Cognitive Reserve: “Money in the Bank”

Running head: COGNITIVE RESERVE 1

Cognitive Reserve: “Money in the Bank”

Myrna Davis Washington

University of the Rockies

COGNITIVE RESERVE 2

Abstract

Cognitive Reserve (CR) is defined as individual differences in the

baseline efficiency of cognitive processing, such that those with

more efficient CR networks have greater capacity and are more

flexible in coping with impairment and those with lower CR are

more susceptible to the effects of aging-related brain

deterioration. CR is commonly measured by achieved education

level, premorbid intelligence, and irregular word reading

ability. CR is analogous to “money in the bank” in that the more

CR one has, the better prepared one is to prevent, offset, and

recover from cognitive (and physical) impairment. This paper

explores the relationship of CR to information processing or

memory, cognitive functioning, brain atrophy, amnesia, and brain

damage by looking at research supporting the CR hypothesis and

examining CR as indicative of hippocampal volume. Findings

indicate that in addition to off-setting cognitive decline,

amnesia, AD, and dementia (diseases that affect memory), CR is an

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effective protective, preventive, therapeutic, and curative

moderator.

Cognitive Reserve: “Money in the Bank”

While assimilating and analyzing current research on memory

and amnesia from a biopsychological perspective, one of the areas

that emerged as being of particular interest to health and

wellness psychology was cognitive reserve. While the topic of

cognitive reserve was limited to a brief paragraph nestled in the

middle of Pinel’s (2011) chapter on “Brain Damage and

Neuroplasticity”, it stood out like a “sore thumb” when

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approached from a lifetime commitment to wellness and health.

What is cognitive reserve? How is cognitive reserve measured?

What is its relationship to information processing or memory,

cognitive functioning, brain atrophy, amnesia, brain damage, and

health and wellness, in general? How does cognitive reserve act

as a preventive measure in off-setting cognitive decline,

amnesia, Alzheimer’s Disease (AD), and dementia; diseases that

affect memory? These questions and research supporting the

subject of cognitive reserve are the focus of this paper, which

explores the cognitive reserve hypothesis, examines cognitive reserve as

indicative of hippocampal volume, and explores its relationship

to memory, brain atrophy, and disease prevention. What is

presented herein is a demonstration that cognitive reserve is

analogous to “money in the bank”; the more one has, the better-

prepared one is to prevent, withstand, and recover from

impairment.

Cognitive Reserve

What is Cognitive Reserve? Simply put, Cognitive Reserve (CR) is

“roughly the equivalent to education and intelligence” (Pinel,

2011p. 260). From a biopsychological perspective, however, CR is

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defined as “individual differences in the baseline efficiency of

cognitive processing, such that those with more efficient CR

networks have greater capacity and are more flexible in coping

with impairment and those with lower CR are more susceptible to

the effects of aging-related brain deterioration” (Benedict et

al., 2011, para. 2). Theoretically, CR includes both passive and

active processes in the brain that modify risk for the clinical

expression of brain disease, with passive reserve or brain

reserve referring to individual differences in the amount of

brain damage one can endure before exhibiting clinical signs and

symptoms (Fick, Kolanowski, Beattie, & McCrow, 2009). Active

reserve, on the other hand, is the CR presented in this paper.

This definition refers to individual differences in the degree of

efficiency with which individuals can use brain networks or

cognitive strategies to cope with brain pathology, differences

which are hypothesized to be due to mental stimulation that

individuals are exposed to over a lifetime, including level of

educational attainment, occupational complexity, and the mental

complexity of leisure activities (Fick et al., 2009).

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The CR Hypothesis. CR is thought to play a role in the

improvements observed after brain damage that do not result from

true brain recovery and has also been used to explain why

educated people are less susceptible to the effects of aging-

related brain deterioration (Pinel, 2011). According to the CR

hypothesis, neuropsychological expression of brain disease is

attenuated among people with higher educational attainment and

premorbid intelligence; persons with higher premorbid

intelligence or educational attainment can withstand more severe

neuropathology before suffering cognitive impairment (Sumowski,

Chiaravalloti, Wylie, & Deluca, 2009). According to the CR

hypothesis, for example, elderly people with higher cognitive

reserve can withstand a greater degree of parietal hypometabolism

on positron emission tomography (a proxy of AD progression)

before developing dementia (Sumowski et al., 2009).

