Abstract
Purpose of Review The article discusses the two most significant modifiable risk factors for dementia, namely, physical
inactivity and lack of stimulating cognitive activity, and their
effects on developing cognitive reserve.
Recent Findings Both of these leisure-time activities were associated with significant reductions in the risk of dementia in
longitudinal studies. In addition, physical activity, particularly
aerobic exercise, is associated with less age-related gray and
white matter loss and with less neurotoxic factors. On the
other hand, cognitive training studies suggest that training
for executive functions (e.g., working memory) improves prefrontal network efficiency, which provides support to brain
functioning in the face of cognitive decline.
Summary While physical activity preserves neuronal structural integrity and brain volume (hardware), cognitive activity
strengthens the functioning and plasticity of neural circuits
(software), thus supporting cognitive reserve in different
ways. Future research should examine whether lifestyle interventions incorporating these two domains can reduce incident
dementia.
Keywords Dementia . Cognitive reserve . Physical activity .
Cognitive activity
Introduction
As the human race celebrates rising longevity, societies have
to confront changing disease profiles. One condition that will
become more and more common is dementia (i.e., major
neurocognitive disorder). Dementia is not a disease in itself;
it is an umbrella term for a myriad of diseases causing cognitive impairment, of which Alzheimer’s disease (AD) is the
most common form. The prevalence rate of dementia doubles
approximately every 6 years from the age of 65 years,
reaching 7 % in those aged 75–79 years, 12 % in those aged
80–84 years, 20 % in those aged 85–89 years, and 40 % in
those aged 90 years or over [1]. Because of population aging,
there is increasing interest in studying the aging brain.
Dementia is the consequence of three processes. The first
of these processes is age-related, or “normal,” cognitive decline. Studies have found that most cognitive functions decline since early adulthood, and the areas affected most are
those that rely on mental speed, volume of processing, and
coordination efficiency, such as attention, working memory,
verbal recall, reasoning, multitasking, task switching, and response inhibition [2, 3]. Knowledge of the world, people,
events, and vocabulary, on the contrary, tends to be well preserved [4].
Parallel to these performance declines is a gradual loss of
brain mass throughout adulthood. Certain cortical and
subcortial regions involved in cognition are particularly susceptible to gray matter loss over time, including the hippocampus, caudate nucleus, putamen, and prefrontal cortex [5, 6].
Furthermore, white matter changes and injuries become prevalent after late midlife, with white matter volume declining
most noticeably in the prefrontal region [5, 7]. The compromised integrity of the white matter tracts affects the connectivity between brain regions, leading to less efficient
networks.
This article is part of the Topical Collection on Geriatric Disorders
* Sheung-Tak Cheng
takcheng@eduhk.hk; s.cheng@uea.ac.uk
1 Department of Health and Physical Education, The Education
University of Hong Kong, 10 Lo Ping Road, Tai Po, N.T., Hong
Kong
2 Department of Clinical Psychology, Norwich Medical School,
University of East Anglia, Norfolk NR4 7TJ,

The second one is a process of pathological changes
brought on by neurological diseases, leading to accelerated
cognitive decline. Take AD as an example. Advances in
in vivo imaging and cerebrospinal fluid (CSF) testing have
opened the window for identifying the presence of betaamyloid fibrils and plaques two decades or more before symptom onset [8]. Although whether it is appropriate or ethical to
diagnose AD in the preclinical phase without effective treatment for it is a matter of debate [9], the newer research findings suggest that the brains of people with AD may be coping
with the disease’s assault many years before daily functioning
starts to suffer. In the preclinical phase, the person appears
normal because the brain recruits additional resources to cope
with injuries to networks. This leads us to the next factor and
the focus of this article—the brain’s ability to redirect its
resources.
Cognitive Reserve
Cognitive reserve is a hypothetical construct that moderates
the effects of age-related decline and pathological damage
[10]. It refers to structural and dynamic capacities of the brain
that buffer against atrophies and lesions. Tissue or functional
loss at a particular brain region may be compensated by other
neurons working harder in order to maintain the same level of
functioning as much as possible. This compensation may happen at the “local” level, in the sense that the neighboring
neurons make up for the lost neural activity from regional
damage. Called “brain reserve” by some scholars [10], this
type of volumetric reserve is also referred to as a passive or
static model of cognitive reserve.
