluid intelligence in knowledge acquisition, which was largely maintained
or even improved into old age (Horn & Cattell, 1967).

Baltes and his colleagues characterized the distinction as involving a decline in basic information-processing
mechanisms labeled the mechanics of cognition (e.g., Baltes, 1997). In contrast, experience with a culture leads to
acquisition of a broad class of declarative and procedural knowledge and skills about how to achieve goals in a
cultural context, labeled the pragmatics of intelligence. Although Baltes’ conceptualization emphasized mechanisms
that influence observed abilities, similar arguments were being made by Horn (e.g., Horn & Hofer, 1992) in
extended versions of fluidcrystallized theory. As a consequence, the differences between these theoretical
viewpoints are subtle at best. Can a two-curve model actually account for most of the age-related variance in adult
intellectual development? If so, it would be surprising, for several reasons. First, theories of psychometric abilities
generally acknowledge that a large number of intellectual abilities exist. Theoretical approaches based on the work
by Thurstone on primary mental abilities (e.g., Thurstone, 1938) typically argue for 30 or more primary abilities
(Carroll, 1993; Horn & Hofer, 1992). It would be surprising if all these abilities declined at the same rate in
adulthood. Second, contemporary hierarchical models of abilities typically acknowledge that fluid and crystallized
intelligence are distinct from other higher order ability factors. Horn (1985; Horn & Hofer, 1992) argued that, for
example, general visualization abilities, general auditory abilities, speediness, and secondary memory are all
empirically distinct from fluid intelligence. To the extent that these second-order factors are indeed differentiable
from fluid intelligence, one might expect their developmental curves in adulthood to also differ. Third, theories of
biological aging identify a large number of potential biological clocks, operating at different levels of basic
physiology, that appear to be associated with rates of biological aging. What do the empirical data tell us? The cross-
sectional age curves for episodic memory, spatial visualization, and measures of fluid intelligence and general
processing speed vary somewhat as a function of issues like how the tests are constructed and scaled, their
processing requirements, and the like. Yet there is surprising similarity in the curves across these different classes of
abilities. Certainly the ability that is typically found to have the largest crosssectional age differences is speed of
processing, such as identified by the Perceptual Speed factor (Carroll, 1993). Salthouse (1996) has evaluated
Perceptual Speed in a plethora of studies, typically finding the largest cross-sectional age differences for that factor
(see also Schaie, 1989). However, fluid intelligence shows considerable similarity in magnitude of estimated decline
to measures of episodic memory, working memory, and spatial visualization (e.g., Hertzog, 1989; Hultsch, Hertzog,
Dixon, & Small, 1998; Park et al., 1996; Salthouse, Pink, & Tucker-Drob, 2008). No one study has examined all the
relevant abilities in a truly representative sample of the adult population, and most observe at least some variation in
cross-sectional age slopes across abilities. Nevertheless, the available crosssectional evidence on the mechanics of
cognition is more or less consistent with the argument that abilities emphasizing cognitive mechanics decline in
adulthood. There are important exceptions – not all processing mechanisms decline, and not all aspects of
pragmatics are maintained (see Hertzog, 2008). Also, cross-sectional data disagree as to whether the cross-sectional
curves are linear or curvilinear – accelerating the magnitude of estimated decline in old age (e.g., compare Hultsch
et al., 1998, with Park et al., 1996, regarding episodic memory). Nevertheless, the negative correlation of age with
fluid intelligence, working memory, spatial visualization, and the like from early adulthood to old age is about –. 4.
There is evidence that the cross-sectional age curves for crystallized intelligence may differ as a function of the type
of knowledge being assessed. Work by Ackerman and colleagues has focused on tracking domain-specific
knowledge that may occur during and after the time that young adults begin to specialize vocational and personal
interests, crystallizing them into a pattern of preferences for information sought, acquired, digested, and assimilated
into existing knowledge structures (e.g., Ackerman, 2000; Beier & Ackerman, 2005). Ackerman’s argument is that
crystallized intelligence, as manifested in general cultural knowledge tests (like WAIS Information) or in
recognition vocabulary tests, underestimate acquisition of new knowledge during adulthood. Thus, although the
existing psychometric data suggesting longterm stability in verbal abilities and cultural knowledge diverges from the
pattern of negative age differences seen with fluid intelligence and other human abilities, it may not capture the
lifelong learning that occurs in the specific domains in which people invest time and effort to acquire knowledge.
