神马文学网cognitive reserve: Information from Answers.com
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cognitive reserve
The term cognitive reserve describes the brain‘s resilience toneuropathological damage. There are two models that can be used when exploring the concept ofreserve: brain reserve and cognitive reserve. These terms, albeit often used interchangeably in theliterature, provide a useful way of discussing the models. Using a computer analogy brain reserve can be seen as hardware andcognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve iscommonly 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 personsunexpectedly revealed that there was a discrepancy between the degree ofAlzheimer’sdiseaseneuropathology and the clinical manifestations of the disease (Katzmanet al. 1988). This is to say that some participants whose brains had extensiveAlzheimer’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 toage-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have hadincipientAlzheimer‘s disease but somehow avoided the loss of large numbers ofneurons, or alternatively, started with larger brains and moreneurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in theliterature in this context.
The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higherreserve was found to provide a greater threshold before clinical deficit appears (Katzman 1993, Satz 1993, Stern 1994).Furthermore those with higher capacity once they become clinically impaired show more rapid decline (Wilson et al. 2000),probably indicating a failure of all compensatory systems and strategies put in place by the individual with greater reserve tocope with the increasingneuropathogical damage.
Brain Reserve
Brain reserve may be defined as the brain‘s resilience, its ability to cope with increasing damage while still functioningadequately. This passive, threshold model presumes the existence of a fixed cut-off which, once reached, would inevitably heraldthe emergence of the clinical manifestations of dementia.
Brain size
A 1997 study found thatAlzheimer’s diseasepathology in large brains did not necessarily result in clinicaldementia(Mori et al. 1997). Another study reported head circumference to be independently associated with a reduced risk ofclinicalAlzheimer’s disease (Mortimer et al. 2003).
While some studies, like those mentioned, find an association, others do not. This is thought to be because head circumferenceand other approximations are indirect measures.
Number of neurons
The number of synapses is lower in early onset dementia that in late onset dementia (Bigio et al. 2002). This mightindicate a vulnerability to the manifestation of clinical cognitive impairment, although there may be other explanations.
The genetic component of cognitive reserve
Evidence from a twin study indicates a genetic contribution to cognitive functions (Ando, Ono & Wright, 2001).Heritability estimates have been found to be high for general cognitive functions but low for memory itself (Swan et al.1990). Adjusting for the effects of education 79% ofexecutive function can beexplained by genetic contribution (Swan & Carmelli 2002). A study combining twin and adoption studies found allcognitive functions to be heritable. Speed of processing had the highest heritability in thisparticular study (Plomin et al. 1994).
Cognitive Reserve
Cognitive reserve also indicates resilience toneuropathological damage, but theemphasis here is in the way the brain uses its damaged resources. It could be defined as the ability to optimise or maximiseperformance through differential recruitment of brain networks and/or alternative cognitive strategies. This is an efficiencymodel, rather than a threshold model, and it implies that the task is processed using less resources and in a way that makeserrors unlikely to occur.
Education and Occupation
Childhood cognition, educational attainment and adult occupation to all contribute to cognitive reserve independently(Richards & Sacker, 2003). The strongest association in this study was found with childhood cognition.
Lifestyle
For any given level of clinical impairment there is a higher degree of neuropathological changes in the brains of thoseAlzheimer’s diseasesufferers who are involved in greater number of activities. Thisis true even when education and IQ are controlled for. This suggeststhat differences in lifestyle may increase cognitive reserveby making the individual more resilient (Scarmeas et al. 2003).
Global Reserve
In spite of the differences in approach between the models of brain reserve and cognitive reserve, there is evidence that bothmight be interdependent and related. This is where the computer analogy ends, as with the brain it seems that hardware can bechanged by software.
The Neurotrophic effect of Knowledge
The posteriorhippocampi of licensed London taxi drivers was famously found to be largerthan that of matched controls (Maguire et al. 2000). Exposure to an enriched environment (defined as a combination of moreopportunities for physical activity, learning and social interaction) produces not only a host of structural and functionalchanges in the brain but also influences the rate of neurogenesis in adult and senescent animal models (Kempermann, Kuhn &Gage 1997; van Praag et al. 1999).
