Cognitive reserve (CR) has been defined as the ability to cope with brain damage in order to delay the onset of clinical, cognitive and functional manifestations of the pathology and minimize their expression (Stern, 2002). The concept of CR arose from the field of dementia, specifically Alzheimer’s disease, in an attempt to find an explanation for the observed lack of relationship between the degree of brain pathology and its manifestation (in terms of symptomatology or of cognitive deficits). One of the pioneers in this area was Roth in 1955 (Roth, 1955), who observed that in some cases the degree of a dementia’s severity did not correlate with the amount of brain damage (measured by the number of senile plaques). Initially, an attempt was made to explain this fact with the threshold theory, which proposed that only when it was surpassed did it lead to the appearance of clinical manifestations. Later, a more complex model was considered in which each person could have a different threshold of tolerance and that clinical manifestations would depend on how the brain used the remaining neural substrate (Stern, 2002). As a result, individuals with higher CR would have a greater ability to use a neural network in a more efficient way, using alternative neural networks or cognitive strategies in order to actively compensate for the effects of a pathology affecting brain function (Stern, 2002). From this perspective, higher CR has been considered a protective factor against the symptomatology and dysfunctionality of brain disease, and lower levels a vulnerability factor. Therefore, CR might explain why some individuals with similar brain pathologies have different clinical presentations (Stern, 2013).
Over the past few years, it has been postulated that this concept can also be adapted to mental disorders. In fact, in 2006 Barnett and collaborators (Barnett et al., 2006) proposed that CR could be used in different neuropsychiatric disorders, using the example of schizophrenia. They assume that, unlike in Alzheimer’s disease, in schizophrenia the pathology can interfere with the quantity of accumulated CR. Another assumption is that it would be impossible to establish CR and the neuropsychiatric pathology itself as totally independent variables. In fact, in all studies that have compared CR levels in people with severe mental disorders and healthy control subjects, patients have shown lower CR than controls.
https://www.sciencedirect.com/science/article/pii/S0924977X2100208X