|Year : 2011 | Volume
| Issue : 2 | Page : 79-82
Cognitive reserve: The warehouse within
Jyoti Prakash, VSSR Ryali, Kalpana Srivastava, PS Bhat, R Shashikumar
Department of Psychiatry, Armed Forces Medical College, Pune, Maharashtra, India
|Date of Web Publication||16-Oct-2012|
Department of Psychiatry, Armed Forces Medical College, Pune - 411 040, Maharashtra
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Dementia is characterized by progressive and mostly irreversible memory loss. Other neuropsychiatric disorders affect cognition in varying manner. Are all people affected with such disorders manifest clinically in similar manner or does our brain have some reserve to tolerate insults? Relevant researches over the last two decades were scrutinized to understand brain reserve, appreciate the conceptual change in the same over years, and how the same can be improved for better cognition and memory over the year. Literature evidence suggests that the cognitive reserve (CR) is a dynamic and functional concept. There is adequate evidence to suggest that enriched environment and various other measures are likely to improve CR across all age. Improving CR may delay or reverse the effects of aging or brain pathology.
Keywords: Cognitive reserve, enriched environment, neurogenesis, synaptogenesis
|How to cite this article:|
Prakash J, Ryali V, Srivastava K, Bhat P S, Shashikumar R. Cognitive reserve: The warehouse within. Ind Psychiatry J 2011;20:79-82
Our life is defined by the memories we possess. Be it mother's affection, father's admonition, childhood friends, or college pranks; sweet or sour, these memories modify our personalities to what we are today. However, as Ben Johnson quotes "Memory, of all the powers of the mind, is the most delicate and frail." One of the diseases which primarily affect these memories is dementia.
Dementia, a disease of the old age is characterized by progressive memory loss and associated behavior problems. Treatment primarily aims at reducing the speed of damage by pharmacological and psychological interventions. With better medical facilities, we have definitely added more years to life but what about more life to years!!! If we gloss over the statistics, dementia accounts for approximately 25 million people in the world, which doubles every 20 years. In developed country, it affects 15% of people less than 80 years and around 25% of people above 80 years of age.  In India, around 3.7 million are affected by this illness, of which 2% are less than 65 years of age. The rate doubles with every 5-year increase of age.  Can we do something to prevent ourselves from this disease? Can we take some preventive measures to avoid, halt, or arrest this decay of memory?
The vision somewhere began in 1988. Katzman et al. brought out a research article in the Annals of Neurology as to why some people develop Alzheimer's dementia and some do not. They studied 137 autopsied brains. Alzheimer's brain revealed characteristic plaque and tangles. However, came out a startling revelation that 10 of the autopsied brain had same level of plaques and tangles, but no symptoms whatsoever of Alzheimer's disease during their lifetime. What made them different? These brains were heavier and had more neurons per age.  This let out the research question that are some people more resilient or adaptive to brain pathology? Can one function normally despite neuronal changes? Do some people have more cognitive capacity than needed and when needed can we draw an extra reserve? Thus, came out the concept of cognitive reserve (CR).
| Cognitive Reserve|| |
CR is a hypothesized capacity of mature adult brain to sustain the effects of disease or injury without manifesting clinically. It accounts for individual differences in the cognitive processes and neural networks which allow one to cope better than others with the brain damage. 
In earlier period, people entertained the concept of what is called as "brain reserve". , This construct was a passive model and stated that each individual had a fixed "brain reserve capacity," which does not change with time, experience, or training. It thus implied that an individual has a prefixed amount of brain damage that can be sustained before reaching threshold for clinical expression. Brain reserve capacity was then measured in brain size or the synaptic count, which was understood as a fixed component and thus a nonmodifiable factor.
Various researches since the landmark revelation point toward an active construct called "cognitive reserve." This reserve is as active as other part of the brain during any activity; it is functional as it augments the functions of other neurons; and it is modifiable with time, experience, and training. This thus implied that even people with similar brain size can have different CRs. 
CR has two components: Neural reserve and neural compensation. Neural reserves are those networks which are less susceptible to damage, are more efficient, have greater capacity, and may be invoked while coping with increased task demand. It thus helps individual cope with brain pathology. Neural compensation is a process by which individual suffering from brain pathology use brain structures or networks not normally used by intact brain to compensate for brain damage. These are networks other than CR network. These compensations occur by two methods. In "compensation to improve performance," the brain recruits additional brain areas which have resilient and healthy networks, i.e., like similar network on contralateral hemisphere. In "compensation to maintain performance," the brain recruits any network. These are not as health and resilient as the prior. Thus, the performance is poor. Such compensations are more in older age.  In general, a better CR implies greater overall cognitive efficiency, greater proliferation of brain neurons, more connection between neurons, enhanced ability to compensate by recruiting generalized neurons for specific task at hand, and better ability to use alternative strategies to solve problems. 
