The cognitive reserve hypothesis, which suggests brain-stimulating activities may stall late-life cognitive decline, received a boost via research published online July 3 in Neurology. The researchers reported more frequent cognitive activity at any age is associated with slower cognitive decline later in life independent of neuropathologic conditions.
Robert S. Wilson, PhD, from the Rush Alzheimer’s Disease Center in Chicago, and colleagues aimed to test the cognitive reserve hypothesis, as the link between participation in cognitively stimulating activities and reduced late-life cognitive decline is not well-delineated. The dominant hypotheses are the cognitive reserve hypothesis and the reverse causality hypothesis, which suggests cognitive inactivity may be a consequence of neuropathologic lesions rather than a risk factor.
Wilson and colleagues reviewed data from 294 participants in the Rush Memory and Aging Project who rated early- and late-life cognitive activities, participated in annual cognitive testing for a mean of 5.8 years and underwent a post-mortem neuropathologic exam to determine chronic gross infarcts, chronic microscopic infarcts, neocortical Lewy bodies, B-amyloid burden and tau-positive tangle density.
The mixed-effects model associated higher frequency late-life cognitive activity with a higher level of cognitive function and a slower rate of cognitive decline. Compared to participants with average activity, those with infrequent activity (10 th percentile) decline increased by 48.4 percent, reported Wilson et al. Decline was reduced by 32.3 percent among those in the 90 th percentile of late-life cognitive activity.
Results for early-life (childhood, young adulthood and middle age) cognitive activities mirrored the late-life findings.
Wilson and colleagues estimated that cognitive activity across life accounted for nearly 15 percent of variability in cognitive decline not attributable to neuropathologic burden. “This finding supports the cognitive reserve hypothesis and suggests that the association of cognitive activity with lack of cognition is not the result of reverse causality.”