Cognitive reserve

Cognitive reserve is the mind's and brain's resistance to damage of the brain. The mind's resilience is evaluated behaviorally, whereas the neuropathological damage is evaluated histologically, although damage may be estimated using blood-based markers and imaging methods. 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] some participants whose brains had extensive Alzheimer's disease pathology, had no or very few clinical 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 has been 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 showed more rapid decline once becoming clinically impaired, probably indicating a failure of all compensatory systems and strategies put in place by the individual with greater reserve to cope with the increasing neuropathological damage.[5]

  1. ^ Katzman R, Terry R, DeTeresa R, Brown T, Davies P, Fuld P, Renbing X, Peck A (February 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. doi:10.1002/ana.410230206. PMID 2897823. S2CID 31389744.
  2. ^ Katzman R (January 1993). "Education and the prevalence of dementia and Alzheimer's disease". Neurology. 43 (1): 13–20. doi:10.1212/wnl.43.1_part_1.13. PMID 8423876. S2CID 42469859.
  3. ^ Stern Y, Gurland B, Tatemichi TK, Tang MX, Wilder D, Mayeux R (April 1994). "Influence of education and occupation on the incidence of Alzheimer's disease". JAMA. 271 (13): 1004–10. doi:10.1001/jama.1994.03510370056032. PMID 8139057.
  4. ^ Satz P, Morgenstern H, Miller EN, Selnes OA, McArthur JC, Cohen BA, Wesch J, Becker JT, Jacobson L, D'Elia LF (May 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 Syndromes. 6 (5): 503–11. doi:10.1097/00126334-199305000-00011. PMID 8483113.
  5. ^ Wilson RS, Bennett DA, Gilley DW, Beckett LA, Barnes LL, Evans DA (December 2000). "Premorbid reading activity and patterns of cognitive decline in Alzheimer disease". Archives of Neurology. 57 (12): 1718–23. doi:10.1001/archneur.57.12.1718. PMID 11115237.