Handbook of Clinical Neurology, Vol.

167 (3rd series)

Geriatric Neurology
S.T. DeKosky and S. Asthana, Editors
https://doi.org/10.1016/B978-0-12-804766-8.00011-X
Copyright © 2019 Elsevier B.V. All rights reserved

Chapter 11

Cognitive reserve
YAAKOV STERN1* AND DANIEL BARULLI2
1
Departments of Neurology, Psychiatry and Taub Institute, Columbia University College of Physicians and Surgeons,
New York, NY, United States
2
Department of Psychology, Columbia University, New York, NY, United States

Abstract
Cognitive reserve is a latent construct theorized to account for the discrepancy between observed brain
deterioration and ultimate clinical outcomes. This review outlines the theoretical development of the
reserve concept and presents major trends within epidemiological and neuroimaging research literatures
in support of such a construct. Particular focus is placed on the implications for cognitive aging and
dementia.

Age-related dementia and normal cognitive decline

THE RESERVE CONCEPT
Disparity is frequently reported between an individual’s
level of brain pathology, such as disease burden as with
Alzheimer’s disease (AD), and their discernible function
on neuropsychologic instruments or on activities of daily
living. This disparity has been explained by the concept
of cognitive reserve (CR) (Stern, 2002; Barulli and Stern,
2013). This chapter discusses epidemiologic evidence
for CR, controversies over its measurement, and the
nature of reserve. Although most of the research being
conducted on CR is centered on cognitive decline and
dementia (and this review focuses on those processes),
it is important to realize that CR is not a mechanism
solely compensatory to aging and age-related maladies.
Prevention or amelioration of cognitive impairment due
to multiple sclerosis (Sumowski et al., 2009), Parkinson’s
disease (Farinpour et al., 2003), and HIV-related dementia
(Kesler et al., 2003) has been shown to be facilitated by
lifelong exposure to CR proxies. It has also been shown
to play a role in the recovery from traumatic brain injuries
(Schneider et al., 2014) and stroke (Robertson and Murre,
1999). CR has also shown to be protective against pathol-
ogy that is traditionally vascular, such as white matter
hyperintensities (Brickman et al., 2009).
can be explained with several theories, all of which have
alternative but possibly interactive etiologic hypotheses.
These include the vascular hypothesis of dementia, the
inflammatory hypothesis, toxin build up within the brain,
and even psychosocial factors (Qiu and Fratiglioni,
2011). Through observational studies, we can say with
some confidence that mixed brain pathologies, such as
neurodegenerative and vascular pathologies, are respon-
sible for a sizeable amount of dementia cases (Schneider
et al., 2007). A number of specific risk factors responsi-
ble for dementia have been brought to light, with age
being the most important one: approximately 70% of
all dementia cases occur in people who are 75 years of
age or older (Fratiglioni et al., 2000). Over time, the accu-
mulation of risk factors can affect dementia susceptibil-
ity, which makes longitudinal studies of all of these
risk factors as well as protective factors simultaneously,
a necessity to fully understand models of dementia
(Kivipelto et al., 2006). As Qiu and Fratiglioni (2011)
state, these considerations suggest that a life course
model of dementia may be a stronger method of studying
this form of chronic disorder, which is often character-
ized by very long (decades) latent periods. This set of fac-
tors, which differentially position some individuals than

*Correspondence to: Yaakov Stern, Ph.D., Professor of Neuropsychology, Columbia University College of Physicians and
Surgeons, 622 W 168th St, PH18-321, New York, NY 10032, United States. Tel: +1-212-342-1350, Fax: +1-212-342-1838,
E-mail: ys11@columbia.edu
182 Y. STERN AND D. BARULLI
others for greater levels of cognitive impairment, is the
first issue that needs to be kept in mind while considering
not just cognitive aging, but the processes meant to
compensate for it, such as CR.