Even within the domain of vocabulary, there may be activity-dependent differences in the types of word knowledge
that are acquired. Frequent crossword puzzle players show major cross-sectional age differences in esoteric
vocabulary terms that are correctly recognized, probably as a direct function of actual experience with encountering
these terms while solving puzzles (Hambrick, Meinz, & Salthouse, 1999). Be that as it may, there is little question
that abilities that reflect specific knowledge acquisition are maintained or improved, at least into the 60s. Beier and
Ackerman’s (2005) work on specificity of knowledge acquisition resonates with other evidence that people of
different ages also differ in historical life contexts that produce cohort differences in knowledge-based abilities.
Schaie (2005) has studied adult intellectual development for over 50 years, using hybrid cross-sectional and
longitudinal designs known as sequential strategies, enabling an evaluation of age changes across different birth
cohorts and epochs of historical time. One of Schaie’s findings is that there are large cohort differences in
vocabulary, which helps to explain why studies of age and cognition that use older vocabulary tests – particularly
with “advanced” and perhaps dated items – tend to find that older adults perform better than younger adults. Such
age differences probably reflect a combination of improvement with experience in the older adults, but lower
knowledge of esoteric word meanings in younger generations. By the same token, it is likely to be true that younger
adults have more word knowledge in domains they commonly employ, such as technical terms and jargon associated
with advanced technology (older adults are less likely to use new technology such as iPhones or iPods; Czaja et al.,
2006). Schaie (2005) has also shown that there are cohort differences favoring earlier born generations in simple
mental calculations such as two column addition. One could view this effect as being a societal consequence of the
use of computers and calculators, slowing the efficiency of mental arithmetic in more recent cohorts apt to rely on
technological support. In sum, the distinction in developmental functions between knowledge and experience-based
abilities, on the one hand, and fluid-like abilities, on the other hand, is consistent with a large body of crosssectional
evidence.
Longitudinal Evidence Regarding Levels of Adult Intellectual Development
As noted earlier, Schaie and colleagues (e.g., Schaie, 2005) have assembled the largest extant database with
combined longitudinal and cross-sectional intelligence test data. A reasonable question to ask, then, is whether these
data produce radically different conclusions regarding age changes in adult intellectual development, relative to the
crosssectional data. On the one hand, Schaie’s (2005) data clearly indicate that cohort differences are not confined to
aspects of knowledge and crystallized intelligence. He also observes substantial generational differences on a tests
of fluid reasoning and spatial relations. Others have noted the changes during the 20th century in performance on
tests of reasoning and fluid intelligence, as manifested in the so-called Flynn effect (Flynn, 2007; Raven, 2000). The
impact of these cohort effects is primarily in attenuating the estimated changes in intelligence from ages 20 to 50,
but they also reduce the magnitude of estimated age change in late life as well (Zelinski, Kennison, Watts, & Lewis,
2009). Certainly the STAMAT Verbal Meaning test shows a prolonged period of maintenance, relative to the other
abilities, but it too manifests evidence of longitudinal decline in old age. Separate evidence, however, suggests that
this pattern of apparent decline is an artifact of the speeded properties of the STAMAT Verbal Meaning test (e.g.,
Hertzog, 1989). In fact, all of the STAMAT tests are substantially influenced by speed of processing, in part because
of limited item difficulty, even for the Letter Series and Space tests. The pattern of mean ability changes based on
sequential data can be separated into three parts. The first is the similarity of age changes across different aspects of
cognitive mechanics. The second is the conclusion that meaningful age-related changes in cognitive mechanics
occur after mid-life and accelerate in magnitude in late life. The third is the presence of substantial cohort effects on
variables measuring different aspects of cognitive mechanics that inflate estimates of age changes made from cross-
sectional data. Regarding cohort effects, there is broad agreement across studies that there are few cohort effects in
general informationprocessing speed, including the Perceptual Speed factor identified by psychometric tests (e.g.,
Hultsch et al., 1998; Schaie, 1990). However, the limited available data from studies other than Schaie’s Seattle
Longitudinal Study confirm substantial cohort effects on tests of reasoning (Raven, 2000; Zelinski & Kennison,
2007; R¨onnlund & Nilsson, 2008) and visuospatial ability (R¨onnlund & Nilsson, 2008; Zelinski & Kennison,
2007). These effects attenuate estimated age changes in cognition. For example, Zelinski and Kennison (2007)
found that six-year effect sizes in reasoning, spatial ability, and episodic memory were reduced in old age by
between 0.2 and 0.3 standard deviations (SD) by controlling on cohort differences. Interestingly, some studies report
few cohort effects on crystallized intelligence while finding larger effects on abilities more related to cognitive
mechanics (see Zelinski et al., 2009; cf. Alwin, 2009). The conclusion that declines in cognitive mechanics are
subtle before age 50 and accelerating thereafter is broadly consistent with reported results from a number of other
longitudinal studies of cognition and intellectual abilities in adulthood, including the Long Beach Longitudinal
Study (Zelinski & Kennison, 2007), the Victoria Longitudinal Study (Hultsch et al., 1998), and the Betula
Longitudinal Study (R¨ onnlund, Nyberg, B¨ackman, & Nilsson, 2005). These studies all suggest curvilinear
patterns of average age changes from the period of midlife through old age, with an acceleration in the rate of aging
effects on fluid intelligence, episodic memory, and spatial visualization and other fluid-like abilities after age 65.