Measurement of CR. CR is an independent predictor of

neuropsychological outcomes that is commonly measured by achieved

education level, premorbid intelligence, and irregular word

reading ability (Benedict et al., 2010; Pinel, 2011). Because

this model emphasizes behavioral adaptation or neuropsychological

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(NP) compensation mediated by increased activation of either

usual or alternate neural networks, it also represents a

potential mechanism for coping with brain damage (Benedict et

al., 2011). CR could explain why a person with high intelligence

or education, for example, can sustain more cerebral injury

before showing a functional deficit or why a person with high CR

experiences less cognitive decline with senile dementias such as

Alzheimer’s Disease (AD) (Benedict et al., 2010). Recent research

in other neurological populations (i.e., frontotemporal dementia,

stroke, head, Parkinson's disease, and ischemic white matter

disease) has also supported the hypothesis that CR moderates

disease prevention and recovery (Benedict et al., 2010).

Cognitive Reserve, Memory and Information Processing

“Money in the Bank”. Think of the human brain as the bank,

memory and learning (both neuroplastic processes) as money, and

cognitive reserve as money deposited into the bank for a “rainy

day” (savings). From this position, the more memory, learning,

and information one processes (information processing or IP), the

better prepared one is to adjust to and overcome change,

adversity, and impairment. In this sense, high cognitive reserve

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(reserves of memory and learning that serve as coping

repertoires) is to the body as a money-laden savings account is

to the owner of the account. This brings to light two very

important questions: 1) what is memory? and 2) what is its

relationship to IP?

Memory. The answer to both of the above questions lies in

the definition of memory as a neuroplastic process that involves

neurogenesis and the ability of the brain to process experiential

information, modify its functioning in response to experiences

(learning), store experiential modifications, and subsequently

recall them as memories (Pinel, 2011). Memories are created when

conscious experiences occur and information is rapidly encoded

and distributed throughout the hippocampus (the primary site or

memory and learning), where it is temporarily stored as short-

term memory until it can be transferred to a more stable cortical

storage system as long-term memory (Parker, Jordan & Grimaldi,

2011; Pinel, 2011). Memory, like learning, involves the brain’s

ability to change in response to experience, with the difference

being that learning deals with how experience changes the brain,

rather than its storage and reactivation (recall) of memories.

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However, what should be noted is that without the ability to

process information, learn and remember, every moment would be

experienced as if one were a newborn; each face would be

unrecognizable, each act novel, and each word incomprehensible

(Pinel, 2011).

Hippocampal Volume. The above information facilitates the

conceptualization of CR as indicative of hippocampal volume, with

high CR indicating high hippocampal volume, low CR indicating low

hippocampal volume, normal aging and various disease pathologies

(i.e., alcoholism, schizophrenia, and major depressive disorder)

depleting hippocampal volume, and hippocampal atrophy predicting

the progression of age-related memory loss and the onset of

diseases characterized by dementia, memory loss, and amnesia

(i.e., AD and Korsakoff’s Syndrome) (Benedict et al., 2010;

Parker et al., 2011).

Cognitive Reserve, Brain Atrophy, and Multiple Sclerosis

Although very little is known about risk and protective

factors for cognitive impairment in multiple sclerosis (MS; a chronic

neurologic disease characterized by central nervous system white

matter lesions and cerebral atrophy, with more than 50% of MS

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patients also suffering cognitive impairment and IP

inefficiency), only one published study (Sumowski et al., 2006,

as cited in Sumowski et al., 2009) has shown that CR moderates

the negative effect of MS on cognition by reporting an

interaction between MS diagnosis and CR, such that the negative

effect of an MS diagnosis on IP efficiency is attenuated at

higher levels of CR. Sumowski et al’s 2006 study (as cited in

Sumowski et al., 2009) demonstrated that persons with MS showed

impaired IP efficiency relative to matched healthy controls at

lower levels of reserve, but that this performance discrepancy

narrowed as CR increased and disappeared completely at higher

levels of reserve. The current study, Sumowski et al. (2009), set

out to provide additional support for the CR hypothesis by

examining CR in MS and investigating whether the negative effect

of brain atrophy on IP efficiency was moderated by premorbid

intelligence and asking the question: “Does CR moderate the

deleterious effect of MS disease severity (i.e., brain atrophy)

on IP efficiency?” Additionally, to move beyond the previous

dichotomous characterization of MS disease as present or absent,

Sumowski et al (2009) used a magnetic resonance imaging (MRI)


estimate of brain atrophy as a continuous measure of MS disease

severity.

Participants. Thirty-eight persons aged 18-55 years with

clinically definite MS were recruited from local MS clinics and a

local chapter of the National MS Society (Sumowski et al., 2009).

The study sample consisted of 33 women and 5 men aged 27-54 years

(44.0 ± 7.5, mean ± SD ) with 12-20 years of education (mean 15.9

± 2.3) (Sumowski et al., 2009). Mild overall gait disturbance was

observed with the Hauser Ambulation Index (HAI; mean 2.1 ± 2.2)

and depressive symptomatology on the Beck Depressive Inventory

(BDI-II; qualified as a regressor in the subsequent analyses) was

minimal (mean 12.0 ± 8.0), with elevations due mostly to somatic

and vegetative symptoms consistent with MS (Sumowski et al.,

2009). Disease duration ranged from 1 to 29 years (mean 10.1 ±

7.1) and MS course included relapsing-remitting (30), secondary

progressive (6), and primary progressive (2) (Sumowski et al.,

2009).