However, when the number of healthy or functional neurons fall below a certain threshold vis-à-vis task demands, the
brain may recruit other regions and networks to help in order
to maintain performance. This functional re-routing of neural
circuits represents an active or dynamic model of reserve.
Studies utilizing functional magnetic resonance imaging
(fMRI) techniques have shown predominantly increased prefrontal, task-based activation in healthy older adults as well as
those with mild cognitive impairment (MCI; i.e., minor
neurocognitive disorder) and early dementia [11–13]. These
over activations in the prefrontal cortex (and, sometimes, other cortices as well) are often bilateral to increase the output.
They play compensatory functions because they are associated with the following: (a) under activations in posterior regions such as medial temporal lobe, precuneus, and visual
cortex; (b) the inability to suppress the default mode network;
and (c) improved performance across a range of tasks, including working memory, episodic memory, inhibitory control,
semantic processing, processing speed, and visual perception
[14]. In fact, younger adults also display similar activation
patterns when cognitively overloaded. The default mode
network, consisting of midline structures from the posterior
cingulate/precuneus to the anterior cingulate/medial prefrontal
cortex, as well as certain lateral parietal areas, is activated
while the brain is not focused on external stimuli and tasks
(e.g., during mind wandering or thinking about past and future) but is deactivated when it is [15, 16]. With age, the brain
is less capable of suppressing the default mode network during
task situations, thus interfering with task performance with
irrelevant stimuli.
All of the age-related brain deteriorations mentioned
above, including gray matter and white matter loss, and less
efficient/functional networks are more pronounced in people
who are on the way to developing cognitive impairment
[17–19]. However, there is substantial heterogeneity in the
clinical manifestation of dementia in individuals with similar
degrees of brain pathology, which is presumably related to
inter-individual differences in cognitive reserve. Cognitive reserve cannot be observed or directly measured, and proxy
measures such as education, premorbid intelligence (IQ), linguistic ability, and occupational complexity are often used.
Indeed, studies have found that cognitive reserve moderates
the relationship between neuropathology and clinical status.
A study of 323 cognitively healthy adults found that lifetime
occupational complexity (e.g., whether synthesizing and analyzing data, supervising and mentoring colleagues, and setting
up and operating precise instruments), averaged up to three jobs
and weighted by years on the job, was associated with more
hippocampal and whole brain atrophy, after controlling for
global cognition, apolipoprotein E ε4 (APOE4) status, and cardiovascular risk factors [20]. Another analysis from the same
sample showed that educational level attenuated the age trend
in CSF biomarkers of AD such that those with higher (especially university) education had lower tau concentrations and
tau/Aβ42 ratios in the CSF [21]. Another study following 245
adults for an average of 11 years operationalized cognitive
reserve in terms of reading level, vocabulary, and years of education combined. Interestingly, the researchers found that the
left entorhinal cortex volume at baseline predicted time to MCI
symptom onset in those with low cognitive reserve only, controlling for baseline cognitive reserve and APOE status.
Among those with high cognitive reserve, there was no connection between the degree of entorhinal atrophy and time to
symptom onset [22•]. Similarly, in a large study involving 2400
individuals, an additional year of education was associated with
a 13–18 % reduction in the likelihood of receiving a diagnosis
of AD at the clinical examination most proximal to, and within
1 year of, death, after controlling for neuropathology examined
at autopsy (e.g., the extent of plagues and/or tangles) and history of stroke [23]. This condition is sometimes referred to as
Alzheimer’s disease without dementia, as the individual has the
pathological condition indicative of AD but is either asymptomatic or has borderline symptoms that do not cross the
threshold for clinical diagnosis.

Cognitive reserve is hypothesized to empower the brain to
tolerate atrophies and insults and, as a result, delay symptom
onset. At the same time, because the brain is more compromised by the time that symptoms appear, those with higher
cognitive reserve tend to experience a more rapid course of
decline afterward. At this point, there is no evidence that cognitive reserve would postpone mortality [24, 25], and hence, a
pattern consistent with compression of morbidity is expected
[26]. To what extent a high cognitive reserve would delay
symptom onset is not at all clear, but any noticeable delay,
be it 1 or 2 years, would translate into tremendous public
health benefits by reducing the prevalence of dementia.
