What provides cerebral reserve?

Abstract

The cerebral reserve hypothesis is a heuristic concept used to explain apparent protection from the onset of cerebral disease and/or cognitive decline in old age. A significant obstacle when investigating the reserve hypothesis is the absence of baseline data with which to compare current cognitive status. We tested the influence of three hypothesized proxies of reserve (education, head size and occupational attainment [OCC]) in 92 volunteers born in 1921, whose cognitive function was measured at age 11 and 79 years, and who underwent brain MRI. The association between each proxy and old age cognitive function was tested, adjusting for variance contributed by childhood mental ability and detrimental age-related pathological changes measured using MRI. The results showed that education and OCC, but not total intracranial volume (TICV), contribute to cerebral reserve and help retain cognitive function in old age. Education was found to contribute between 5 and 6% of the variance found in old age memory function but was found to have no significant association with reasoning abilities. OCC was found to contribute around 5% of the variance found in old age memory function and between 6 and 8% of the variance found in old age reasoning abilities. We conclude that the intellectual challenges experienced during life, such as education and occupation, accumulate reserve and allow cognitive function to be maintained in old age.

Use it or lose it? SES mitigates age-related decline in a recency/recognition task

“…On the contrary, there was no evidence for a protective role of larger total intracranial brain volume as proposed by brain reserve capacity models. Hence, this study provides empirical evidence for the protective effect of education and occupation above and beyond differences in individual memory abilities that had been present in childhood [62].…”

“…A recent MRI study by Staff et al [62] tested this hypothesis empirically. In order to dissociate the protective effects of three proxies for reserve (total brain volume, education and occupational attainment) from pre-existing differences in the level of cognitive ability, a large sample of elderly volunteers whose cognitive abilities had been evaluated previously at age 11 was re-examined at age 79.…”

Ageing and the brain

“…Elevated cholesterol and blood pressure, both linked to obesity and excess calorie intake, and elevated blood homocysteine are risk factors for the development both of AD and cerebrovascular disease [87][88][89]. Other beneficial influences on brain function in old age are physical exercise [90], extended years of education [91,92], cognitive stimulation [93] and a high intake of polyunsaturated fatty acids [94] and B vitamins, particularly vitamins B6, B12 and folate [95] and statins [96]. The influence of toxins in causing brain damage in normal brain ageing is not clear but vigilance is called for, as some environmental toxins have been implicated as risk factors in age-related disease, for example, the pesticide rotenone and the herbicide paraquat in PD [97] and a product of cycad seeds, β-methylamino-L-alanine (BMAA), in Guam disease [98].…”

Traumatic Brain Injury and Executive Functioning in an Incarcerated Sample

“…Neural reserves are pre-existing cognitive processes that are efficient and effective enough to withstand disruptions by brain damage, and neural compensation is the development of new cognitive processes to work around significant disruptions caused by brain damage (Stern, 2007 (Manly, Touradji, Tang & Stern, 2003;Staff et al, 2004;Ardila, Ostrosky-Solis, Rosselli, & Gomez, 2000).…”

“…Research has also demonstrated relationships between later cognitive decline and premorbid intellectual ability (Alexander et al, 1997;Richards & Sacker, 2003) and occupational attainment (Staff et al, 2004). Siedlecki and colleagues (2009) tested the validity of cognitive reserve as a distinct construct and found strong convergent validity and moderate discriminant validity.…”