Methodology. Subjects were asked to complete a vocabulary-

based estimate of premorbid intelligence (Wechsler Vocabulary)

and a composite measure of IP efficiency (Symbol Digit Modalities Test


[SDMT] and Paced Auditory Serial Addition Task [PASAT]). Brain atrophy was

estimated from measurements of third ventricle width using high-

resolution anatomical brain MRI (magnetization-prepared rapid

gradient echo) (Sumowski et al., 2009).

Results. In a hierarchical regression analysis controlling

for age and depressive symptomatology, findings indicated that

brain atrophy predicted worse IP efficiency (R2 = .23, p = .003)

and cognitive reserve predicted better IP efficiency (R2 = .13, p

= .013), with these effects moderated by an Atrophy x Cognitive

Reserve interaction (R2 = .15, p = .004) (Sumowski et al., 2009).

Findings also demonstrated that while MS subjects with minimal

atrophy (2.9 mm = -1 SD) produced normal IP efficiency regardless

of cognitive reserve and that t higher atrophy (7.0 mm = +1 SD),

MS subjects with high cognitive reserve maintained performance

within the average range (25th percentile), those with normal

reserve demonstrated mild impairment (5th percentile), and those

with lower reserve showed severe impairment (1st percentile)

(Sumowski et al., 2009). What this demonstrated to the

researchers was that higher cognitive reserve allowed MS subjects

to better withstand the increased cerebral demands associated


with advancing disease (i.e., atrophy) (Sumowski et al., 2009).

These results indicated that the negative effect of brain atrophy

on IP efficiency is attenuated at higher levels of reserve, such

that MS subjects with higher reserve are better able to withstand

MS neuropathology without suffering cognitive impairment and

helps explain the incomplete and inconsistent relationship

between brain atrophy and IP efficiency in previous research

(Sumowski, 2009).

A Second Look at Cognitive Reserve

A second study (Benedict et al., 2011) replicated Sumowski

et al. (2009) and added validity to the CR hypothesis by

demonstrating that CR (as indexed by more years of education or

higher premorbid intelligence) not only moderates cognitive

decline in patients with senile dementias such as AD, but

protects against the progression of cognitive dysfunction in

persons with MS.

Participants. Benedict et al. (2011) studied 91 patients

with clinically definite MS, who entered the study for one of

three reasons: participation in research (n = 52; 57%), routine

monitoring of cognitive function (n = 10; 11%), or referral for


evaluation of a specified management problem related to suspected

cognitive impairment (n = 29; 32%). The baseline mean (± SD ) age

was 44.8 ± 8.8 years, with 70% female, 92% Caucasian patients,

and 14.3 ± 2.0 average years of education (Benedict et al.,

2011). Mean disease duration was 11.0 ± 8.3 years and patients

were characterized according to their current disease course,

with 78% of the sample having relapsing-remitting (n = 71), 18.7%

having secondary-progressive (n = 17), and 3.3% having primary

progressive (n = 3) (Benedict et al., 2011). Patients were

excluded from the study if: 1) they had a past history of a

medical or psychiatric disorder that could substantially

influence cognitive function or have a lasting impact on brain

integrity (including but not limited to craniocerebral trauma

with > 5-min loss of consciousness, alcohol or drug dependence,

and learning disability); 2) current major depression or

alcohol/substance abuse; 3) neurological impairment that might

interfere with cognitive testing; and/or 4) an MS relapse or

acute corticosteroid treatment within 6 weeks of testing

(Benedict et al., 2011).


Methodology. Information processing speed and efficiency

were investigated at a mean test-retest interval of 1743± 440.6

days (roughly 57 years) using the PASAT (which measured auditory

processing speed and working memory), the SDMT (used as a

measure of processing speed in the visual modality), an Information

Processing (IP) composite index (the mean Z score of the SDMT and PASAT

based on previously published normative values, and the Expanded

Disability Status Scale (EDSS) (Benedict et al., 2011).

Cognitive reserve was estimated using years of completed

education and the North American Adult Reading Test (NAART)

(Benedict et al., 2011).