While characteristics such as education and intelligence are
relatively stable since young adulthood, there is increasing
interest in the role of leisure activities in building up cognitive
reserve, which will be the focus of this article. The emphasis
will be on physical and cognitive activities as these have received the strongest support in the literature in terms of the
prevention of dementia. The hypothesis proposed is that physical (especially aerobic) exercise and cognitive activity work
together to protect brain health in general, thus reducing the
loss of brain mass with age and strengthening compensatory
circuits primarily through enhancing executive function.
Physical Activity
A recent analysis examined the relative contributions of seven
potentially modifiable risk factors (i.e., diabetes mellitus, midlife hypertension, midlife obesity, depression, physical inactivity, smoking, and low education) to AD disease burden.
Diet was excluded because of the difficulty in aggregating
data from diverse dietary factors. Physical inactivity was defined as not doing 20 min of vigorous activity for at least
3 days per week or 30 min of moderate activity for at least
5 days per week. Low educational attainment was defined as
having lower secondary education or less. By calculating the
population attributable risks, the authors estimated that, for the
world as a whole, low education and physical inactivity were
the two most important modifiable risk factors, accounting for
19 and 13 % of AD prevalence, respectively, or nearly 11
million cases combined in 2010. The contribution of low education was not as pronounced in the developed regions such
as the USA and Europe, where physical inactivity accounted
for over 20 % of the prevalence [27••].
Longitudinal studies controlling for risk factors such as
lipids, hypertension, diabetes, obesity, history of stroke, depression, smoking, educational level, APOE status, and so on
generally confirm the importance of physical activity in reducing dementia risk [28]. For instance, in a study of 2492 older
Germans, engagement in any additional physical activity on a
regular basis was associated with a 20 % risk reduction in
terms of dementia onset over the next 4.5 years. No effect
was found for cognitive activities [29]. Such medium
follow-up interval is typical in this literature, but a longer
interval would be needed to examine the long-term effects of
physical activity as a potential preventive agent. A study of
803 older adults residing in a suburban area of Japan found
that those with self-reported leisure-time physical activity of at
least 1 day per week had a 41 % reduction in the risk of
developing AD (but not other types of dementia) over the next
12 years, compared with those who were less active. Other
types of physical activity, such as household chores, were not
examined in this study [30]. That any physical activity, when
compared with a sedentary lifestyle, could reduce the odds of
dementia or dementia-related mortality also received support
from other longitudinal studies of older adults [31–33]. The
magnitude of risk reduction reported in the Japanese study
was consistent with the effect size found in a recent metaanalysis of nine other studies [34].
It is not difficult to understand why light physical activity
would be beneficial for older adults. Yet, even physical activity of suboptimal amount and intensity at midlife appears to be
similarly beneficial. A study following over 1200 Swedish
adults for 21 years found that engaging in leisure-time physical activities of moderate intensity for at least twice a week at
midlife was associated with a 53 and 65 % reduced chance of
developing all-cause dementia and AD, respectively, in old
age, compared with less frequent activities [35]. While studies
tend to use the amount/intensity of physical activity at one
point in time as the predictor of future dementia risk, the
implicit assumption is that this one-time measure reflects a
more stable habit. Indeed, studies have also found that an
increase or decrease of physical activity over time changes
the odds of getting dementia in the expected direction [36•,
37].
Longitudinal studies, however, do not prove causality.
Those with an underlying disease process, though not yet
diagnosable with dementia, may start reducing activity long
before symptom onset. Randomized controlled trials (RCTs)
are needed to demonstrate causality. However, the follow-up
intervals in RCTs are usually not long enough to make any
meaningful assessment of potential effects on dementia incidence. One study has attempted to address this question.
Three hundred eighty-nine Hong Kong older adults with
MCI were randomized to a Tai Chi group and a toning and
stretching exercise group (control). Tai Chi, a mind-body exercise, also has an aerobic component and improves cardiorespiratory fitness [60]. After some initial training, participants
were instructed to continue practicing the exercise at least
three times a week, each for a minimum of 30 min, for a total
of 12 months from the start of intervention. Experimental
effect in terms of conversion to dementia was found for the
54 and 78 % of the Tai Chi and control participants, respectively, who adhered to the regime throughout, but not for the
whole sample (note the higher attrition in the former). Among

these completers, 4 and 17 % of the Tai Chi and the control
group, respectively, progressed to dementia by the end of the
year, representing an 80 % risk reduction in multivariate
models [38]. However, because of differential attrition rates
between the two groups and because of a lack of treatment
effect in the intent-to-treat analysis, the results have to be
taken with caution.
