The term cognitive reserve
describes the mind's resilience to neuropathological
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. 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. 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.
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.
A 1997 study found that Alzheimer’s disease pathology
in large brains did not necessarily result in clinical dementia
. Another study reported head circumference to be independently associated with a reduced risk of clinical Alzheimer’s disease
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 neurons
The number of synapses is lower in early onset dementia that in late onset dementia. This might indicate a vulnerability to the manifestation of clinical cognitive impairment, although there may be other explanations.
Genetic component of cognitive reserve
Evidence from a twin study indicates a genetic contribution to cognitive functions. Heritability estimates have been found to be high for general cognitive functions but low for memory itself. Adjusting for the effects of education 79% of executive function
can be explained by genetic contribution . 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.
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 occupation
Childhood cognition, educational attainment, and adult occupation all contribute to cognitive reserve independently. The strongest association in this study was found with childhood cognition.
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. 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 neocortical plaques survived with mild deficits, despite (or due to) low brain weight.
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.
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. 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. Interestingly, many changes can be effected merely by introducing a physical exercise regimen.
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.