Cognitive reserve and cortical thickness in preclinical Alzheimer’s disease

Abstract

This study examined whether cognitive reserve (CR) alters the relationship between magnetic resonance imaging (MRI) measures of cortical thickness and risk of progression from normal cognition to the onset of clinical symptoms associated with mild cognitive impairment (MCI). The analyses included 232 participants from the BIOCARD study. Participants were cognitively normal and largely middle aged (M age = 56.5) at their baseline MRI scan. After an average of 11.8 years of longitudinal follow-up, 48 have developed clinical symptoms of MCI or dementia (M time from baseline to clinical symptom onset = 7.0 years). Mean thickness was measured over eight ‘AD vulnerable’ cortical regions, and cognitive reserve was indexed by a composite score consisting of years of education, reading, and vocabulary measures. Using Cox regression models, CR and cortical thickness were each independently associated with risk of clinical symptom onset within 7 years of baseline, suggesting that the neuronal injury occurring proximal to symptom onset has a direct association with clinical outcomes, regardless of CR. In contrast, there was a significant interaction between CR and mean cortical thickness for risk of progression more than 7 years from baseline, suggesting that individuals with high CR are better able to compensate for cortical thinning that is beginning to occur at the very earliest phase of AD.

The impact of education on cortical thickness in amyloid-negative subcortical vascular dementia: cognitive reserve hypothesis

“…However, there was no correlation between education and cortical thickness in patients with svMCI in our study. The results are also consistent with studies in patients with AD dementia, showing higher education levels to be associated with more cortical thinning [ 10 ], whereas these effects were not prominent in MCI stage [ 40 , 41 ]. In terms of MCI, not subcortical vascular type, there are several studies with inconsistent results regarding cognitive reserve.…”

Relationship Between Risk Factors and Brain Reserve in Late Middle Age: Implications for Cognitive Aging

“…Whereas three of the four the dynamic brain reserve measures we used were associated with multiple general health factors. Importantly, our work builds upon recent studies that have started to expand our view of brain reserve with the incorporation of glucose metabolism, white matter integrity, and patterns of gray matter volume and cortical thickness (Querbes et al, 2009;Smith et al, 2010;Arenaza-Urquijo et al, 2013;Ewers et al, 2013;Morbelli et al, 2013;Malpetti et al, 2017;Pettigrew et al, 2017;Laubach et al, 2018). As shown in our results, the incorporation of carefully selected dynamic neuroimaging measures associated with cognitive aging may provide additional tools for the study of brain reserve; however, this will require future studies in independent samples.…”

Simvastatin ameliorates cognitive impairments via inhibition of oxidative stress‑induced apoptosis of hippocampal cells through the ERK/AKT signaling pathway in a rat model of senile dementia

“…Previous reviews have discussed the effectiveness of statins in the prevention of dementia, but there is insufficient evidence to recommend statins for the treatment of Alzheimer's disease, a condition that leads to the development of numerous forms of dementia (9,10). Pathogenesis of senile dementia mainly targets the hippocampal area associated with memory and cognition, and leads to cognitive function disorders and impairments of cognition including, memory, language and attention (11,12). Elevated rates of apoptosis and oxidative stress in hippocampal cells are frequently observed in patients with senile dementia (13).…”