Why should physical activity work in reducing the risk of
dementia? It is likely that physical activity protects brain
health via a number of pathways. Although the benefits of
exercise have primarily been demonstrated in animal studies
previously, more recent studies, including RCTs, have been
able to replicate these findings in humans [39, 40]. In a nutshell, physical activity protects brain health and fuels
neuroplasticity by reducing the likelihood of vascular diseases
and improving cerebral perfusion (e.g., plaque deposits in arteries, atherosclerosis, hypertension, and stroke) [41–47], improves respiratory function [48], stimulates growth factors
particularly brain-derived neurotrophic factor (BDNF) and
insulin-like growth factor-1 [49–52], and downregulates oxidative stress and inflammatory responses [43, 44, 53]. It also
reduces the brain’s exposure to neurotoxic factors, including
beta-amyloid and excessive glucose [41, 54–56]. For these
reasons, it is no wonder that the cognitive benefits of physical
activity appear to be limited to aerobic exercise [57–59]. At the
same time, it is important to note that many physical activities
also have mental stimulation properties such as those that
require eye-hand coordination and visuospatial memory, thus
further augmenting their effects on cognitive functioning.
The association between physical activity and amyloid burden in the brain deserves special attention because of the latter’s significance for AD pathology. A few studies have demonstrated, on a cross-sectional basis, a negative association
between physical activity level and beta-amyloid load in the
brain, whether measured by Pittsburgh Compound B (PIB)
positron emission tomography (PET) or CSF analysis, in older
adults, although this association was not consistently found
[61]. Liang and colleagues reported that cognitively intact
older adults who performed 30 min of moderately intense
exercise for at least 5 days a week had lower PIB uptake or
higher levels of CSF Aβ42 (i.e., more amyloid clearance from
the brain), compared with less active individuals; however, no
relationship between physical activity and CSF tau was found
after controlling for cardiovascular risk factors, APOE4 status,
and depressive symptoms [54]. Brown and colleagues found
that a relationship between high levels of physical activity and
reduced PIB uptake existed even among physically active, but
APOE4-positive, individuals [55]. However, these crosssectional relationships are difficult to interpret because a lack
of, or decrease in, activity may be the result of brain changes.
Without longitudinal studies, it is difficult to judge whether
physical activity actually downregulates beta-amyloid production, especially in at-risk individuals.
Despite certain ambiguities in the state of the field, the
broader picture remains supportive of the neuroprotective effects of physical activity. Importantly, the improvements in
cognition attributable to physical exercise appear to be mediated by gains in brain volume and network connectivity [46],
which in turn are partially mediated by increases in perfusion
and growth factors [46, 47, 52, 62]. Two recent systematic
reviews support the positive effects of long-term physical activity on white matter volume and white matter integrity [63]
as well as gray matter volume [64], although the effects on the
former were small and inconsistent. For instance, one RCT
reported no improvements in white matter integrity in older
adults after a 1-year walking exercise intervention, compared
with those having stretching exercise; both groups had three
40-min sessions per week led by an exercise trainer. However,
gains in cardiorespiratory fitness in terms of maximal oxygen
consumption (VO2 max) in the walking group were moderately correlated with white matter integrity (as measured by
fractional anisotropy from diffusion tensor imaging) in the
frontal and temporal lobes.
The benefit of physical activity on slowing age-related decline in gray matter is not limited to cognitively healthy adults
but exists for those with MCI or dementia as well [65, 66].
Thus, it is never too late to increase physical activity. The
hippocampal volume and its relationship to long-term physical activity have been a subject of much research interest partly because of neurogenesis in the dentate gyrus section
throughout adulthood [67] and partly because hippocampal
atrophy is one of the hallmarks of early AD. An RCT comparing moderate-intensity aerobic exercise with stretching and
toning exercise of 1-year duration, 3 days a week, reported a
2 % increase in bilateral hippocampal volume in the former,
versus a 1.4 % decrease in the latter, representing a 1–2-year
reverse in age-related decline in hippocampal volume.
Furthermore, the increase in hippocampal volume in the aerobic exercise group was associated with changes in VO2 max
and serum BDNF [62]. Other studies have found positive
effects on brain regions other than the hippocampus. In another RCT, older adults who participated in exercise interventions
for 6 months showed increases in physical activity, which in
turn was correlated with increased gray matter volume in the
prefrontal and the cingulate cortex, compared with those without intervention [68]. Another intervention study suggested
that the effects of aerobic exercise on gray and white matter
volumes may be specific to older, but not younger, adults [69].