The development of the reserve theory hinges on
the ability to understand complex interactions among
risk and protective lifestyle factors. Reserve proposes
that certain environmental factors can explain and
predict why some individuals seem to respond more
favorably in the presence of pathology than others. In
a pioneering postmortem study of cognitively normal
women, Katzman et al. (1989) discovered advanced
Alzheimer’s pathology in 10 of these women; this was
accounted for by the “brain reserve” hypothesis, which
proposed that larger brains would be more durable to
pathology, effectively not allowing the effects of
dementia to make themselves clinically or behaviorally
manifest (Katzman, 1993). The rationale behind this
concept is that the larger the brain, the larger the number
of neurons and synapses, and hence the greater the
threshold to be reached before pathologic changes make
themselves present behaviorally. The brain reserve (BR)
theory is present in several modified forms today. Studies
indicate that roughly 25%–32% of individuals who at
autopsy show plaques and neurofibrillary tangles charac-
teristic of AD are not diagnosed with dementia in their
lifetime (Ince, 2001; Riley et al., 2002; Roe et al.,
2007). More nuanced structural variables have been pro-
posed to explain this observation: one suggested metric
that can help predict the rate of cognitive decline in
response to certain pathologies is the combined number
of pyramidal neurons (Sachdev and Valenzuela, 2009),
which can effectively complement other measures such
as the circumference of one’s head, which has been
linked to the risk of dementia (Mortimer et al., 2003).
Recently cortical fractal dimensionality or the fractal
structure of the cortical surface has been proposed as
another advanced metric for quantifying a reserve-like
variable (Whalley et al., 2016). The associations among
these variables, however, is affected by other variables
within the model, such as genetic factors that may put
one at greater or lesser risk for dementia (Graves
et al., 2001).
The development of the concept of CR, in contrast, can
be attributed to the subsequent observation of protective
effects of experiential, rather than biometric, factors. BR
and CR differ in that BR is viewed as a predominantly
passive model wherein once some biologic threshold of
disease burden or neural loss has been reached, cognitive
decline is inevitable; and CR is viewed as an active process
where such thresholds can be manipulated with certain
lifetime experiences (Stern, 2002). Education seems to
have a profound, protective effect on long-term cognition
and is one of the most extensively studied factors
(Qiu et al., 2001). Education at higher levels has been
shown to correlate with lower levels of cognitive decline
and lower risk of dementia (Meng and D’Arcy, 2012).
This protection is strongly supported in the literature on
reserve, being found by several research teams (Albert
et al., 1995; Butler et al., 1996; Chodosh et al., 2002;
Christensen et al., 1997; Lyketsos et al., 1999; Farmer
et al., 1995; Zahodne et al., 2014).
MEASURING RESERVE AND ITS
ALTERNATIVES
The measurement of CR is controversial because of
the vast array of evidence for a protective set of lifestyle
factors as well as the theoretical nature of CR. As dis-
cussed in this chapter, the first theoretical difference
drawn when considering the epidemiologic data is the
distinction between passive and active concept, with
the former being more closely related to brain reserve
(Satz et al., 2011) and the latter being more in relation
to CR (Stern, 2002). If reserve was simply a quantifiable
metric that was able to be measured within the brain
itself, then response to pathology would likely not be
highly modified by life-long exposure factors, such as
the ones discussed later. However, we know this is not
the case. CR proposes that the relationships between
the numerous lifetime exposure factors can lead to a brain
that is much more resilient with respect to the presence of
damage and pathology, and knowledge of how many fac-
tors are present in an individual’s life is useful to predict
to a given level of pathology (Stern, 2002). A further
major distinction must be drawn between CR and the
newer notion of brain maintenance (BM). Brain mainte-
nance can be defined as the theory that lifestyle factors
give an individual protection from the development of
pathology itself, as opposed to protection given against
the manifestation of harmful cognitive decline in the
presence of increasing pathologic burden (Nyberg
et al., 2012). While brain maintenance may be viewed
as internally protective, CR does not prevent the preor-
dained, biologic factors from spurring on dementia; it
acts as a complementary mechanism, which modifies
how the brain responds to said factors, once they are pre-
sent. Discerning differences between these two theories
is challenging, seeing as they both assume that similar
variables, such as education and complex mental activi-
ties, are responsible for granting protection. Valenzuela
et al. (2008) discovered less hippocampal atrophy over
a 3-year period within individuals who engaged in com-
plex mental activities over their lifetimes, consistent with
the brain maintenance model. However, most of featured
research shows greater support for the compensation
model CR, than the protection model, BM (e.g.,
Steffener et al., 2014). Assessing outcomes in a clinical
 COGNITIVE RESERVE
setting, Brayne et al. (2010) found that education had
an indirect effect on the neurodegenerative and vas-
cular pathologies. The pathologies were not prevented
directly. Thus, it seems that brain maintenance may be
the most applicable to normal aging, where lifestyle
and physical activity can, evidently, affect the mainte-
nance of the brain itself. However, some evidence has
shown that AD and other brain pathology may be directly
impacted by lifestyle. Therefore, CR and brain mainte-
nance may complement one another and be differentially
applicable depending on the type of brain deterioration
present. Indeed, recent work directly analyzing the two
concepts (Habeck et al., 2016) has found that while the
two measures can both be correlated with the same prox-
ies (e.g., education and verbal IQ), they themselves can
remain unassociated.