Measures of cognitive reserve
The anatomical or structural measures of CR constitute hardware model. These are measured by brain volume, head circumference, synaptic count, dendritic branching, etc. The functional measure is akin to software model which focuses on process than structures. These measures are intelligence quotient (IQ) or premorbid IQ, level of activation in functional magnetic resonance imaging (fMRI), efficiency of neural network, active compensation by alternative/more extensive network after challenge, etc. Most of these measures are malleable with time and life experiences. Summations of these are taken as proxy equivalent of CR. These proxy measures are income, occupational attainment, educational attainment, and degree of literacy. Although educational attainment is more widely used proxy, the degree of literacy is a more sensitive measure. 
Where is that specific CR network? Recent findings suggest that these networks are located in frontal lobe. It was seen that a higher CR individual was able to activate this network while working on more difficult task, whereas lower CR individual was unable to tap this network. These networks were found more often in younger people.  Do these networks degrade during natural aging process? Can this degradation be slowed or halted?
How to improve the cognitive reserve
Various literatures suggest that enriched environment (EE), cognitively stimulating activities, cognitive training, and physical training are likely to increase our CR, thus making us more resilient to cognitive decline and damage.
1. Enriched environment: This term has been given to environmental conditions that facilitate enhanced sensory, cognitive, and motor stimulation. EE has been seen to improve experience-dependent microdevelopment. EE has been found to promote neurogenesis, synaptogenesis, and transgenerational transmission. 
EEs are meaningful social engagement and activities that provide a sense of mastery.  These are complex, highly structured enjoyable activity that provide opportunity for self-expression, e.g., charity, clubs, group games, voluntary work, and caring for sick.  A separate study on cohabitation revealed that single, widowed, or separated had three times higher risk for cognitive impairment and 7.67 higher risk for Alzheimer's disease vis a vis their married/cohabiting counterparts. 
- Neurogenesis: Concept in neurology till last decade held that brain cells cannot reproduce. However, adequate evidences suggest that brain structures could generate new cells. Evidence is strongest for hippocampus and neocortex.  Short-term exposure to EE has led to fivefold increase in new neurons, substantial improvement in learning, exploratory behavior, and locomotor activity. These effects were seen even beyond the age of 65 years and potential exists throughout the lifespan. 
- Synaptogenesis: Physical activity enhances growth of neurons and learning promotes new connection between the neurons. Neuronal aging diminished by active and challenging life even if starts later in life. 
2. Cognitively stimulating task: In a unique study, 6- to 12-year old learnt in company of older adults in an intergenerational Charter School Cleveland where older adults contributed by sharing knowledge and experience. Improvement in cognition and QOL was seen in these elderlies  A China-based study found gardening and other community activities protective for incident dementia.  Crossword puzzles led to better performance on complex cognitive tasks.  Learning magic was found to be protective.  A German study worked on the effects of juggling. A volume increase was found in visual cortex, nucleus accumbens, and hippocampus. Effect was temporary in later two.  Formal education, reading book, magazines, etc. led to increased cognitive activity, the practice of which was associated with reduction in risk for Alzheimer's dementia and slower rates of cognitive decline. , Prospective cohort study from New York found that musical instruments, dancing, and leisure activity accounted for reduced risk for incident dementia and memory decline  La Rue recommendation (2008) suggests following for better memory: to carve out time for cognitively stimulating activities that one enjoys, to add some new challenging pursuits as time and energy allow, to engage in these pursuits several times a week, and to participate in social interaction. 
3. Cognitive training: Advanced cognitive training for independent and vital elderly (ACTIVE) study undertook training of older adults in areas of reasoning, memory, and processing speed. Generalized benefit was seen in cognition in adult 65 years and older. Improvement lasted at least 5 years with booster training.  In Experience Corps (EC) project, elders were taught literacy, mathematics, and conflict resolution in elementary school. Training showed improvement in executive function and memory  There are many cognitive training websites available, few of these include www.fitbrains.comnone , www.gamesforthebrain.comnone , www.mybraintrainer.comnone , www.luminosity.comnone , and www.sharpbrains.comnone . Many books are also available which elucidates the concept of CR and ways to improve it. These books are "The sharp brain guide to brain fitness-Alvaro and Elkhonon 2009," "Magnificient mind at any age-Amen D G 2008," "The mature mind: the positive power of ageing brain-Cohen G D 2005," "Cognitive reserve: theory and application-Yakov Stern 2006," etc. 