Erickson and colleagues suggest that the main neurological
benefit of physical activity is the preservation of neurons and
synapses in areas where age-related atrophy is most apparent,
namely, the prefrontal cortex and the hippocampus [64].
Nevertheless, this body of literature is mostly correlational,
and only a handful of studies have employed longitudinal or
experimental designs. Despite such a limitation, these neurological findings corroborate the results of RCTs of cognitive

outcomes. Although the overall effect sizes tend to be small,
executive functions, attention, processing speed, and memory
are the cognitive domains most responsive to physical activity
interventions [51, 70, 71]. These domains happen to correspond well with the same brain regions where volumetric
advantages associated with physical exercise have been found
[64].
The effect on executive function is noteworthy as those
with poor executive function, probably because of deficits in
goal-directed behavior, performance monitoring, and inhibition of prepotent responses, tend to reduce physical activity
over time, leading to a vicious cycle [72]. In an RCT comparing a 1-year resistance training program to a balance and toning control in older women, the long-term maintenance of
physical activity, up to 1 year post-intervention, was predicted
by gains in executive function during the intervention [73].
Cognitive Activity
The London taxi driver study showing that taxi drivers (who
had to navigate through the streets of London purely from
memory, per license requirements) had larger posterior hippocampus than bus drivers (who drove fixed routes) [74] was
seminal in suggesting the effect of cognitive activity on
neurogenesis in the hippocampus. Yet, experimental studies
in humans are few. An exception was a recent study comparing a virtual-reality spatial-navigation training, conducted every other day over a 4-month period, with a leisure walking
exercise on treadmill as control. Results showed maintenance
of hippocampal volume for up to 4 months after the training
for both older and younger adults who were in the navigation
training group, compared to a decline in hippocampal volume
in the walking group [75].
A prospective study showed a moderate correlation between engagement in complex mental activities and both volume and reduced atrophy rate of the hippocampus after
3 years. However, only 37 older adults were included in the
study [76]. On the other hand, there was no correlation between past cognitive activity, measured retrospectively, and
gray and white matter volumes in a large sample of older
women (N = 393) [77].
Other studies attempted to study the relationship of cognitive activity with AD biomarkers. In an interesting study [78],
65 cognitively intact adults provided data on current cognitive
activity as well as cognitive activity at 6, 12, 18, and 40 years
old on a retrospective basis. Only past cognitive activity
summed across the previous ages was correlated inversely
with PIB retention. Physical activity as measured by calorie
consumption in a recent 2-week period was also negatively
correlated with PIB retention, but the correlation disappeared
after controlling for past cognitive activity. Moreover, when
these cognitively healthy participants were divided into
tertiles according to past cognitive activity, the least active
ones had beta-amyloid levels similar to that of ten agematched participants with AD, whereas those most active
had levels similar to that of 11 young adults. Although it is
tempting to read the data as supporting the protective role of
lifetime cognitive activity, the data are actually difficult to
interpret as the inactive individuals were asymptomatic at similar amyloid levels to those with AD. The data may be
interpreted as low cognitive activity being protective as the
higher amyloid burden in these individuals did not cause
symptoms, unless there were longitudinal data showing that
these individuals were on an impending decline into dementia.
In addition, a study of 186 older adults did not find any correlation between past/current cognitive activity and a number
of biomarkers, including PIB uptake, glucose metabolism
(fluorodeoxyglucose PET), and hippocampal volume [79],
while another study of 118 older adults found that lifetime
cognitive activity was associated with less PIB uptake in
APOE4 carriers [80].
At best, the available evidence is mixed and inconclusive as
to whether cognitive activity has direct impacts on brain structure and physiology. One difficulty with this line of research is
accounting for the variety of cognitive activities and the relationship of each activity to neuropathology. For instance, while
challenging spatial navigation conducted frequently enough
(e.g., what London taxi drivers do on a daily basis) may stimulate noticeable neurogenesis in the hippocampus, we are not
entirely sure what playing chess would do to the brain.