Salthouse (2009) has argued that the type of longitudinal gradients produced by Schaie (2005) are contaminated by
practice effects on the tests, an internal validity threat (Shadish, Cook, & Campell, 2002) that is problematic for
longitudinal designs (Schaie, 1977). Because individuals are repeatedly given the same tests, they may show some
savings in generating problem answers. If it were the case that younger adults manifest larger practice effects (an
age X practice interaction), perhaps due to retention of prior test answers, then the contamination by practice would
produce shallower age slopes. One way to address the problem of practice effects has been to incorporate effects of
number of occasions of measurement as a proxy for exposure that would benefit from practice. Models that use this
approach also tend to increase the magnitude of age-related decline and estimate an earlier onset of reliable age-
related decline (e.g., Ferrer, Salthouse, Stewart, & Schwartz, 2004; Rabbitt, Diggle, Holland, & McInnes, 2004).
However, this modeling approach is controversial (see the exchange between Salthouse, 2009, Schaie, 2009, and
Nilsson, Stern¨ang, R¨ onnlund, & Nyberg, 2009). A model that uses all available data in a standard longitudinal
panel and then jointly estimates age changes and practice effects (under the convergence assumption – see McArdle
& Bell, 2001) confounds the estimates of practice effects with other influences that are not modeled, including
historical period (time), experimental mortality (attrition), and selection X period interactions. Sliwinski, Hoffman,
and Hofer (2010) argue that such models inevitably assign within-person changes that deviate from cross-sectional
trends to estimates of practice, morphing the estimated age effects away from within person change toward between-
person differences. As pointed out by Nilsson et al. (2009), studies that use an independent samples comparison
group to estimate practice effects report far less impressive practice adjustments than studies like Ferrer et al.
(2004).
Age Changes in the Factor Structure of Intelligence Tests
Another important question about aging is whether it influences the underlying factor structure of human abilities. A
leading developmental hypothesis has been the dedifferentiation hypothesis (deFrias, L¨ovd´en, Lindenberger, &
Nilsson, 2007). It states that shared causes of age effects across different kinds of human abilities will produce
increased correlations among ability factors. In the extreme, such changes could lead to a reduced number of distinct
human abilities. Factor analytic questions of this type cannot be separated from issues of how broadly or narrowly
tests are selected. A unifying perspective on this issue derives from hierarchical models of abilities, such as in
Carroll (1993). This view suggests that one can evaluate factor structure at a relatively narrow level (how different
tests define primary abilities, such as inductive reasoning or working memory), at a second-order level (how
different primary abilities define higher order factors like fluid intelligence, general speed of processing, or spatial
visualization), or at the highest levels (how second-order factors define a highest order general intelligence factor).
