The notion of ‘cognitive reserve’ has been deployed to help deal with the fact that people who have been found to have similar levels of damage/pathology in their brains at death (from, for example, Alzheimer’s Disease) exhibited different levels of cognitive functioning during life(Stern, 2002, 2006). These observations suggest some people’s brains can cope with damage better than others and they raise the question – why? ‘Cognitive reserve’ works to help frame the answers to that question.
‘Cognitive reserve’ functions in a similar fashion to the phrase ‘emergent property’; they are both ways of drawing together ideas to clarify what we know and to direct our questions regarding what we don’t know. Stern describes‘cognitive reserve’ as a heuristic to guide future research.
Anyway, Stern helpfully breaks down ‘cognitive reserve’ into three components that will probably prove to be inter-dependent when people begin to understand their physiological underpinnings.
(1) Passive reserve or “Brain Reserve Capacity” and the notion of a threshold.
This idea rests on an assumption that our ability to cope with damage to the brain is pretty much hardwired into us. It might correlate with the overall size of our brains or the number of neurons or the degree of interconnectedness between them. It also rests on the notion that there is some sort of threshold to the amount of damage that can be absorbed by the brain before that damage is reflected in outward changes in cognitive or behavioural functioning. So, if you have a higher brain reserve you can absorb more damage than those who have a lower reserve.
This is not an unreasonable model. But the work by, for example, Chen et al. (2010) and Taki et al. (2011) show that the brain is changing over time even in healthy adults and that the changes are distributed heterogeneously across the brain. Chen et al. (2010) “found that the anterior hippocampus showed greater age-related atrophy. Additionally, [they] observed that right hippocampal tail volume correlated with spatial memory and learning, while left hippocampal body volume correlated with delayed verbal memory.” Meanwhile, Taki et al. (2011) concluded that white matter integrity, rather than white matter volume, is important to cognitive functioning in healthy elderly subjects. However, they also found significant positive correlations between gray matter volume and the cognitive functions of semantic memory and short-term memory. Both white matter integrity and grey matter volume change with age. So the notion of brain reserve is, perhaps, not fine grained enough to deal with this.
(2) Active reserve models.
These are split into 2 models – “Cognitive Reserve” and “Compensation”.
(2a) “Cognitive Reserve”
With this notion, Stern wants to give voice to the idea that over the courses of our lives, the structure of our brains shifts and changes. We develop through our education, our working life experiences, through our hobbies and interests; in doing so we develop cognitive strategies for dealing with certain tasks. If we become expert at certain tasks we might develop multiple strategies for dealing with them. If not then we might only have one way of dealing with a cognitive task. If our brains are damaged in some ways impairing a certain function then people who have richer life experiences or higher education, might be able to unknowingly make use of other cognitive strategies in order to get around that damage; whilst other people may not. Those then that can invoke multiple, ‘normal’ ways to get around the damaged function will therefore not exhibit the same symptoms as those with limited cognitive options.
Here we are dealing with a slightly different notion that taps into ideas about neural plasticity. This suggests that where brain damage inhibits a certain function, the brain can adapt by co-opting other parts of the brain not normally employed in that function to help compensate for the lack of functioning. The more people can do that then the fewer symptoms they may display for a given level of damage or pathology.
The paper by Cherry et al. (2010) gives some insight into this. They looked at tasks requiring uni-lateral or bi-lateral functioning, i.e when a task could be dealt with using only one half of their brain or shared out across both halves. Their conclusions were that bi-lateralisation was possible but that the cognitive function was less efficient than when the task could be carried out uni-laterally.
However, Stern also notes that both active models require a neural substrate. Implicitly there is a limit to them, when the pathology is sufficient to damage large swathes of the neural substrate then neither cognitive reserve nor compensation have the capacity to act.
The active models are the more interesting because they suggest that people have the capacity to adapt and change. We can infer that interventions can facilitate such processes. Strauch (2011) rightly raises the questions – When do those interventions needs to take place? Is there an upper age limit? Can we continue to intervene and possibly improve the active reserve capacity even when a disease such as dementia has already begun to take effect?
Chen, K.H.M., Chuah , L.Y.H, Sim, S.K.Y & Chee, M.W.L. (2010) ‘Hippocampal region-specific contributions to memory performance in normal elderly’, Brain and Cognition, 72, 400–407
Cherry, B.J., Yamashiro, M., Anderson, E., Barrett, C., Adamson, M.M. & Hellige, J.B. (2010)
‘Exploring interhemispheric collaboration in older compared to younger adults’, Brain and Cognition, 72, 218–227
Stern, Y. (2002) ‘What is cognitive reserve? Theory and research application of the reserve concept’, Journal of the International Neuropsychological Society, 8, 448–460
Stern. Y. (2006) ‘Cognitive Reserve and Alzheimer Disease’, Alzheimer Dis. Assoc. Disord., 20, 112–117
Strauch, B. (2011) The Secret Life of the Grown-Up Brain: Discover the Surprising Talents of the Middle-Aged Mind, London: Penguin Books
Taki, Y., Kinomura, S., Sato, K., Goto, R., Wub, K., Kawashima, R. & Fukuda, H., (2011) ‘Correlation between gray/white matter volume and cognition in healthy elderly people’, Brain and Cognition, 75, 170–176