Conclusions
The clinical diagnosis of dementia does not tally with level of underlyingneuropathology. The theory of cognitive reserve explains this phenomenon. People with high reserve goundiagnosed 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 brainsize.
If we accept the validity of this model it is important to note that cognitive reserve and all the variables associated withit do not protect fromAlzheimer’s disease. This means that the traditional ideathat 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 sufferingneuropathologicalchanges in the brain will not be picked up by standard clinicalcognitive testing.Conversely anyone who has used these instruments clinically knows thatthey can yield false positives in people with very lowreserve. From this point of view the concept of ‘adequate level ofchallenge’ easily emerges. Conceivably one could measurecognitive reserve and then offer specifically tailored tests that wouldpose enough level of challenge to accurately detect earlycognitive impairment both in individuals with high and low reserve.This has implications for treatment and care. Currently somepeople who would be eligible for it are not offered treatment while itmay offered in other cases needlessly.
In people with high reserve deterioration occurs rapidly once thethreshold is reached. In these individuals and their carersearly diagnosis might provide an opportunity to plan future care and toadjust to the diagnosis while they are still able to makedecisions.
References
Ando J, Ono Y, Wright MJ (2001). Genetic structure of spatial and verbal working memory. Behavioral Genetics. 31(6):615-24.
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.
Katzman R (1993). Education and the prevalence of dementia and Alzheimer‘s disease. Neurology. 43(1):13-20.
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.
Kempermann G, Kuhn HG, Gage FH (1997). More hippocampal neurons in adult mice living in an enriched environment. Nature. 386(6624):493-5.
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.
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.
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.
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.
Richards M, Sacker A (2003). Lifetime antecedents of cognitive reserve. Journal of Clinical and Experimental Neuropsychology. 25(5):614-24.
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.
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.
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.
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.
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.
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.
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.
External Resources
Cognitive Reserve and Lifestyle- SharpBrains blog on brain fitness.
The term cognitive reserve describes the brain‘s resilience toneuropathological damage. There are two models that can be used when exploring the concept ofreserve: brain reserve and cognitive reserve. These terms, albeit often used interchangeably in theliterature, provide a useful way of discussing the models. Using a computer analogy brain reserve can be seen as hardware andcognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve iscommonly 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 personsunexpectedly revealed that there was a discrepancy between the degree ofAlzheimer’sdiseaseneuropathology and the clinical manifestations of the disease (Katzmanet al. 1988). This is to say that some participants whose brains had extensiveAlzheimer’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 toage-matched controls. The investigators speculated with two possible explanations for this phenomenon: these people may have hadincipientAlzheimer‘s disease but somehow avoided the loss of large numbers ofneurons, or alternatively, started with larger brains and moreneurons and thus might be said to have had a greater ‘reserve’. This is the first time this term is used in theliterature in this context.
The study sparked off interest in this area and to try to confirm these initial findings further studies were done. Higherreserve was found to provide a greater threshold before clinical deficit appears (Katzman 1993, Satz 1993, Stern 1994).Furthermore those with higher capacity once they become clinically impaired show more rapid decline (Wilson et al. 2000),probably indicating a failure of all compensatory systems and strategies put in place by the individual with greater reserve tocope with the increasingneuropathogical damage.
Brain Reserve
Brain reserve may be defined as the brain‘s resilience, its ability to cope with increasing damage while still functioningadequately. This passive, threshold model presumes the existence of a fixed cut-off which, once reached, would inevitably heraldthe emergence of the clinical manifestations of dementia.
Brain size
A 1997 study found thatAlzheimer’s diseasepathology in large brains did not necessarily result in clinicaldementia(Mori et al. 1997). Another study reported head circumference to be independently associated with a reduced risk ofclinicalAlzheimer’s disease (Mortimer et al. 2003).
While some studies, like those mentioned, find an association, others do not. This is thought to be because head circumferenceand other approximations are indirect measures.
Number of neurons
The number of synapses is lower in early onset dementia that in late onset dementia (Bigio et al. 2002). This mightindicate a vulnerability to the manifestation of clinical cognitive impairment, although there may be other explanations.
