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The term cognitive reserve describes the brain's resilience to neuropathological damage. There are two models that can be used when exploring the concept of reserve: brain reserve and cognitive reserve. These terms, albeit often used interchangeably in the literature, provide a useful way of discussing the models. Using a computer analogy brain reserve can be seen as hardware and cognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve is commonly used to refer to both brain and cognitive reserves in the literature.

In 1988 a study published in Annals of Neurology reporting findings from post-mortem examinations on 137 elderly persons unexpectedly revealed that there was a discrepancy between the degree of Alzheimer’s disease neuropathology and the clinical manifestations of the disease.[1] This is to say that some participants whose brains had extensive Alzheimer’s disease pathology clinically had no or very little manifestations of the disease. Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have had incipient Alzheimer's disease but somehow avoided the loss of large numbers of neurons, or alternatively, started with larger brains and more neurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in the literature in this context.

The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higher reserve was found to provide a greater threshold before clinical deficit appears.[2][3][4] Furthermore those with higher capacity once they become clinically impaired show more rapid decline, probably indicating a failure of all compensatory systems and strategies put in place by the individual with greater reserve to cope with the increasing neuropathogical damage.[5]

Brain reserveEdit

Brain reserve may be defined as the brain's resilience, its ability to cope with increasing damage while still functioning adequately. This passive, threshold model presumes the existence of a fixed cut-off which, once reached, would inevitably herald the emergence of the clinical manifestations of dementia.

Brain sizeEdit

A 1997 study found that Alzheimer’s disease pathology in large brains did not necessarily result in clinical dementia.[6] Another study reported head circumference to be independently associated with a reduced risk of clinical Alzheimer’s disease.[7]

While some studies, like those mentioned, find an association, others do not. This is thought to be because head circumference and other approximations are indirect measures.

Number of neuronsEdit

The number of synapses is lower in early onset dementia that in late onset dementia.[8] This might indicate a vulnerability to the manifestation of clinical cognitive impairment, although there may be other explanations.

Genetic component of cognitive reserveEdit

Evidence from a twin study indicates a genetic contribution to cognitive functions.[9] Heritability estimates have been found to be high for general cognitive functions but low for memory itself.[10] Adjusting for the effects of education 79% of executive function can be explained by genetic contribution .[11] A study combining twin and adoption studies found all cognitive functions to be heritable. Speed of processing had the highest heritability in this particular study.[12]

Cognitive reserveEdit

Cognitive reserve also indicates a resilience to neuropathological damage, but the emphasis here is in the way the brain uses its damaged resources. It could be defined as the ability to optimise or maximise performance through differential recruitment of brain networks and/or alternative cognitive strategies. This is an efficiency model, rather than a threshold model, and it implies that the task is processed using less resources and in a way that makes errors unlikely to occur.

Education and occupationEdit

Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently.[13] The strongest association in this study was found with childhood cognition.

LifestyleEdit

For any given level of clinical impairment, there is a higher degree of neuropathological change in the brains of those Alzheimer’s disease sufferers who are involved in greater number of activities. This is true even when education and IQ are controlled for. This suggests that differences in lifestyle may increase cognitive reserve by making the individual more resilient.[14] Mortimer et al performed cognitive testing on a population of 678 nuns in 1997, in which they showed that different levels of cognitive activity and performance were possible in patients diagnosed with Alzheimers. One subject showing reduced neocrotical plaques survived with mild deficits, despite (or due to) low brain weight.

Global reserveEdit

In spite of the differences in approach between the models of brain reserve and cognitive reserve, there is evidence that both might be interdependent and related. This is where the computer analogy ends, as with the brain it seems that hardware can be changed by software.

Neurotrophic effect of knowledgeEdit

The posterior hippocampi of licensed London taxi drivers was famously found to be larger than that of matched controls, while the anterior hippocampi were smaller.[15] Exposure to an enriched environment, defined as a combination of more opportunities for physical activity, learning and social interaction, produces not only a host of structural and functional changes in the brain but also influences the rate of neurogenesis in adult and senescent animal model hippocampi.[16] Interestingly, many changes can be effected merely by introducing a physical exercise regimen. [17]

ConclusionsEdit

The clinical diagnosis of dementia does not tally with level of underlying neuropathology. The theory of cognitive reserve explains this phenomenon. People with high reserve go undiagnosed until damage is severe, then rapid decline ensues.

Cognitive reserve is measurable clinically. The variables that seem to contribute to it independently are: IQ, education, professional attainment, leisure activities, familial antecedents and brain size.

If we accept the validity of this model it is important to note that cognitive reserve and all the variables associated with it do not protect from Alzheimer’s disease. This means that the traditional idea that education protects from Alzhemier’s disease is false, albeit it does protect from its clinical manifestations.