While the CR theory does not seek to exclude brain
related structural measures, it assumes that prediction
of dementia susceptibility is possible, independent of
physical or biologic measurements, unlike brain reserve.
However, as we gain greater understanding of the micro-
structural foundations and functional networks of the
brain through the use of tools such as MRI-based Diffu-
sion Tensor Imaging (DTI), brain reserve and CR
become increasingly interrelated, as there is usually a
neurophysiologic correlate of the environmental expo-
sures of a given individual (Barulli and Stern, 2013).
Additionally, there are increasingly fewer distinctions
between the two theories, as evidence of environmental
exposures such as exercise having neuroplastic modifi-
cations to brain structure accumulate (Whalley et al.,
2004). Structural brain measures have also been recently
linked to active compensation present in CR. Piras and
colleagues (2011), for instance, have observed differ-
ences in the microstructure of the hippocampus, in rela-
tion to education. Midlife physical activity also seems to
protect against dementia risk (Rovio et al., 2005). Addi-
tionally, some success has been demonstrated with aero-
bic exercise intervention with individuals already living
with dementia; depression has been shown to be reduced,
as well as primary neuropsychiatric symptoms (Paillard
et al., 2015). One suggestion for the mechanism
behind this type of intervention ties strongly into existing
lines of animal research within enriched environments
(Nithianantharajah and Hannan, 2009). As reviewed
by Brown et al. (2003) and Van Praag et al. (2005), pro-
motion of neurogenesis in areas of the hippocampus such
as the dentate gyrus leads to new neurons playing an
active role in pattern integration, spawning new task-
related networks. This was found to be present in rodents
when placed in stimulating environments and made to
exercise (Deng et al., 2010). Environmental enrichment
could also serve as a factor that prevents or slows down
the progression of AD pathology (Lazarov et al., 2005).
183
Nithianantharajah and Hannan (2009) argue that a strong
correlation between environmental enrichment and CR is
present, and understanding one could shed light on the
other. Environmental enrichment, however, can be more
easily studied using more invasive experimental manip-
ulations in animal models. It can, therefore, potentially
help us understand how the how mechanisms of CR
develop and operate over the course of one’s life and
even across generations. Such an epigenetic implemen-
tation of CR can be seen in the increase of long-term
potentiation within babies of mothers exposed to envi-
ronmental enrichment, even when the offspring are not
(Arai et al., 2009).
In addition, the two theories exhibit different mecha-
nisms as explanations of observations. CR suggests that
cognitive responses play a role in the brain’s response
over a long period of time to certain types of exposure
variables outlined later, while the short-term response
is present to address challenges once the pathology is
present, in the form of functional activation changes
(Stern, 2009). Stern suggested neural reserve and neural
compensation are characteristic of the neural implemen-
tation of CR. Neural reserve proposes that differences
in the efficiency, capacity, or flexibility of cognitive
networks are a result of lifelong exposures. This may
account for the noticeable differences between individ-
uals with high and low CR; the former have networks
which exhibit greater capacity (i.e., a larger range of acti-
vation, due to the response to a neural challenge, such
as performing a difficult task) and/or greater efficiency
(i.e., at the exact same level of activation as measured
with the Blood Oxygen Level Dependent (BOLD) sig-
nal), greater performance (possibly due to more direct
and less repetitive synaptic wiring within said networks
or in a more expedient hemodynamic response). This
hypothesis is supported empirically, with recent findings
demonstrating lower levels of activation with similar
performance during a working memory task in those
with a higher CR, measured with education and premor-
bid IQ (Sol
e-Padull
es et al., 2009).