At the primary ability or second-order level, one can also evaluate the correlations among ability factors, treating
these correlations as an index of differentiation. In addressing these questions one can run into difficulty separating
measurement invariance and suboptimal measurement properties of tests from changes in relationships among
constructs. For example, use of speeded tests of intelligence may produce a substantial degree of dedifferentiation
that is attributable to the global effects of speed of processing on test performance, rather than because the
underlying ability constructs are becoming more correlated (Hertzog & Bleckley, 2001). The best available evidence
suggests that the factor structure of intelligence is not materially affected by aging. A large number of confirmatory
factor analytic studies, using both cross-sectional and longitudinal data, indicate that the same human abilities can be
identified in young adulthood, middle age, and old age (e.g., Anstey, Hofer, & Luszcz, 2003; Hertzog & Schaie,
1986; Hertzog, Dixon, Hultsch, & Mac-Donald, 2003; Hultsch et al., 1998; Brickley, Keith, & Wolfe, 1995; Lane &
Zelinski, 2003; Schaie et al., 1998). In all cases, the hypothesis of configural invariance (i.e., that the same variables
load on the same factors at all ages; Meredith & Horn, 2001) has been supported. In most cases, the evidence
supports the stronger hypothesis of metric invariance, that the unstandardized factor pattern weights, or factor
loadings (Meredith & Horn, 2001), are equivalent across time in longitudinal studies or are equivalent across age
groups. This is a broad generalization, and there are some interesting exceptions. Nevertheless, the developmental
changes that occur in adulthood do not appear to radically alter the underlying nature of human abilities. On the
other hand, the evidence regarding whether adult development results in increasing correlations among human
ability factors is mixed. Some studies have not found such effects (e.g., Zelinski et al, 2009; Bickley et al., 1995),
whereas other studies have (deFrias et al., 2007; Hertzog & Bleckley, 2001; Hertzog et al., 2003; Hultsch et al.,
1998; Schaie et al., 1998; Verhaeghen & Salthouse, 1997). However, major increases in factor correlations may be
restricted to old age (deFrias et al., 2007; Schaie et al., 1998). One methodological concern with agecomparative
factor analysis is that aggregation over long epochs of age is often needed to generate sufficient sample sizes for
factor analysis of cross-sectional data. For example, one might pool data from people within the ages of 20 and 39,
40 and 59, 60 and 79 to create “young,” “middle aged,” and “old” age groups. Aggregation over wide age spans
(such as 20 years) can create spurious increases in factor correlations because of the inflating influence of age-
heterogeneity on variable correlations (Hofer, Flaherty, & Hoffman, 2006). Given greater average age change after
age 60 that is similar across variables, factor correlations in the oldest group would be inflated. Forming narrower
age spans, if possible given the sample size, avoids this effect. In sum, factor analytic evidence indicates subtle
changes, if any, in the factor structure of human abilities. Thus, quantitative comparisons of ability test scores may
not be compromised by age-related changes in the measurement properties of the tests (Baltes & Nesselroade,
1970).

Individual Differences in Cognitive Change

One of the remarkable features of human intelligence is its relative stability of individual differences over years,
even decades. When longitudinal data are collected on the same person over time, it is possible to compute
correlations of ability test scores across that interval. These correlations can be remarkably high. For example, Ian
Deary and colleagues discovered large sample data on a general ability test for cohorts of Scottish schoolchildren in
multiple cohorts, and readministered the test over 60 years later to those who could be located. Test-retest
correlations were approximately .65 across the different cohorts (e.g., Deary et al., 2004). Similar findings have been
reported in long-term longitudinal studies using a wider range and variety of intelligence test and cognitive tasks
(e.g., Schaie, 2005). Moreover, when statistical corrections are possible to correct for attenuation of the stability
estimates for measurement error, the correlations are even higher. Hertzog and Schaie (1986) reported that the latent
seven-year stability of a general intelligence factor formed from primary ability tests was about .9. Hence it is
reasonable to conclude that individual differences in abilities are to a reasonable degree preserved as a function of
aging. Those individuals who perform well in a particular domain are likely to continue to do so across their adult
lives. Longitudinal studies may overestimate the stability of individual differences. Selective attrition has been
universally demonstrated in longitudinal studies of human abilities – those individuals who return for testing
performed higher at the inception of the study than those who fail to return (e.g., Ghisletta, McArdle, &
Lindenberger, 2006; Schaie, 2005). Selective attrition and population mortality are also likely to upwardly bias
estimates of stability of individual differences in intelligence. Nevertheless, even in positively selected samples, the
stability observed still implies that there are reliable individual differences in rates of change. When growth curve
analyses or latent difference score analyses are performed on longitudinal cognitive data, it is generally the case that
there are reliable variances in the slopes of the growth curves (e.g., deFrias et al., 2007; Ghisletta et al. 2006;
McArdle et al., 2002). Not all individuals are changing at the same rate; some decline faster than others, and some
even show improvements. Schaie (2005) has argued that, although the modal pattern of individual change is one of
relative stability in mid-life, one can identify also individuals who reliably decline or who reliably improve, even on
abilities related to cognitive mechanics. Data on six-year stability from the Victoria Longitudinal Study (VLS) on a
number of different cognitive variables, including working memory, episodic memory, fluid intelligence, ideational
fluency, verbal comprehension, and speed of processing show reliable variances in latent difference scores (Hertzog
et al., 2003), despite corrected stabilities that were typically in the 0.8 to 0.9 range. As pointed out by deFrias et al.
(2007), these individual differences in cognitive changes may be more pronounced in old age than in middle age.