The genetic component of cognitive reserve
Evidence from a twin study indicates a genetic contribution to cognitive functions (Ando, Ono & Wright, 2001).Heritability estimates have been found to be high for general cognitive functions but low for memory itself (Swan et al.1990). Adjusting for the effects of education 79% ofexecutive function can beexplained by genetic contribution (Swan & Carmelli 2002). A study combining twin and adoption studies found allcognitive functions to be heritable. Speed of processing had the highest heritability in thisparticular study (Plomin et al. 1994).
Cognitive Reserve
Cognitive reserve also indicates resilience toneuropathological damage, but theemphasis here is in the way the brain uses its damaged resources. It could be defined as the ability to optimise or maximiseperformance through differential recruitment of brain networks and/or alternative cognitive strategies. This is an efficiencymodel, rather than a threshold model, and it implies that the task is processed using less resources and in a way that makeserrors unlikely to occur.
Education and Occupation
Childhood cognition, educational attainment and adult occupation to all contribute to cognitive reserve independently(Richards & Sacker, 2003). The strongest association in this study was found with childhood cognition.
Lifestyle
For any given level of clinical impairment there is a higher degree of neuropathological changes in the brains of thoseAlzheimer’s diseasesufferers who are involved in greater number of activities. Thisis true even when education and IQ are controlled for. This suggeststhat differences in lifestyle may increase cognitive reserveby making the individual more resilient (Scarmeas et al. 2003).
Global Reserve
In spite of the differences in approach between the models of brain reserve and cognitive reserve, there is evidence that bothmight be interdependent and related. This is where the computer analogy ends, as with the brain it seems that hardware can bechanged by software.
The Neurotrophic effect of Knowledge
The posteriorhippocampi of licensed London taxi drivers was famously found to be largerthan that of matched controls (Maguire et al. 2000). Exposure to an enriched environment (defined as a combination of moreopportunities for physical activity, learning and social interaction) produces not only a host of structural and functionalchanges in the brain but also influences the rate of neurogenesis in adult and senescent animal models (Kempermann, Kuhn &Gage 1997; van Praag et al. 1999).
Conclusions
The clinical diagnosis of dementia does not tally with level of underlyingneuropathology. The theory of cognitive reserve explains this phenomenon. People with high reserve goundiagnosed 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 brainsize.
If we accept the validity of this model it is important to note that cognitive reserve and all the variables associated withit do not protect fromAlzheimer’s disease. This means that the traditional ideathat 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 sufferingneuropathologicalchanges in the brain will not be picked up by standard clinicalcognitive testing.Conversely anyone who has used these instruments clinically knows thatthey can yield false positives in people with very lowreserve. From this point of view the concept of ‘adequate level ofchallenge’ easily emerges. Conceivably one could measurecognitive reserve and then offer specifically tailored tests that wouldpose enough level of challenge to accurately detect earlycognitive impairment both in individuals with high and low reserve.This has implications for treatment and care. Currently somepeople who would be eligible for it are not offered treatment while itmay offered in other cases needlessly.
In people with high reserve deterioration occurs rapidly once thethreshold is reached. In these individuals and their carersearly diagnosis might provide an opportunity to plan future care and toadjust to the diagnosis while they are still able to makedecisions.
References
Ando J, Ono Y, Wright MJ (2001). Genetic structure of spatial and verbal working memory. Behavioral Genetics. 31(6):615-24.
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.
Katzman R (1993). Education and the prevalence of dementia and Alzheimer‘s disease. Neurology. 43(1):13-20.
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.
Kempermann G, Kuhn HG, Gage FH (1997). More hippocampal neurons in adult mice living in an enriched environment. Nature. 386(6624):493-5.
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.
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.
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.
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.
Richards M, Sacker A (2003). Lifetime antecedents of cognitive reserve. Journal of Clinical and Experimental Neuropsychology. 25(5):614-24.
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.
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.
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.
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.
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.
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.
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.
External Resources
Cognitive Reserve and Lifestyle- SharpBrains blog on brain fitness.
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