Another proposed mechanism of reserve is known as
neural compensation. This is where individuals afflicted
by pathology must use another cognitive network to
compensate for the loss of a primary task-related cogni-
tive network once it has become too damaged (Stern,
2009). In general, neural compensation is difficult to
interpret because additional functional magnetic reso-
nance imaging (fMRI) activity can be associated with
both improved and diminished performance. This is con-
sistent with what we know now of the wide array of
neural networks (Boyle et al., 2008; Steffener and
Stern, 2012). Findings from fMRI provide this mecha-
nism with a vast amount of empirical evidence, in which
studies have found areas of additional activation in
184 Y. STERN AND D. BARULLI
older adults but not younger adults and have interpreted
these as compensatory activation (see Morcom and
Johnson, 2015 for a review). Without activating these
secondary networks, in theory, older subjects would
not be able to perform tasks as well as younger, healthier
subjects. There are, however, reports of compensatory
networks being associated with poorer performance
(Craik, 2006; Steffener and Stern, 2012). It is fair to
assume, in these situations, that the compensatory net-
work is utilized in the place of damaged primary
networks and, thus, is not as effective. The alternative
network acts as a cane to a pair of legs; it allows one
to walk, but not nearly as well.
An alternative way to approach CR is to find cognitive
processes that might underlie it. CR, for example, could
be associated with one’s ability to figure out and use
alternative cognitive processes and strategies (Barulli
and Stern, 2013; Barulli et al., 2013). This stance on
CR is heavily cognitive-oriented and is in tandem with
results of factor analyses of CR proxies and neuropsy-
chologic variables. These studies tend to find high
levels of overlap between cognitive control components
of executive function factors and CR (Siedlecki et al.,
2009). Similar theories of CR propose that it is primarily
brought about by working memory ability (Sandry and
Sumowski, 2014), can be obtained by the long-term
deployment and enhancement of the noradrenergic sys-
tem, and because of this, is mainly a function of attention
(Robertson, 2013) or is essentially a product of decision-
making factors through the lifespan (Boyle et al., 2013).
Ideally, research will be able to find ways to augment
and utilize CR through understanding it in both the cog-
nitive and neurophysiologic terms. The noradrenergic
theory of reserve recently received not only theoretical
support but also demonstrated methodological utility;
following up on observations that neuronal density in
the locus coeruleus (a major source of norepinephrine)
was inversely associated with dementia risk, Clewett
et al. (2015) reported that signal intensity in this region
using neuromelanin-sensitive MRI is positively associ-
ated with CR proxies such as education and verbal
intelligence. These authors argue that these results point
to the first bona fide biomarker of CR.
Putting aside the ontologic considerations about CR,
the question becomes how it is best measured, as numer-
ous exposure variables have been associated with it.
Proxy variables seem to be the most dominant way to
approach this task, using variables such as premorbid
IQ, education, or occupational history. These approaches
can be problematic since reserve is thought to be a cumu-
lative process based on experiences that occur in both
early and late life (Richards and Sacker, 2003). But
Siedlecki et al. (2009) found that within structural equa-
tion models, IQ and exposure variables share common
statistical variance. This is distinct from broader defini-
tions of cognitive functions. Measures such as these
display congruent and discriminant validity, which sug-
gests that their lumping is appropriate and, thus, may be a
good way to estimate reserve. This proxy variable
approach has yielded many standardized ways to esti-
mate lifetime exposures which are thought be in line with
CR (Harrison et al., 2015). Valenzuela and Sachdev
(2007) for instance, developed the “Lifetime Experi-
ences Questionnaire” to convey academic, social, occu-
pational, and leisure mental stimulation throughout
lifetime. In addition to showing validity and reliability,
it has been useful in weeding out individuals that will
experience cognitive decline over the next 18 months.
Problematically, in a meta-review of operationalizations
of CR, Harrison et al. (2015) found a notable lack of
consensus among research teams as to the definition
and agreed proxies of CR. There certainly is no “gold
standard” CR composite, and there is high variation
between groups and across studies, but proxies have been
a generally effective approach with regard to making
predictions about the conversion of dementia.