The existence of individual differences in change on different human abilities raises an intriguing question. Are
these changes related to each other? Rabbitt (1993) once framed the question this way: Does it all go together when
it goes? There is good evidence that changes across variables are not independent but are instead correlated. Given
the extended measurement batteries in studies like the Betula Longitudinal Study and the VLS, we probably know
the most about associations in age-related changes in different aspects of memory. In the case of the VLS, analyses
in two different six year longitudinal samples show that individual differences in changes in working memory are
correlated with changes in episodic memory (measured by free recall of word lists and narrative text content) and in
a measure of semantic memory (fact recall). In addition, changes in working memory also correlate with changes in
other abilities, including ideational fluency, inductive reasoning, and speed of processing (Hultsch et al., 1998;
Hertzog et al., 2003). Betula study data indicates correlations among different aspects of episodic memory and
processing speed (L ¨ovd´en et al., 2004). Hertzog et al. (2003) showed that one could fit a higher order general
factor of change to the latent change factors for multiple cognitive abilities. This latent variable was defined
principally by working memory but also had substantial loadings on most other variables, with the exception of
changes in vocabulary. One interesting feature of the VLS data was the strong association of changes in fact recall
with changes in working memory. The fact recall measure assessed cultural knowledge (e.g., “who is the cartoon
character who gets his strength from eating spinach?”). Cross-sectionally, the fact recall measure behaves like a
measure of crystallized intelligence, as one would expect (Hultsch et al., 1998). Longitudinally, it dissociates from
verbal comprehension. Instead, changes in fact recall are more highly correlated with changes in working memory
and episodic memory. Such a pattern suggests late life changes in retrieval or access to information held in semantic
memory that are shared across episodic and semantic memory tasks. One typically observes high correlations of
measures of inductive reasoning and working memory. The strong association of working memory and reasoning
has been observed in a number of individual differences studies (e.g., Kane & Engle, 2002; Salthouse et al., 2008).
Kyllonen and Chrystal (1990) once remarked that reasoning might not be, in fact, differentiable from working
memory. Yet working memory changes and reasoning changes are only moderately correlated in the VLS data
(Hertzog et al., 2003); instead, changes in working memory are more highly correlated with changes in fact recall
than with changes in reasoning. The influences that drive age changes may not be the same influences that determine
the factor structure of abilities in young adulthood. Perhaps the most interesting aspect of the VLS change factor is
that there is reliable change variance in almost all human abilities that is unique to each variable. Figure 9.1, taken
from Hertzog et al. (2003), shows the results of a model where a higher order factor of general cognitive change is
used to account for the correlations of change among the different cognitive variables. The general change factor has
moderate to strong relationships to change in most of the cognitive variables. Thus there is a coherence to the
individual differences in rates of cognitive change in later life. Nevertheless, changes in the latent variables do not
correlate up to the limit defined by the variance of their changes. Cognitive change is both common and unique, in
the factor analytic sense of those terms. There are certainly shared aspects of change, but different human abilities
change independent of each other. The answer to Rabbitt’s (1993) question, it seems, is not that everything goes
together, but that, when working memory goes, a lot of other abilities seem to go too, to at least a degree. These
results are therefore divergent from the similarity of average age trends in fluid intelligence and other aspects of
cognitive mechanics. The coherence to cognitive change – as manifested in moderate correlations of longitudinal
changes across variables obscures the fact that variables are changing independently, such that people will have
different profiles of change across a set of cognitive variables. Unlike the inferences about the dimensions of change
from cross-sectional data (e.g., Salthouse et al., 2008), such findings indicate that a potentially large number of
causes influence agerelated changes in cognition. Why the discrepancy between crosssectional and longitudinal
results? Certainly, there are potential issues with the validity of the longitudinal estimates of correlated change. For
instance, Ferrer et al. (2005) noted that differential practice effects across variables could distort the estimated
longitudinal change correlations. It is difficult to believe, however, that such effects could produce artifactual
variable-specific change variance of the type observed in the VLS data, given that the VLS uses rotating alternate
forms to measure word recall, text recall, and fact recall with different items at each occasion of measurement. To
my mind the difference arises essentially because the question cannot be adequately addressed by statistical models
of cross-sectional data (Hofer et al., 2006; Lindenberger et al., 2009). Cross-sectional analyses can only estimate, in
effect, correlations among cross-sectional age curves by testing for whether cognitive variables have a partial
correlation with age, controlling on other cognitive variables. This approach can reveal whether average age trends
differ between variables (e.g., Horn, Donaldson, & Engstrom, 1981). Failing to detect different shapes of cross-
sectional curves neither implies that the variables in question change in lockstep nor that their changes have the
same underlying causes. To actually assess individual differences in change, one must repeatedly measure the same
people (Baltes & Nesselroade, 1979). In sum, there is a high degree of stability in human abilities across the adult
life course, but at the same time there are individual differences in cognitive changes, particularly in old age. A
critical question, then, is what determines these individual differences in cognitive trajectories.