4. Physical training: Aerobic fitness training in older adult promoted significant increase in gray (cortical neurons) and white matter (connecting pathways) Physical and cognitive training combined had multiplier effect. 
Richards and Deary have brought out a life course model for better memory. [Figure 1] shows the role of multiple factors in the same. The model lays emphasis on the role of genetics and the environment. It lays stress on the structural neuronal complexity as well as the dynamic functional processing capacity and efficacy. From the above, it is obvious that the CR has a role to play in almost all aspects of cognitive and at all stage of development.  Improving CR will not only improve the function capacity but also delay the expressions of cognitive disorders such as Alzheimer's disease significantly [Figure 2].
|Figure 2: Factors affecting cognitive reserve at various stages of human development|
Click here to view
Role of cognitive reserve in other disorders
CRs have implications in various other disorders. Common neurological disorders include traumatic brain injury,  epilepsy,  multiple sclerosis,  Huntington's disease,  and Parkinson's disease.  Psychiatric disorders where CR was found to have positive role were schizophrenia,  affective disorders,  substance abuse,  sleep apnea-related cognitive deficits,  etc.
| Conclusion|| |
Available research evidences support the construct of CR structurally and functionally. Reserve is dynamic, interactive, and malleable. EE and cognitively and physically stimulating activities affect the CR positively in all stages of life and development. These reserves are determined by efficiency and capacity of existing brain networks and ability to enlist new compensatory networks and pure CR networks. CR has prophylactic and therapeutic implication in a wide range of neuropsychiatric conditions across all ages. Improving CR may delay or reverse the effects of aging or brain pathology.
| References|| |
|1.||Håkansson K, Rovio S, Helkala EL, Vilska AR, Winblad B, Soininen H, et al. Association between mid-life marital status and cognitive function in later life: Population based cohort study. BMJ 2009;339:b2462. |
|2.||Prevalence, impact, costs and services for dementia. Executive Summary the Dementia India Report; 2010. |
|3.||Katzman R, Terry R, DeTeresa R, Brown T, Davies P, Fuld P,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. |
|4.||Starr MJ, Lonie J. Estimated pre-morbid IQ effects on cognitive and functional outcomes in Alzheimer disease: A longitudinal study in a treated cohort. BMC Psychiatry 2008;8:27. |
|5.||Katzman R. Education and the prevalence of dementia and Alzheimer's disease. Neurology 1993;43:13-20. |
|6.||Satz P. Brain reserve capacity on symptom onset after brain injury: A formulation and review of evidence for threshold theory. Neuropsychology 1993;7:273-95. |
|7.||Stern Y. What is cognitive reserve? Theory and research application of the reserve concept. J Int Neuropsychol Soc 2002;8:448-60. |
|8.||Stern Y. Cognitive reserve and Alzheimer disease. Alzheimer Dis Assoc Disord 2006;20:112-7. |
|9.||Grady CL. In: Stern Y, editor. Cognitive reserve: Theory and application. New York, NY: Taylor and Francis, Inc; 2006. p. 265-83. |
|10.||Stern Y. Imaging cognitive reserve. In: Stern Y, editor. Cognitive Reserve: Theory and Applications. New York: Taylor and Francis; 2007. p. 251-64. |
|11.||Studenski S, Carlson MC, Fillit H, Greenough WT, Kramer A, Rebok GW. From bedside to bench: Does mental and physical activity promote cognitive vitality in late life? Sci Aging Knowledge Environ 2006;2006:pe21. |
|12.||Potkanowicz E, Hartman-Stein P, Biermann J. "Behavioral Determinants of Health Aging Revisited: An Update on the Good News for the Baby Boomer Generation" OJIN. Online J Issues Nurs 2009;14(3) |
|13.||Gould E, Beylin A, Tanapat P, Reeves A, Shors TJ. Learning enhances adult neurogenesis in the hippocampal formation. Nat Neurosci 1999;2:260-5. |
|14.||Olson AK, Eadie BD, Ernst C, Christie BR. Environmental enrichment and voluntary exercise massively increase neurogenesis in the adult hippocampus via dissociable pathways. Hippocampus 2006;16:250-60. |
