Update: we now have an in-depth interview with Yaakov Stern, leading advocate of the cognitive reserve theory, and one of the authors of the paper we review below: click on Build Your Cognitive Reserve-Yaakov Stern. 

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In honor of the Week of Science presented at Just Science from Monday, February 5, through Sunday, February 11, we will be writing about “just science” this week. We thought we would take this time to discuss more deeply some of the key scientific publications in brain fitness.

Today, we will highlight the key points in an excellent review of cognitive reserve: Scarmeas, Nikolaos and Stern, Yaakov. Cognitive reserve and lifestyle. Journal of Clinical and Experimental Neuropsychology. 2003;25:625-33.

What is Cognitive Reserve?
The concept of a cognitive reserve has been around since 1998 when a post mortem analysis of 137 people with Alzheimer’s Disease showed that the patients exhibited fewer clinical symptoms than their actual pathology suggested. (Katzman et al. 1988) They also showed higher brain weights and greater number of neurons when compared to age-matched controls. The investigators hypothesized that the patients had a larger “reserve” of neurons and abilities that offset the losses caused by Alzheimer’s. Since then the concept of cognitive reserve has been defined as the ability of an individual to tolerate progressive brain pathology without demonstrating clinical cognitive symptoms.

Despite many studies that demonstrate an association between higher participation in more intellectual, social and physical activities and more reserve, most of these studies were not done over a long enough time period to rule out whether the stimulating activities were promoting higher cognitive performance or higher performers were more likely to engage in stimulating activities. The longitudinal studies show a mutually reinforcing cycle between an initially high intellectual functioning person, an engaged lifestyle, and more cognitive reserve, but also a maintenance of intellectual performance. (Arbuckle et al. 1992, Gold et al. 1995, Hultsch et al 1999, Schaie 1984, Schaie 1996, Schooler and Mulatu 2001)

In one study of 1772 nondemented individuals over seven years that controlled for factors like ethnic group, education, and occupation, participants with high leisure activity had 38% less risk of developing dementia, and that risk was reduced by approximately 12% for each additional leisure activity adopted. (Scarmeas, Levy, et al. 2001) Later studies, including imaging studies of cerebral blood flow, continue to build up data showing frequent participation in cognitively stimulating activities reduces risk for Alzheimer’s and slows the rate of cognitive decline. Interestingly, physical, social, and intellectual activities all help, although intellectual activities were associated with the lowest risk of incident dementia. Furthermore, it has been shown that people with high cognitive reserve decline more rapidly, supporting the idea that the pathology is more advanced by the time it is clinically apparent. (Stern, Tang, et al. 1995)

Causality

The association between engaged lifestyle and dementia risk could be either mediated or confounded by abilities like IQ or education. If this is the case then it could be that either IQ or education represent the true causal links with dementia or that subjects with higher IQ or education tend to adopt lifestyles which themselves causally reduce the risk of dementia (such as exercise, diet, etc.). Nevertheless, in studies where education and occupation (Scarmeas et al. 2001) or education and IQ (Scarmeas et al. 2003) were controlled for, the association between leisure activities and dementia risk was still there.

Other possibilities are that high functioning and engaged lifestyle are results of an innate capacity. Or perhaps borderline dementia patients are less active as a result of the pathology. Or perhaps the connection has yet to be found.

How Does it Work?
If it is a causal relationship, there are four possible explanations of how it might work:

1. Participation in stimulating activities spurs neuronal growth and a larger number of neurons to compensate for the pathology
2. High activity people use the same number of neural networks more efficiently
3. High activity people use alternate neural networks more efficiently to compensate for the pathology
4. The factors that affect cognitive reserve disrupt the development of the disease pathology by decreasing neurodegeneration

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Update: we now have an in-depth interview with Yaakov Stern, leading advocate of the cognitive reserve theory, and one of the authors of the paper we review below: click on Build Your Cognitive Reserve-Yaakov Stern.  

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Further Reading

• Arbuckle TY, Gold DP, Andres D, Schwartzman A, Chaikelson J. The role of psychosocial context, age, and intelligence in memory performance of older men. Psychol Aging. 1992;7:25–36.
• Gold DP, Andres D, Etezadi J, Arbuckle T, Schwartzman A, Chaikelson J. Structural equation model of intellectual change and continuity and predictors of intelligence in older men [published erratum appears in Psychol Aging 1998;13(3):434]. Psychol Aging. 1995;10:294–303.
• Hultsch D, Hertzog C, Small BJ, Dixon RA. Use it or lose it: Engaged lifestyle as a buffer of cognitive decline in aging? Psychol Aging. 1999;14:245-63.
• Katzman R, Terry R, DeTeresa R, et al. Clinical, pathological, and neurochemical changes in dementia: A subgroup with preserved mental status and numerous neocortical plaques. Ann Neurol. 1988;23:138-44.
• Roe CM, Xiong C, Miller JP, Morris JC. Education and Alzheimer disease without dementia: support for the cognitive reserve hypothesis. Neurology. 2007;68:223-8.
• Scarmeas N, Levy G, Tang MX, Manly J, Stern Y. Influence of leisure activity on the incidence of Alzheimer’s disease. Neurology. 2001;57:2236-42.
• Scarmeas N, Stern Y. Cognitive reserve and lifestyle. J Clin Exp Neuropsychol. 2003;25:625-33.
• Scarmeas N, Zarahn E, Anderson KE, et al. Cognitive reserve-mediated modulation of positron emission tomographic activations during memory tasks in Alzheimer disease. Arch Neurol. 2004;61:73-8.
• Scarmeas N, Zarahn E, Anderson KE, et al. Association of life activities with cerebral blood flow in Alzheimer disease: implications for the cognitive reserve hypothesis. Arch Neurol. 2003;60:359-65.
• Schaie KW. Intellectual development in adulthood: The Seattle longitudinal study. San Diego: Academic Press, 1996.
• Schaie K. Midlife influences upon intellectual functioning in old age. International Journal of Behavioral Development. 1984;7:463–78.
• Schooler C, Mulatu MS. The reciprocal effects of leisure time activities and intellectual functioning in older people: A longitudinal analysis. Psychol Aging. 2001;16:466–82.
• Stern Y. Cognitive reserve and Alzheimer disease. Alzheimer Dis Assoc Disord. 2006;20:S69-74.
• Stern Y. Cognitive reserve and Alzheimer disease. Alzheimer Dis Assoc Disord. 2006;20:112-7.
• Stern Y, Habeck C, Moeller J, et al. Brain networks associated with cognitive reserve in healthy young and old adults. Cereb Cortex. 2005;15:394-402.
• Stern Y, Tang MX, Denaro J, Mayeux R. Increased risk of mortality in Alzheimer’s disease patients with more advanced educational and occupational attainment. Ann Neurol. 1995;37:590-5.