Influences on Adult Cognitive Development

The individual differences in cognitive change just reviewed could in principle reflect a number of different
influences. Cognitive psychologists tend to focus on processing mechanisms that are associated with changes in
complex cognition. As noted earlier, resources like working memory, processing speed, and inhibitory aspects of
attention are often cited as causes of age changes in intelligence (see Hertzog, 2008; Salthouse, 1996; Verhaeghen &
Salthouse, 1997). Even if one emphasizes a componential approach to human intelligence, the question remains as to
what determines agerelated changes in fundamental processing mechanisms. One important influence is individual
differences in genetically programmed biological aging – often termed senescence. In essence, the idea is that our
biological aging clocks may be ticking in different metrics of time. Newer research derived from insights into the
human genomic code indicates that genetic polymorphisms associated with neurotransmitters, neurotrophins, and
related hormones influence adult cognitive development (e.g., Harris et al., 2006; Lindenberger et al., 2008).
Behavioral genetic studies indicate a considerable degree of heritability in cognitive change in late life (Reynolds,
2008). However, genetic predispositions interact with social and psychological mechanisms to produce cognitive
phenotypes. When we organize our data by chronological age, we are not measuring individual differences in rates
of biological aging. The effects of age revealed in group mean changes or in individual differences in change reflect
variation in cognition that is systematically correlated with how old people are. But there are many contextual
variables that are correlated with chronological age as well, including age-graded events like retirement, experience,
and shrinkage of one’s social network. Furthermore, nonnormative, negative life events are correlated with age, such
as risks for contracting different kinds of chronic disease that can impact cognition, either directly through
influences on the brain or indirectly through psychological effects of medications used to treat them (Birren, 1964).
The longitudinal studies that generate the data in question may measure physical health but typically cannot control
on disease by only assessing disease-free older adults. The average older adult has three or more chronic health
conditions, including arthritis, vascular disease, Type II diabetes, reduced hormonal secretion, pulmonary or renal
disease, and declining sensory and perceptual function (e.g., macular degeneration; see Spiro & Brady, 2008). There
is also a host of brain pathologies that are correlated with age and which may have impact on cognition before they
are clinically detected, including different forms of dementia and Parkinson’s disease). Lifestyles also change as
people grow older, sometimes as a consequence of limitations produced by chronic disease, in other cases as a
function of changing patterns of behavior that have psychological and social origins. Certainly, structural features in
the brain undergo changes that are correlated with cognition. For instance, Raz et al. (2008) analyzed a longitudinal
sample that had been measured with structural magnetic resonance imaging to evaluate changes in gray matter
volume in the cerebral cortex. Individual differences in the structural changes in dorsolateral prefrontal cortex and
hippocampal areas of the brain were correlated with changes in fluid intelligence.

Disease and brain pathology. The findings of Raz et al. (2008) do not necessarily imply that neurobiological aging
in the brain drives cognitive changes. The morphological changes in the brain can also be caused by disease, such as
cardiovascular disease and dementia. Sliwinski et al. (2003) conducted a fascinating study in this regard, using data
from the Bronx Longitudinal Study (Sliwinski & Buschke, 2004). The study involved a prospective design of the
incidence of dementing illnesses in a nondemented control group collected as part of a larger study of Alzheimer’s
disease and related disorders. Individuals in this group were measured cognitively at regular intervals, but they were
also assessed for dementia. Over time some of the participants were clinically diagnosed as having dementia, and
this allowed Sliwinski and colleagues to compare cognitive change in the preclinical phase with change in those
individuals who did not convert to dementia. As might be expected, individuals who had not yet been diagnosed
with dementia (but undoubtedly had contracted the disease) showed greater change in episodic memory during their
preclinical phase, compared to individuals who did not later receive a dementia diagnosis. Even more interesting,
however, was the fact that the aggregate control sample manifested individual differences in cognitive change, as
well as correlations of changes across cognitive variables. However, the magnitude of individual differences was
reduced by controlling on later dementia diagnosis, as were the correlations of change among different variables.