A different view was expressed in a review by Satz
et al. (2011), stating that while reserve is successful based
on the fact that the proxies it uses are found to modulate
effects of pathology on cognition, it is unsuccessful as an
explanatory construct because of the narrow amount of
support for the a priori grouping of these indicators, such
as education, socioeconomic status, or IQ, together.
Additionally, reserve is often touted as dissociable from
constructs, such as a construct of general intelligence (g),
which themselves are often used to predict disease
outcomes (Gottfredson, 2004; Gottfredson and Deary,
2004). Satz argues that few studies show the necessary
dual validity among the reserve proxies or the discrimi-
nant validity that should exist between such concepts and
supposedly dissociable factors. He argues reserve is
more likely a 2-factor model (brain and CR) or even a
4-factor model (where “reserve” decays into individual
factors such as processing resources, executive function,
complex mental activities, and g) rather than a model uti-
lizing a single latent factor. Jones et al. (2011) also voice
these concerns and argue that prior to utilizing the reserve
concept, certain a priori decisions must be explicated.
One of these decisions is whether to handle reserve as
a reflective (proxies for reserve each occur individually
because of the underlying latent variable that is usually
antecedent to them but do not affect one another) or as
a formative latent variable (proxies affect one another,
but collectively contribute to an emergent reserve con-
struct). The former model would work well with a
fixed genetic interpretation of disease risk, whereas
the latter raises questions about a single reserve vari-
able’s construct validity, but is consistent with the
 COGNITIVE RESERVE
theory of CR. Another concern voiced by Jones and
others is the close relationship between socioeconomic
status (SES) and standard reserve proxies. Low SES is
powerfully associated with disease, and with proxies for
CR correlating highly with SES, it is not surprising that
the correlation is used to predict health outcomes. The
argument is present in animal research (van Praag et al.,
2000), where enriched environment paradigm critics
note that enrichment may not be protective, but the
depravity of a standard housing condition could affect
and exaggerate study outcomes. Indeed, this perspec-
tive seems to conform well with recent findings that
parental education and income are major determinants
of brain volumes in children from infancy through ado-
lescence (Noble et al., 2015). As Whalley et al. (2016)
speculate, this could reflect any number of possible
causal sequences, including not only less access to edu-
cational resources but also more biologic deprivations
such as poor nutrition or increased psychosocial stress.
Regardless of the cause, one study by the same authors
even found that childhood SES was predictive of
adult hippocampal volume even after controlling for
education, gender, adult SES, and intelligence at age
11 (Whalley et al., 2016).
Reed et al. (2010), with respect to quantifying reserve
that doesn’t rely on proxies, have taken a different
approach—a technique wherein they broke down the
variance of episodic memory performance and denoted
CR as the residual variance after subtracting the variance
accounted for by variables like age, sex, and ethnicity,
as well as by structural brain measures and education.
The leftover variance should, in theory, correspond to
“reserve” in a more basic sense or maintain function
despite the predictions of pathology and other confounding
demographics. Indeed, this calculated version of CR paral-
leled with word reading scores and seemed to slightly
decrease the rate of conversion from mild cognitive impair-
ment (MCI) to dementia, as well as the rate of decline in the
executive abilities of individuals. Moreover, in individuals
with high levels of CR, baseline brain status was less pre-
dictive. We should expect this, if this is a truly pure mea-
sure of reserve. Interesting and potentially useful, this
measure of reserve could work well if we are willing to
accept the varying nature of the measure, given its reliance
on varying tasks and utilization of certain brain measure.
However, if researchers can discover more substantial cog-
nitive and neural mechanisms for reserve and demonstrate
the validity of the construct using a method like Structural
Equation Modeling (SEM), then a realistic interpretation
like the one discussed later seems more plausible.
A CR network is a collection of networks that could
mediate among sets of lifetime variables that are thought
to give reserve and the compensatory mechanism seen in
mental task performance. This is a potential for a CR
185
measure that is beyond proxy variables. Stern et al.