Moreover, activities cross domains; that is, many cognitive
activities have social components (e.g., playing bridge), and
there is no easy way to separate the effects of the different
components (the same may be said of physical exercises with
mentally stimulating properties). For example, Leung and colleagues classified the following as primarily cognitive activities: reading, using computer, board/card games, mahjong, participating in forums or discussions, writing, calligraphy and
painting, handicraft, playing musical instruments, investment
in stock market, and gambling [81]. Not every researcher
would agree with this list; unfortunately, there is not a standard
list of activities to use in research (some studies include singing,
going to museum, etc.). In any case, the point is that the list
includes activities of quite a diverse nature in terms of their
mental stimulation properties. Researchers typically ask respondents to indicate the frequency of engaging in each activity
and then sum the ratings up to form a total activity score. But,
since the mental stimulation property of each activity is not the
same, much noise is introduced into the measure with people
who have the same score but very different degrees and types
of mental stimulation in everyday life. Passive cognitive activities, such as watching television, appear not to be helpful.
Studies have actually shown watching television to increase
the odds of dementia and mortality [82–84], partly because
those who watch television a lot tend to be sedentary

In addition, while there are established ways to rate or
define the intensity of physical activity, no such methods exist
for cognitive activity. What constitutes moderate- or highintensity cognitive activity, for example? Thus, when there is
a negative finding between cognitive activity and brain measures, it is not sure whether the wrong measure of cognitive
activity was used or whether the nil finding should have been
expected.
Despite the fact that there exists no strong evidence of
cognitive activity on brain health, cognitive activity is often
found, in large-scale longitudinal surveys, to be a stronger,
even the sole, predictor of cognitive decline and incident dementia when compared with physical and social activity [81,
85–88], although there are exceptions [89–91]. As individuals
who are physically active also tend to be intellectually active
[92], the effect of physical activity may be difficult to parse
out from the effect of cognitive activity. Typically, a high level
of cognitive activity is associated with a roughly 50 % reduction in the risk of developing dementia in the next 4–5 years,
after controlling for APOE4 status, cardiovascular risk factors,
educational level, and so on. These findings are consistent
with studies suggesting that for those who subsequently develop dementia, a high level of premorbid cognitive activity is
associated with delayed symptom onset, followed by an accelerated course of decline [93–95], as is predicted by the
cognitive reserve hypothesis. Such a relationship has not been
observed for physical activity [94].
Despite these research findings, it would be premature to
conclude that cognitive activity is necessarily more important
than physical activity. A recent study followed 864 older
adults over 6 years. Participants were divided into four groups
based on a median split on the frequency of habitual cognitive
activity and whether the participant obtained moderateintensity exercise from everyday activities. Those with low
cognitive activity and without moderately intense physical
activity were the reference group. The results showed that
those without physical activity, despite being high in cognitive
activity, did not differ from the reference group in terms of the
odds of incident MCI during the follow-up period. But,
among those with any physical activity, the odds were lower,
being 48 % lower in those with low cognitive activity and
80 % lower in those with high cognitive activity [91]. The
data suggest that physical activity is essential, while cognitive
activity adds further benefits. More research is needed to replicate this finding.
Again, RCTs are needed to ascertain causality. However,
RCTs of cognitive leisure activity are difficult to do. It is
difficult to pick one leisure activity (or several ones forming
a package) among such a wide variety that would appeal to,
and be maintained by, study participants who had been “inactive cognitively.” And, it would be unrealistic to do an RCT
for every single activity (e.g., chess, crossword puzzle). While
inactivity at baseline is an ideal precondition for testing the
effect of adding activity to participants’ lives, exactly what
constitutes cognitive inactivity is not clear. To date, RCTs on
cognitive leisure activity have been limited to samples with
cognitive impairment only [96, 97]. And, there is some evidence that mahjong can modulate the trajectory of decline in
people with mild-to-moderate dementia in the medium term,
as evidenced in the maintenance of Mini-Mental State
Examination and a slower rate of increase in the Clinical
Dementia Rating Sum-of-Box score up to 9 months from
baseline [98•, 99].
It should be noted that the protective effect of cognitive
activity may be disguised under other names in the literature.
For instance, low educational level accounts for more AD
cases worldwide than physical inactivity [27]. While advanced educational attainment is considered a proxy of cognitive reserve, it probably derives its benefits from enabling a
lifetime of higher-level cognitive activity [25, 93], partly via
holding cognitively stimulating jobs [100]. An occupation
with complex duties may be characterized as an enriched environment for cognitive stimulation on a day-to-day basis.
Another related topic concerns whether speaking more than
one language protects one against dementia, and the research
evidence to date is mixed [101–103]. Gold’s review [104]
suggests that the benefits of lifelong bilingualism appear not
to be related to the possession of another language per se. The
benefits are more likely due to the neural effects of switching
between languages and inhibiting one while using the other.