Furthermore, within the dementia group, organizing the time scale by point of diagnosis rather than chronological
age eliminated the individual differences in rates of cognitive change. What does this pattern imply? It would appear
that in this sample, the presence of preclinical dementia was a major source of individual differences in change.
Because people vary in the age at which the disease is contracted and later diagnosed, organizing the data by age
(without knowledge of the disease and its progression) produces larger individual differences in rates of change.
Given that other prospective studies of Alzheimer’s disease, vascular dementia, and other dementing illnesses
indicate a fairly long preclinical period in which cognition may be affected (e.g., B¨ackman & Small, 2007), it
would appear that a major influence on individual differences in cognitive change in old age is the presence or
absence of dementia. Furthermore, a number of studies have directly linked magnitudes of longitudinal changes in
cognitive abilities to different kinds of disease, including cardiovascular and cerebrovascular disease, late-onset
diabetes, and their precursors, or risk factors, such as obesity, hypertension, poor cholesterol profiles, and the like
(Spiro & Brady, 2008).

Disease and terminal decline. A focus on disease effects on cognition raises an additional set of important questions
about aging and intellectual development. To what extent are the average curves for cognitive abilities and age
misleading, in the sense that they are not representative of the actual developmental trajectories of individuals?
Means, even if generated from longitudinal data, are simply best guesses as to the level of function, on average, at a
particular age. We link the means of different ages with a line (or fit a curve to the data), but this does not imply that
the developmental pathways of individuals have the shape implied by the shape of the aggregate mean curve. The
population of adults might be quite heterogeneous in nature, with the major changes in psychological functioning,
including cognition, occurring during a period of decline preceding death (e.g., Berg, 1996; Bosworth, Schaie, &
Willis, 1999). Indeed, time to death may be a more important way of indexing cognitive loss in old age than
chronological age (Singer et al. 2003). Some new and impressive data on this score come from models of
longitudinal data that jointly use time to death and age to organize the data (Ram et al., 2010). The modeling
approach is fairly complex, requiring estimation of a change point (Hall, Sliwinski, Stewart, & Lipton, 2000), at
which the slope of decline prior to a change point is lower than the slope immediately prior to death. Thorvaldsson
et al. (2008) used this method to demonstrate accelerated cognitive decline occurring about seven years before death
in the Swedish Goteborg Longitudinal Study data. Wilson, Beck, Bienias, and Bennett (2007) found evidence for a
shorter period of terminal decline of about four years. Terminal decline was associated with the apolipoprotein E ε4
allele, a genetic polymorphism thought to be associated with risk for Alzheimer’s disease (AD). Laukka,
MacDonald, and Backman (2008) also concluded that a substantial proportion of the variance in terminal cognitive
decline might be due to emergence of dementia, but there was evidence of decline in individuals who did not
develop AD. Undoubtedly future research will clarify the extent to which other disease factors play a role in
terminal cognitive decline, including vascular disease and organ failure (e.g., renal dysfunction, see Buchman et al.,
2009). In light of the evidence for terminal decline effects, the possibility exists that the curvilinear age trends for
cognitive function in late life are actually an artifact of aggregation over individuals with different functions. This
idea was nicely illustrated by Baltes and Labouvie (1973), who showed that a combination of (1) a change point
function of stable level of cognition, followed by terminal decline, and (2) a variable onset of the terminal decline
that was correlated with advancing age could produce aggregate curvilinear functions that did not capture the
functional form of individual change (see Figure 9.2). The aggregate function could be influenced by the increasing
risk of terminal decline, with its curvature reflecting an averaging of persons in terminal decline with persons who
are still stable.

Exercise and an engaged life style. A critical question regarding adult intellectual development is whether health-
promoting behaviors such as exercise, nutrition, and an active lifestyle promote better developmental outcomes
(Hertzog, Kramer, Wilson, & Lindenberger, 2009). Over the last decade, compelling evidence has emerged that
aerobic exercise in middle age and old age promotes enhanced cognitive function in older adults. Colcombe and
Kramer’s (2003) metaanalysis evaluated aerobic exercise intervention studies in older adults and compared exercise
groups’ cognitive performance to performance in a groups doing toning and stretching only. Short-term aerobic
exercise resulted in substantial improvements in tasks assessing executive functioning and controlled attention
(domains highly correlated with fluid intelligence; Salthouse et al., 2008). The data are broadly consistent with
cross-sectional studies suggesting an association of self-reported exercise with human abilities (e.g., Eggermont et
al., 2009), but the intervention effects help to argue for a causal influence of exercise on cognition. Unfortunately,
there are at present no longitudinal studies that contrast longer term adherence with exercise regimens and degree of
cognitive change in adulthood. Does engaging in intellectually stimulating activities also promote better cognitive
outcomes? Salthouse (2006) expressed skepticism on this score, given that his cross-sectional data on self-reported
activities have failed to observe age X activity interactions (see Hertzog et al., 2009, for a critique of this argument).