|15.||Cohen GD, Perlstein S, Chapline J, Kelly J, Firth KM, Simmens S. The impact of professionally conducted cultural programs on the physical health, mental health, and social functioning of older adults. Gerontologist 2006;46:726-34. |
|16.||Fave D, Massimini F. The relevance of subjective well-being to social policies: Optimal experience and tailored intervention. In: Huppert FA, Baylis N, Keverne B, editors. The Science of well-being. New York: Oxford University Press; 2005. p. 379-404. |
|17.||Carlson MC, Saczynski JS, Rebok GW, Seeman T, Glass TA, McGill S et al, Tielsch J, Frick KD, Hill J, Fried LP. Exploring the effects of an "everyday" activity program on executive function and memory in older adults: experience corps. Gerontologist. 2008 Dec;48(6):793-801. |
|18.||Zhang X, Li C, Zhang M. Psychosocial risk factors of Alzheimer's disease. Zhonghua Yi Xue Za Zhi 1999;79:335-8. |
|19.||Newson RS, Kemps EB. The influence of physical and cognitive activities on simple and complex cognitive tasks in older adults. Exp Aging Res 2006;32:341-62. |
|20.||Kwong E, Cullen N. Do you believe in magic? Teaching Magic Tricks to Patients as an Adjunct to their Rehabilitation Program. CAPM&R Annual Conference London, Ont, Jun 2007. |
|21.||Draganski B, Gaser C, Kempermann G, Kuhn HG, Winkler J, Büchel C, et al. Temporal and spatial dynamics of brain structure changes during extensive learning. J Neurosci 2006;26:6314-7. |
|22.||Scarmeas N, Stern Y. Cognitive reserve and lifestyle. J Clin Exp Neuropsychol 2003;25:625-33. |
|23.||Wilson RS, Mendes De Leon CF, Barnes LL, Schneider JA, Bienias JL, Evans DA, et al. Participation in cognitively stimulating activities and risk of incident Alzheimer disease. JAMA 2002;287:742-8 |
|24.||Verghese J, Lipton RB, Katz MJ, Hall CB, Derby CA, Kuslansky G, et al. Leisure activities and the risk of dementia in the elderly. N Engl J Med 2003;348:2508-16. |
|25.||Willis SL, Tennstedt SL, Marsiske M, Ball K, Elias J, Koepke KM,et al. Long-term effects of cognitive training on everyday functional outcomes in older adults. JAMA 2006;296:2805-14. |
|26.||Colcombe SJ, Erickson KI, Scalf PE, Kim JS, Prakash R, McAuley E, et al. Aerobic exercise training increases brain volume in aging humans. J Gerontol A Biol Sci Med Sci 2006;61:1166-70. |
|27.||Richards M, Deary IJ. A life course to cognitive reserve: A model for cognitive ageing and development. Annals of Neurology. 2058:617-62206. |
|28.||Kesler SR, Adams HF, BlaseyCM, Bigler ED. Premorbid intellectual functioning, education, and brain size in traumatic brain injury: An investigation of the cognitive reserve hypothesis. Appl Neuropsychol 2003;10:153-62. |
|29.||Pai MC, Tsai JJ. Is cognitive reserve applicable to epilepsy? The effect of educational level on the cognitive decline after onset of epilepsy. Epilepsia 2005;46 Suppl 1:7-10. |
|30.||Cader S, Cifelli A, Abu-Omar Y, Palace J, Matthews PM. Reduced brain functional reserve and altered functional connectivity in patients with multiple sclerosis. Brain 2005;129:527-37. |
|31.||Zajac MS, Pang TY, Wong N, Weinrich B, Leang LS, Craig JM, et al. Wheel running and environmental enrichment differentially modify exon-specific BDNF expression in the hippocampus of wild-type and pre-motor symptomatic male and female Huntington's disease mice. Hippocampus 2010;20:621-36. |
|32.||Jadavji NM, Kolb B, Metz GA. Enriched environment improves motor function in intact and unilateral dopamine-depleted rats. Neuroscience 2006;140:1127-38. |
|33.||Barnett JH, Salmond CH, Jones PB, Sahakian BJ. Cognitive reserve in neuropsychiatry. Psychol Med 2006;36:1053-64. |
|34.||Chourbaji S, Brandwein C, Vogt MA, Dormann C, Hellweg R, Gass P. Nature vs. nurture: Can enrichment rescue the behavioural phenotype of BDNF heterozygous mice? Behav Brain Res 2008;192:254-8. |
|35.||Solinas M, Thiriet N, El Rawas R, Lardeux V, Jaber M. Environmental enrichment during early stages of life reduces the behavioral, neurochemical, and molecular effects of cocaine. Neuropsychopharmacology 2009;34:1102-11. |
|36.||Alchanatis M, Zias N, Deligiorgis N, Amfilochiou A, Dionellis G, Orphanidou D. Sleep apnea-related cognitive deficits and intelligence: An implication of cognitive reserve theory. J Sleep Res 2005;14:69-75. |
[Figure 1], [Figure 2]