Frequent engagement in this activity leads to reduced neural
costs (i.e., requiring less efforts, as evidenced by lower activation in the prefrontal executive control circuitry) in mental
switching that are generalized to non-language domains. In
this sense, speaking more than one language in daily life
(but not simply acquiring another language) is an intellectual
activity that strengthens executive control.
The review so far has focused on leisure activities that are
cognitively stimulating. As leisure, these cognitive activities
have the properties of being interesting, pleasant, and motivating to the individual and are therefore more likely to be
sustained over time [97, 105]. Group activities facilitate social
integration, which may also be cognitively protective [90,
106]. Moreover, picking up abandoned hobbies again may
bring back memories of old times when the activities were
enjoyed together with family and friends, making these activities more stimulating (the same may be said of other kinds of
activities).
While the exact neurocognitive effects of many leisure activities are not known, there are plenty of cognitive training
programs tailor-made to stimulate specific functions or abilities, such as memory, attention, speed of processing, and executive function. This is a large body of literature that will not
be reviewed here in detail, and readers are referred to other
expert reviews [107, 108], including Gates’ article earlier in
this journal [109]. Typically, cognitively healthy older adults,

after training, can behave like younger adults at baseline
(without training), although the training effects are noticeably
weaker in those with cognitive impairment. Owing to the
growing interest in this area, some researchers have attempted
to evaluate the relative effects of cognitive training and physical exercise, and the results tend to suggest that adding physical exercise to cognitive training does not yield additional
cognitive benefits [96, 110, 111], suggesting a possible ceiling
effect in these interventions.
Also echoing the above observation are preliminary results
from the Finnish Geriatric Intervention Study to Prevent
Cognitive Impairment and Disability (FINGER), a largescale RCT combining dietary regime, physical exercise, and
cognitive training in a sample of about 1200 adults aged 60–
77 years at baseline. Those in the control group received regular health advice. Both intervention and control participants
showed improvements in global cognition as measured by a
comprehensive neuropsychological battery, with a larger improvement in the former equivalent to a 0.02 SD differential in
the first year and a 0.04 SD differential in the second year.
When subcomponents of the battery were analyzed separately,
significant treatment effects were found for executive function
and processing speed, but not for memory [112••]. Overall, the
effect size was very small, suggesting that there may be a
ceiling effect for lifestyle interventions and that the effects of
components do not necessarily add up.
A long-standing issue with cognitive training is the lack of
transfer to untrained tasks (i.e., tasks that were not directly
trained), though tasks that are more similar to the trained ones
have more success. The lack of “far and broad transfer” (e.g.,
from memory training to gains in verbal reasoning) means that
the gains in training would not lead to meaningful improvements in everyday functioning, and so, they were of limited
relevance to people’s lives. Moreover, many cognitive training
programs, by virtue of the stimuli used or the repetition of the
same stimuli over time, fail to capture people’s attention for
long periods or to maintain their interest and motivation in the
long run. Thus, these programs tend to lack ecological value.
In addition, for older adults with relatively limited cognitive
resources, let alone those with cognitive impairment, learning
a novel intellectual exercise may prove to be difficult [113].
An emerging view is that many of these training programs
may have targeted the wrong domains. In particular, the early
focus on memory and memory strategy training (e.g., using
visualization techniques as memory aids) has produced disappointing results in relation to transfer [107, 108]. More recently, there has been growing interest in the efficacy of working
memory training (i.e., exercises that require holding and manipulating information mentally for brief periods). The rationale is that with age, many performance issues, including
reasoning, mental switching, multitasking, and decision making, have deficits in working memory in common. While researchers have attempted to summarize the effects using metaanalyses, the results appear to be very sensitive to which studies were included and the way that the data were coded, leading to conclusions that working memory training has small
far-transfer effects equivalent to a 0.20 SD between intervention and control participants [114, 115], as well as nil effects
[116]. Another meta-analysis of computerized training programs found no effect of working memory training on untrained domains [117].
The meta-analysis by Karbach and Verhaegen [114] also
included a separate analysis of studies training executive control processes, including speed of processing, task switching,
updating, and inhibitory control, based on studies listed in
PsycINFO and PsycARTICLES only (a potential flaw).