Results. Baseline and follow-up data were compared using

analysis of the variance (ANOVA) and correlations were examined

using Pearson calculation (p < .05). Results indicated that

there was significant progression in EDSS from a median value of

2.5 to 3.5 over the 5-year course of the study, a significant

worsening on the SDMT (p < .003), and a trend for worsening on

the PASAT (p = .189) (Benedict et al., 2011). The mean change in

SDMT raw score was -3.0 ± 8.4 (F [1,94] = 7.50; p = .007) with

low educational reserve subjects showing significant reduction in


SDMT and the high sub-group showing little change. ANOVA showed

that the difference between the sub-groups on SDMT at baseline

was not significant (p > .05) (Benedict et al., 2011).These

findings indicate that CR not only helps MS patients with brain

atrophy function normally on cognitive processing tasks that

require memory, but that MS patients with higher CR are less

likely to evidence cognitive decline in IP over time (Benedict et

al., 2011). This is good news for those people with genetic

markers for AD and MS, but can CR prevent AD and retard the rate

of cognitive decline?

Enhancing Cognitive Reserve as a Possible Preventive Measure

Because of the aging of the American population, the

incidence of dementia and delirium (a disorder of acute onset

with fluctuating symptoms and is characterized by inattention,

disorganized thinking and altered levels of consciousness) is

increasing worldwide (Fick, Kolanowski, Beattie, & McCrow, 2009).

The onset of delirium is associated with poor outcomes, including

functional decline, increased hospitalizations, increased health

care use, nursing home placement, and death (Fick et al., 2009).

Although several clinical trials have tested interventions for


delirium prevention in individuals without dementia, little is

known about the ways to prevent delirium in patients with early-

stage AD (Fick et al., 2009). One seminal study (Fick et al.,

2009) used a literature review to the explore mechanisms for

preventing delirium and slowing the rate of cognitive decline in

early-stage AD by enhancing cognitive reserve. Results uncovered

an expanding body of evidence supporting CR as a mechanism for

preventing and retarding delirium and dementia in early-stage AD

(Fick et al., 2009). The implications of this evidence on memory

and amnesia lie in the correlation of CR to more neurons, brain

size, synapse density, and high hippocampal volume (Fick et al;,

2009).

The question of whether decline can be altered in cognition

was answered in part in Fick et al.’s (2009) presentation of the

Advanced Cognitive Training for Independent and Vital Elderly

(ACTIVE) Study, a randomized, controlled, single-blind study (N =

2,832, age range = 65 to 94) that investigated the effect of

cognitive training on mental ability with a 5-year follow up.

Most interestingly, findings from this study suggested that

cognitive training can improve cognitive functioning, and that


improvements can be sustained over 5 years (Fick et al., 2009).

Additional support for this came from a small case-control study

(N = 24, 12 cases and 12 controls) that evaluated the benefit of

cognitive stimulation in elderly people with mild cognitive

impairment compared with cognitively intact participants and used

reality orientation techniques, mental imaging, recall and

delayed recall, and executive exercises as cognitive stimulating

exercises (Fick et al., 2009). Findings from this second study

suggested that cognitive stimulation can improve memory in older

adults with mild cognitive impairment (Fick et al., 2009). Not

surprisingly, several home-based cognitive stimulating studies

demonstrated that reading newspapers, pursuing hobbies, and

participating in leisure activities are all capable of improving

cognition and increasing cognitive reserve in older adults (Fick

et al., 2009). Fick et al. (2009) also added three additional

sources that have protective influences on cognitive function:

regular physical activity, social activities, and social support.

In addition, frequent interactions with large social networks,

leisure pursuits, being married, and perceived positive support

from friends were positively correlated with maintenance of


cognitive function (Fick et al., 2009). From a health-and-

wellness, biopsychological perspective, this is evidence that

cognitive and physical exercise, as well as social networking and

social engagement, protect and improve cognitive reserve by

stimulating neurogenesis – “money in the bank” (Fick et al.,

2009).

Discussion and Concluding Remarks

In summation, CR is analogous to “money in the bank”; the

more information that is processed in the form of memory and

learning, the better prepared an individual is to meet, recover

from, and survive mental and physical impairment. CR is commonly

measured by achieved education level, premorbid intelligence, and

irregular word reading ability. The relationship of CR to

information processing or memory, cognitive functioning, brain

atrophy, amnesia, brain damage, and health and wellness, in

general, is that of a protective, preventive, therapeutic, and

curative moderator. In addition, CR has been shown to be

effective in off-setting cognitive decline, amnesia, AD, and

dementia; diseases that affect memory. However, this is not

news; CR is also analogous to Socio-Economic Status (SES), which


has confounded a plethora of previous studies with its moderating

effects on neurogenesis, aging, cognitive functioning and

decline, health status, and recovery from impairment (Hackman,

Farah, & Meaney, 2010). For future studies, the investigation of

SES and neural development may prove to be a promising area of

study that can refine strategies to address cognitive decline in

diseases that affect memory and learning (Hackman et al., 2010).

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Cognitive Reserve: “Money in the Bank”

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