Furthermore, the study showed that these persons had higher brain weights and greater number of neurons as compared to age-matched controls.
[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.
This passive, threshold model presumes the existence of a fixed cut-off which, once reached, would inevitably lead to clinical manifestations of dementia.
A 1997 study found that Alzheimer's disease pathology in large brains did not necessarily result in clinical dementia.
[6] Another study reported head circumference to be independently associated with a reduced risk of clinical Alzheimer's disease.
[10] Cerebellar circuitry is a site of multiple forms of neuronal plasticity, a factor playing a major role in terms of brain reserve.
It could be defined as the ability to optimize or maximize performance through differential recruitment of brain networks and/or alternative cognitive strategies.
Education is known to play a role in cognitive decline in normal aging, as well as in degenerative diseases or traumatic brain injuries.
Level of education is measured by the number of years an individual spends in school or alternatively, the degree of literacy.
[17] Possibly, the level of education itself provides a set of cognitive tools that allow the individual to compensate for the pathological changes.
[23] In addition to the level of education, it has been shown that bilingualism enhances attention and cognitive control in both children and older adults and delays the onset of dementia.
It allows the brain to better tolerate the underlying pathologies and can be considered as a protective factor contributing positively to the cognitive reserve.
Studies suggest that occupation may provide additive and independent source of cognitive reserve throughout person's life.
[17] Occupation as a proxy for cognitive reserve is positively correlated with local efficiency and functional connectivity in the right medial temporal lobe.
[21] A genetic study using Mendelian randomization analysis demonstrated that high occupation levels were associated with reduced risk for Alzheimer’s disease.
[28] 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.
[29] In other words, everyday experience affecting cognition is analogous to physical exercise influencing musculoskeletal and cardiovascular functions.
One subject showing reduced neocortical plaques survived with mild deficits, despite (or due to) low brain weight.
Previous investigation into Parkinson's disease implicated a possible influence of cognitive reserve in the human brain.
According to some studies[32] the so-called Cognitive Lifestyle is seen as a general protective factor that can be mediated though several different mechanisms.
525 participants with Parkinson’s disease completed different baseline assessments of cognition and provided clinical, social and demographic data.
Exposure to an enriched environment, defined as a combination of more opportunities for physical activity, learning and social interaction, may produce structural and functional changes in the brain and influence the rate of neurogenesis in adult and senescent animal model hippocampi.
[34] Many of these changes can be effected merely by introducing a physical exercise regimen rather than requiring cognitive activity per se.
Katzman et al. (1998) conducted a study on the autopsy results of 10 people and found a pathology related to Alzheimer's disease.