(2008), for example, were able to find an overarching
neural network that was utilized during a common visual
and verbal delayed match-to-sample test, whose expres-
sion differed as a function of CR within a group of young
adults, and was independent of task performance. Iden-
tification of these networks is of utmost importance to
researchers. Unlike proxy measures, this measure of
reserve would be much more direct. Furthermore, it
would require making fewer assumptions about the
convergent and discriminant validity of reserve proxies.
Because this measure is modifiable by lifetime experi-
ences but does not clearly fluctuate, it would capture
the essence of reserve, such as the previously discussed
CR measure. Lastly, many of the extant theoretical ques-
tions about the nature of the mechanisms of reserve
would be settled if a measure like this was identified. For-
tunately, extensive research in the field of neuroimaging
is underway, utilizing a vast spectrum of cognitive tasks,
measures of brain structure and demographics, fMRI
function, performance outcomes, and traditional proxy
measures of CR (e.g., Stern et al., 2014).
FACTORS THAT IMPART RESERVE
Studies indicate that control of risk factors such as hyper-
tension, abstinence from smoking, and regular physical
activity may effectively slow the progression of demen-
tia, and even counter the risk of dementia in the first place
(Flicker et al., 2010). Although these may seem like fea-
sible preventive measures, there is still controversy sur-
rounding the establishment of a universal approach to
prevent cognitive decline (Williams et al., 2010). Identi-
fication of these gradual steps can be crucial to learning
to cope with the public health crisis of Alzheimer’s and
dementia. Estimates show that almost half of AD cases
may result from risk factors that would have been possi-
ble to modify. Three million cases of Alzheimer’s could
have been prevented with a reduction of just 10%–25%
of these risk factors, according to some estimates (Barnes
and Yaffe, 2011). There is evidence that delaying the
onset of the disease by just 1 year could be enough to
reduce the global prevalence of the disease by as many
as 9.2 million in 2050 (Brookmeyer et al., 2007). Failure
in identifying working interventions can be attributed in
part to the common approach of analyzing only a single
avenue of prevention, as opposed to analyzing the myr-
iad factors that play a part in dementia (Mangialasche
et al., 2012).
Education has been proven to be such a powerful, pro-
tective force that it lowers the risk of dementia by about
50% in humans with the ApoE-4 allele, the strongest
known genetic risk factor for AD that is not a mutation
(Wang et al., 2011). In an early epidemiologic study of
186 Y. STERN AND D. BARULLI
the relation of education and occupation to dementia risk,
a longitudinal sample consisting of 593 nondemented
elderly was followed for up to 4 years, and 106 converted
to dementia; 101 of these dementia cases were AD. Edu-
cation played a crucial role in the conversion rates of
this study, with the conversion being 2.2 times greater
in those with less than 8 years of education as compared
to those with more education. It was also 2.25 times
higher in those with a low level of occupational attain-
ment compared to high, and the risk increased to 2.87
when the factors were considered together, suggesting
the profound effect that the two variables have collabo-
ratively (Stern et al., 1994).
Stern et al. (1992) also used Xenon blood flow imag-
ing to investigate how education might moderate the
effect of AD pathology on clinical disease severity.
When patients were matched for overall disease severity,
parietotemporal cerebral blood circulation was lower in
individuals with higher education. This suggests that
the pathology of their AD was more advanced, but
that those with higher education were in some way
compensating for it. Additionally, negative correlations
have been found between cerebral metabolism in the pre-
frontal, premotor, and left superior parietal areas and
higher education, after controlling for dementia severity.
This again hints at a compensatory role for additional
regional activation when disease severity increases
(Alexander et al., 1997). Later studies have confirmed
using positron emission tomography (PET) imaging that
patients with a greater level of education exhibit more
profound AD-related blood flow decline (Garibotto
et al., 2008; Kemppainen et al., 2008; Oh et al., 2015),
suggesting that their brains are showing resilience and
protection in the face of the deleterious nature of the
disease, because of their levels of education. The over-
arching message of these studies is that highly educated
people are less likely to be diagnosed with dementia and
higher education results in better cognitive function
(Bennett et al., 2003) when brain pathology is at a con-
stant, even while controlling for pathology (Roe et al.,
2007). These findings do not dismiss the concept of
brain reserve. However, they do stress the need for a
more active version of compensation, rather than just
the presence of a larger brain to begin with or an
increased number of neurons.