This implies that people with greater reserve who already are suffering neuropathological changes in the brain will not be picked up by standard clinical cognitive testing. Conversely anyone who has used these instruments clinically knows that they can yield false positives in people with very low reserve. From this point of view the concept of ‘adequate level of challenge’ easily emerges. Conceivably one could measure cognitive reserve and then offer specifically tailored tests that would pose enough level of challenge to accurately detect early cognitive impairment both in individuals with high and low reserve. This has implications for treatment and care. Currently some people who would be eligible for it are not offered treatment while it may offered in other cases needlessly.

In people with high reserve deterioration occurs rapidly once the threshold is reached. In these individuals and their carers early diagnosis might provide an opportunity to plan future care and to adjust to the diagnosis while they are still able to make decisions.


ReferencesEdit

  1. Katzman R, Terry R, DeTeresa R, Brown T, Davies P, Fuld P, Renbing X, Peck A (1988). Clinical, pathological, and neurochemical changes in dementia: a subgroup with preserved mental status and numerous neocortical plaques. Annals of Neurology. 23(2):138-44.
  2. Katzman R (1993). Education and the prevalence of dementia and Alzheimer's disease. Neurology. 43(1):13-20
  3. Stern Y, Gurland B, Tatemichi TK, Tang MX, Wilder D, Mayeux R (1994). Influence of education and occupation on the incidence of Alzheimer's disease. JAMA. 271(13):1004-10
  4. Satz P, Morgenstern H, Miller EN, Selnes OA, McArthur JC, Cohen BA, Wesch J, Becker JT, Jacobson L, D'Elia LF, et al. (1993). Low education as a possible risk factor for cognitive abnormalities in HIV-1: findings from the multicenter AIDS Cohort Study (MACS). Journal of Acquired Immune Deficiency Syndrome. 6(5):503-11
  5. Wilson RS, Bennett DA, Gilley DW, Beckett LA, Barnes LL, Evans DA (2000). Premorbid reading activity and patterns of cognitive decline in Alzheimer disease. Archives of Neurology. 57(12):1718-23
  6. Mori E, Hirono N, Yamashita H, Imamura T, Ikejiri Y, Ikeda M, Kitagaki H, Shimomura T, Yoneda Y (1997). Premorbid brain size as a determinant of reserve capacity against intellectual decline in Alzheimer's disease. American Journal of Psychiatry. 154(1):18-24
  7. Mortimer JA, Snowdon DA, Markesbery WR (2003). Head circumference, education and risk of dementia: findings from the Nun Study. Journal of Clinical and Experimental Neuropsychology. 25(5):671-9
  8. Bigio EH, Hynan LS, Sontag E, Satumtira S, White CL (2002). Synapse loss is greater in presenile than senile onset Alzheimer disease: implications for the cognitive reserve hypothesis. Neuropathology and Applied Neurobiology. 28(3):218-27
  9. Ando J, Ono Y, Wright MJ (2001). Genetic structure of spatial and verbal working memory. Behavioral Genetics. 31(6):615-24
  10. Swan GE, Carmelli D, Reed T, Harshfield GA, Fabsitz RR, Eslinger PJ (1990). Heritability of cognitive performance in aging twins. The National Heart, Lung, and Blood Institute Twin Study. Archives of Neurology. 47(3):259-62
  11. Swan GE, Carmelli D (2002). Evidence for genetic mediation of executive control: a study of aging male twins. Journals of Gerontology Series B: Psychological Sciences and Social Sciences. 57(2):P133-43
  12. Plomin R, Pedersen NL, Lichtenstein P, McClearn GE (1994). Variability and stability in cognitive abilities are largely genetic later in life. Behavioral Genetics. 24(3):207-15
  13. Richards M, Sacker A (2003). Lifetime antecedents of cognitive reserve. Journal of Clinical and Experimental Neuropsychology. 25(5):614-24
  14. Scarmeas N, Zarahn E, Anderson KE, Habeck CG, Hilton J, Flynn J, Marder KS, Bell KL, Sackeim HA, Van Heertum RL, Moeller JR, Stern Y (2003). Association of life activities with cerebral blood flow in Alzheimer disease: implications for the cognitive reserve hypothesis. Archives of Neurology. 60(3):359-65
  15. Maguire EA, Gadian DG, Johnsrude IS, Good CD, Ashburner J, Frackowiak RS, Frith CD (2000). Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Science U S A. 97(8):4398-403.
  16. Enriched environment and physical activity stimulate hippocampal but not olfactory bulb neurogenesis. Brown et al Eur J Neurosci. 2003 May;17(10):2042-6
  17. van Praag H, Christie BR, Sejnowski TJ, Gage FH (1999). Running enhances neurogenesis, learning, and long-term potentiation in mice. Proceedings of the National Academy of Science U S A. 96(23):13427-31.
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