They found slightly smaller far-transfer effects pooled across
these training programs than that found for working memory
training, but the difference in effect size did not reach statistical significance.
More research is needed to ascertain the far-transfer effects
of executive function training. Equally important, however,
are studies that reveal why executive function training should
work, if it does, by examining how the brain changes with it.
Studies in this area are only beginning to emerge. In healthy
older adults, but not those with MCI [118], working memory
training is associated with a decreased prefrontal activation
when performing n-back tasks that require participants to continuously update information while comparing the new stimuli
presented to the one n step (i.e., number of steps) backward,
with a higher n demanding a higher cognitive load of processing. Whereas Heinzel and colleagues [119] reported such a
finding in a low load condition (1-back), Vermeij and colleagues [118] found it in a medium load condition (2-back).
The decreased activation, relative to performance, was taken
to imply improved network efficiency. However, none of
these studies had a control group and none assessed untrained
tasks. Another study included a matched control, and the results suggested transfer of reduced neural activation to an
untrained updating task as well as transfer of performance to
other neuropsychological measures of executive functioning
and fluid intelligence [120]. RCTs with larger samples are
needed in future research.
Probably, very few persons, if any, would do n-back training on a regular basis in order to stem cognitive decline.
Moreover, the laboratory tasks used to assess transfer often
have little relevance to everyday functioning. Nevertheless,
these preliminary studies suggest that certain training activities targeting executive function may improve the efficiency
of prefrontal networks, potentially releasing resources for
compensatory functions when the brain is overloaded. The
fact that the improved neural efficiency is found at low-tomedium cognitive load (i.e., 1- to 2-back only, but not 3-back)
suggests a possible limit to the capacity of cognitive reserve
that may be just suitable for handling most everyday functional tasks. More research is needed to find out the kinds of

training task or activity that will most likely strengthen compensatory resources. These investigations may have implications for guiding the kinds of leisure cognitive activity that we
choose in daily life.
Concluding Comments
In the absence of a vaccine or a disease-modifying agent
against dementia, nonpharmacological interventions such as
lifestyle modification remain the only feasible, populationbased approach to preventing dementia. Leisure activities are
generally low-cost options with physical and cognitive health
benefits. Those that are culturally valued [97] will likely draw
widespread participation and family/peer involvement to increase the likelihood of long-term maintenance [105]. While it
would be optimal to start adopting healthy practices early in
life, the available research evidence suggests that it is not too
late to increase physical and cognitive activity in old age.
The current state of knowledge regarding what cognitive
activity actually does to protect the brain against dementia is
very nonspecific. Thus, we need to refer to the literature on
cognitive training for clues. Echoing the literature in clinical
neuroscience about the compensatory role of prefrontal networks, studies of cognitive training suggest that executive
function training may be strategic, although the literature is
not clear whether certain executive functions (such as working
memory) are more crucial than the others. At the same time,
the protective effect of occupational complexity may also be
related to the demands for executive function in challenging
jobs. Thus, it is possible that not all cognitive activities are
equal in terms of offering protection against dementia. In the
long run, training programs need to address barriers to real-life
implementation. Video games that are fun to play with may be
one of the most effective cognitive exercises [121].
The comparisons between cognitive activity and physical
exercise, though of academic value, will likely have little practical value as the general population will be recommended to
do both. Without ignoring the mental stimulation properties of
many physical activities, the most sensible conclusion that one
can draw from the current state of the literature is that while
physical activity, especially aerobic exercise, supports neuronal structural integrity and preserves brain mass (hardware
or static brain reserve), cognitive activity strengthens the
functioning and plasticity of neural circuits (software or dynamic cognitive reserve). Without healthy neuronal structures,
one’s ability to participate in and respond to cognitive training
is undermined. At the same time, cognitive function, especially executive processes, appears to enhance adherence to physical activity program [72, 73]. The two go together. Thus, the
prospect of dementia prevention depends on population-based
interventions that incorporate these multiple domains.
Although the preliminary effect size of the FINGER trial
was small, it should be borne in mind that a small effect in
the general population may be translated into large public
health benefits. The field awaits results from longer followups to see whether such lifestyle interventions can truly reduce
the likelihood of dementia.
Compliance with Ethical Standards
Conflict of Interest The author declares that he has no conflict of
interest.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
Open Access This article is distributed under the terms of the Creative
Commons Attribution 4.0 International License (http://
creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the
Creative Commons license, and indicate if changes were made.
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