Slower rates of cognitive decline have been attributed
to other factors, outside of education. Earlier, a study by
Stern and colleagues indicated a negative correlation
between occupational status and signs of dementia in late
life (Stern et al., 1994, 1995). Karp et al. (2004) later dis-
covered that mentally strenuous or challenging activities
at work, during midlife, substantially reduced dementia
risk. Beneficial results have been shown to arise from
stimulating leisure activities as well with respect to
cognitive outcomes (Scarmeas et al., 2001) and have
been shown to protect against the onset of dementia
(Akbaraly et al., 2009). Engagement in intellectually or
socially stimulating activities has been shown to reduce
risk of developing dementia by 30% (Akbaraly et al.,
2009). In addition, studies have shown that living with
a partner in midlife decreases risks of dementia later in
life (Håkansson et al., 2009). Another study showed that
with a greater number of leisure activities, the likelihood
of dementia developing decreased (Scarmeas et al.,
2003). While the ideal time to engage in the aforemen-
tioned activities is still up for debate, the effectiveness
of the said activities is certain and has shown to delay
the onset of dementia (Paillard-Borg et al., 2009). One
form of cognitive stimulation, bilingualism, has garnered
special empirical attention. Craik et al. (2010) investi-
gated the medical records of 211 patients who were
elderly and had AD. Of these 211, 102 were bilingual
and showed a dementia onset 5.1 years later than those
out of the group who were monolingual. Using CT scans,
neuroimaging has also shown that bilinguals show much
more AD pathology than elderly individuals who are
monolingual on average, when matched for cognitive
function (Schweizer et al., 2012). This again suggests
that the bilinguals are compensating for a greater under-
lying disease burden. However, some findings still
suggest that studies that show that bilingualism delays
the dementing process were cross sectional and relied
too much on estimations of dementia duration. One inci-
dence study did not find that bilingualism had any
protective effect (Zahodne et al., 2014).
Premorbid IQ also has been shown to act as a shield
against the onset of dementia (Schmand et al., 1997).
Rentz et al. (2010) found that within a group of cogni-
tively normal people, when memory scores were
adjusted based on IQ, they showed correlation with cere-
bral perfusion in areas of the brain that were vulnerable
to the early pathology of AD. Greater pathology was
observed, despite intact memory, in those with higher
IQ. These individuals also exhibited higher cognitive
decline over the next three years. This decline is charac-
teristic of CR, which theorizes that once symptoms are
present, dementia progresses at faster rates in people with
higher CR (Stern et al., 1999; Scarmeas et al., 2006; Hall
et al., 2007). Valenzuela and Sachdev (2005), in a meta-
analysis of 33 studies over the course of 7 years, found
that 25 of 33 studies displayed substantial protective
effects through variables ranging from education to
stimulating leisure activities. An overall decreased risk
of dementia at 46% was observed in individuals who
engaged in the widest array of these activities. Although
this can be observed as beneficial, the relationships that
each of the factors has with one another need to be taken
into account, simultaneously, to paint the most accurate
 COGNITIVE RESERVE
picture. For example, one study found that the protective
effects of education became a noncontributing factor
for preventing cognitive decline, after controlling for
late-life leisure activities (Hall et al., 2009). This shows
the impact on research that investigating risk factors in
isolation can have.
CONCLUSION
Understanding the full spectrum of risk and protective
factors not only allows us to understand dementia and
reserve from an epidemiologic stance, but it is also crit-
ical to helping develop CR-based interventions. Recent
work suggests that differential levels of CR can affect
the efficacy of cognitive training programs in demented
adults; Mondini et al. (2016) showed that older adults
with lower levels of CR benefitted from cognitive train-
ing more intensely than older adults with high CR, which
could reflect the fact that high CR may be masking an
already highly advanced disease state. Alternatively,
findings such as this may support the environmental
enrichment critics; those with lower CR may simply
have been cognitively “impoverished” prior to the train-
ing regimen and so actually have room for improvement,
while those with high CR do not. Regardless, findings
such as these point to the relevance of understanding
CR for not just epidemiologic understanding, but
pragmatic implementation as well.
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