Cognitive Reserve

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Neuropsychologia. Author manuscript; available in PMC 2010 August 1.

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Published in final edited form as:
Neuropsychologia. 2009 August ; 47(10): 2015–2028. doi:10.1016/j.neuropsychologia.2009.03.004.

Cognitive Reserve
Yaakov Stern
Cognitive Neuroscience Division of the Taub Institute, and the Departments of Neurology andPsychiatry, Columbia University College of Physicians and Surgeons

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The concept of reserve has been proposed to account for the disjunction between the degree
of brain damage or pathology and its clinical manifestations. For example, a head injury of the
same magnitude can result in different levels of cognitive impairment, and that impairment
can vary in its rateof recovery. Similarly, several prospective studies of aging have reported
that up to 25% of elders whose neuropsychological testing is unimpaired prior to death meet
full pathologic criteria for Alzheimer's disease (Ince, 2001), suggesting that this degree of
pathology does not invariably result in clinical dementia. As will be described in detail below,
many studies indicate that a set oflife experiences such as educational and occupational
exposure and leisure activities are associated with reduced risk of developing dementia and
with a slower rate of memory decline in normal aging. Cognitive reserve (CR) postulates that
individual differences in the cognitive processes or neural networks underlying task
performance allow some people to cope better than others with brain damage.This paper
attempts to produce a coherent theoretical account of reserve in general and of cognitive reserve
in particular. It then reviews some of my group's epidemiologic and imaging research that has
lent support to the concept of cognitive reserve and helped elucidate its neural underpinnings.
It should be stressed that this review is focused on my group's work, and is not a thoroughreview on the entire literature on the topic.
Because my work has focused on aging and dementia, I will discuss CR's relation to these brain
changes. The concept of CR, however, is applicable to almost any situation where brain
function is disrupted. Thus, for example, proxies for higher CR have also been reported to
mediate incidence of dementia in HIV (Farinpour et al., 2003), as well ascognitive changes
associated with schizophrenia, bipolar disorder and depression (Barnett, Salmond, Jones, &
Sahakian, 2006), and traumatic brain injury (Kesler, Adams, Blasey, & Bigler.E.D., 2003).

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Brain Reserve and Cognitive Reserve
Reserve can be roughly classified into passive and active models. Brain reserve (Katzman,
1993) is an example of a passive model, wherereserve derives from brain size or neuronal
count. Larger brains can sustain more insult before clinical deficit emerges, because sufficient
neural substrate remains to support normal function. This approach to reserve has been codified
in the threshold model (Satz, 1993), which revolves around the construct of “brain reserve
capacity”. The model recognizes that there are individualdifferences in brain reserve capacity.
It also presupposes that once brain reserve capacity is depleted past some fixed critical threshold
specific clinical or functional deficits emerge. Thus, individual differences in brain reserve

Correspondence to Yaakov Stern, Taub Institute, 630 W 168th Street, New York, NY 10032. Telephone: 212-342-1350, Fax:
212-342-1838, Email: ys11@columbia.edu.
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