Certainly, simple cross-sectional correlations of activities and intelligence are insufficient grounds for arguing that
activities help preserve cognitive functioning, because individuals with high intelligence tend to manifest higher
levels of intellectual engagement in early adulthood (Ackerman & Heggestad, 1997). However, longitudinal
evidence is needed, given the potential lack of sensitivity of cross-sectional data to change alluded to earlier.
Longitudinal studies have often found relationships of self-reported intellectual engagement with cognition (e.g.,
Schooler, Mulatu, & Oates, 1999; Wilson et al., 2003; see Hertzog et al., 2009 for a review). However, as noted by
Hultsch, Hertzog, Small, and Dixon (1999), longitudinal correlations of activities with cognitive change could still
be due to latelife cognitive changes leading to curtailed activity (MacKinnon et al., 2003). There are fewer
intervention studies with activities, but there is at least some indication that encouraging older adults to engage in
stimulating activities may have cognitive benefits (Carlson et al., 2009; Stine-Morrow et al., 2007; Tranter &
Koutstaal, 2008). In one recent study, participation in a complex videogame environment led to short-term
improvements in attentional control and executive function (Basak, Boot, Voss, &Kramer, 2008). This outcome is
consistent with intervention studies that target executive control (Hertzog et al., 2009), producing more transfer of
training than is typically observed when training focuses on teaching specific processing strategies (e.g., Ball et al.,
2002). The evidence favors an impact of activities on cognitive function, but there is still some disagreement and
controversy on this point.

Functional Aspects of Adult Intelligence

Given that there are, on average, adult age changes in cognitive abilities, what are the practical consequences of
these changes? Evidence is beginning to emerge that there are fewer practical implications for cognitive functioning
in everyday life than some might have supposed. For example, older workers, even those with intellectually
demanding jobs, function well on the job even into old age (e.g., Ng & Feldman, 2008). Work by Colonia-Willner
(1998) may suggest a reason for this maintenance; experience on the job (which correlates with age) brings with it
increases in tacit knowledge (Cianciolo et al., 2006) about how to perform effectively on the job. Colonia-Willner
studied bankers of different ages in Brazil. Although her crosssectional sample showed typical age differences in
fluid intelligence, expert ratings of tacit knowledge about hypothetical banking situations indicated age-related
improvements in this domain. Such effects can be observed in intellectually demanding game situations as well.
Masunaga and Horn (2001) studied the relationship of fluid intelligence to performance on the Japanese game of
Go, a cognitively demanding task with some resemblance to chess. Go performance was less correlated with
standard measures of fluid intelligence and working memory than with measures of reasoning that directly
represented reasoning about Go moves. In a similar vein, Charness and colleagues have demonstrated good memory
retention for chess positions by older chess experts, relative to their impaired episodic memory for chess pieces
placed in random positions on the chess board (e.g., Charness, 1981). Hershey, Jacobs-Lawson, and Walsh (2003)
reported sound simulated financial decision making by older adults who had prior experience in investing or gained
it through structured task experience. Performance in familiar environmental contexts is associated with beneficial
effects of pragmatic knowledge about typical scripts and scenarios, common decisions and choice points, and intact
access to effective strategies for performance that help older adults preserve effective cognitive functioning, even in
the face of decline in fluid ability (Hertzog, 2008). Older adults may also be effective at using strategies that
enhance cognition in everyday life, such as through the use of external aids or behavioral routines that support
timely remembering of what to do and when to do it. For instance, older adults are sometimes better at remembering
to take medications than middle-aged and younger adults, despite age deficits in standard tests of reasoning and
episodic memory (Park et al., 1999). In general, older adults do well in everyday prospective memory tasks relative
to laboratory tasks (Phillips, Henry, & Martin, 2008), probably because of a more active use of strategies to promote
remembering.
Conclusions
The study of adult cognitive and intellectual development is entering a vibrant new phase, one in which the advances
in statistical methods for modeling individual differences are being integrated with designs and measures that permit
a subtle understanding of individual differences in cognitive change. The next decades are likely to see an expanded
understanding of how social and psychological forces interact with biological and genetic influences to shape
individual trajectories of adult cognitive development, at the level of both brain structure and behavior.