Higher education is not associated with greater cortical thickness in brain areas related to literacy or intelligence in normal aging or mild cognitive impairment
Education may reduce risk of dementia through passive reserve, by increasing neural substrate. We tested the hypotheses that education is associated with thicker cortex and reduced rates of atrophy in brain regions related to literacy and intellectual ability. Healthy older adults and those with mild cognitive impairment were categorized into high (≥18 years) and low (≤13 years) education groups. Higher education was associated with thinner cortices in several areas, but one-year atrophy rates in these areas did not differ by education group. These results do not support a passive reserve model in which early-life education protects against dementia by increasing cortical thickness. Connectivity and synaptic efficiency or other lifestyle factors may more directly reflect cognitive reserve.
Available from: Barbara Basile
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ABSTRACT: Cognitive reserve (CR), for which formal education represents a proxy index, has been claimed as a factor mitigating the clinical manifestations of Alzheimer disease (AD). The aim of this study was to assess the impact of formal education in modifying the relationship between cerebral grey matter (GM) damage and clinical manifestations in a large cohort of patients with AD or amnesic mild cognitive impairment (a-MCI). We recruited 22 patients with AD and 23 with a-MCI, and we classified them in subjects with high (HEL) or low educational level (LEL). All patients underwent a neuropsychological assessment and magnetic resonance imaging (MRI) scanning at 3T. T1-weighted volumes were analyzed, using voxel-based morphometry, for GM investigation. A 1-year clinical follow-up was available for part of the a-MCI patients. There were no between-groups differences in clinical features, memory, and language functions. Conversely, HEL subjects performed better in all tests assessing visuo-spatial abilities. GM volumes of LEL compared with HEL patients were reduced in the supramarginal gyrus bilaterally and in the right posterior cingulate/precuneus and frontal opercular cortex. Conversely, HEL compared with LEL patients showed reduced GM volumes in the entorhinal cortices and temporal poles, regions typically affected by AD pathology. These results remained unchanged when including in the analysis of only patients with clinically proven AD (AD and a-MCI converters). This study suggests that CR produces selective GM changes that mitigate the clinical impact of AD. Moreover, it supports the idea that CR is based on several "brain reserves" rather than on a generalized increase of brain plasticity.
Rejuvenation Research 04/2011; 14(2):143-51. DOI:10.1089/rej.2010.1103 · 3.31 Impact Factor
Available from: Enrico Premi
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ABSTRACT: BACKGROUND: The brain reserve hypothesis posits that there are individual differences in the ability to cope with brain pathology, and that brain damage extent and clinical symptoms are not tightly linked. If cognitive reserve hypothesis has been demonstrated in Alzheimer Disease and Frontotemporal Dementia (FTD), no evidence of reserve mechanisms on behavioural disturbances has been corroborated yet. In FTD, distinct behavioural phenotypes may be identified. OBJECTIVE: To test the behavioural reserve hypothesis in behavioural variant FTD (bvFTD). METHODS: As previously demonstrated, bvFTD patients were grouped into four behavioural phenotypes, i.e. "disinhibited", "apathetic", "language", and "aggressive", by means of Confirmatory Factor Analysis on behavioural assessment. Educational achievement was considered as proxy measure of reserve on behavioural disturbances, and cerebral SPECT as an indirect expression of brain pathology. On each group, the effect of education on brain damage was assessed by slope analysis. RESULTS: A specific effect of education attainment on "disinhibited" phenotype was observed, the higher the education, the greater the hypoperfusion in the right inferior frontal gyrus and the left medial frontal gyrus and right caudate (P<0.001). On the other behavioural phenotypes, no effect of education was reported in modulating brain damage. CONCLUSIONS: We suggest that in neurodegenerative diseases the concept of brain reserve might be extended, as compensatory mechanisms are in action not only for cognitive deficits but for behavioural disturbances as well.
Behavioural brain research 02/2013; 245. DOI:10.1016/j.bbr.2013.01.030 · 3.03 Impact Factor
Available from: Katell Mevel
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ABSTRACT: More educated elders are less susceptible to age-related or pathological cognitive changes. We aimed at providing a comprehensive contribution to the neural mechanism underlying this effect thanks to a multimodal approach. Thirty-six healthy elders were selected based on neuropsychological assessments and cerebral amyloid imaging, i.e. as presenting normal cognition and a negative florbetapir-PET scan. All subjects underwent structural MRI, FDG-PET and resting-state functional MRI scans. We assessed the relationships between years of education and i) gray matter volume, ii) gray matter metabolism and iii) functional connectivity in the brain areas showing associations with both volume and metabolism. Higher years of education were related to greater volume in the superior temporal gyrus, insula and anterior cingulate cortex and to greater metabolism in the anterior cingulate cortex. The latter thus showed both volume and metabolism increases with education. Seed connectivity analyses based on this region showed that education was positively related to the functional connectivity between the anterior cingulate cortex and the hippocampus as well as the inferior frontal lobe, posterior cingulate cortex and angular gyrus. Increased connectivity was in turn related with improved cognitive performances. Reinforcement of the connectivity of the anterior cingulate cortex with distant cortical areas of the frontal, temporal and parietal lobes appears as one of the mechanisms underlying education-related reserve in healthy elders.
NeuroImage 06/2013; 83. DOI:10.1016/j.neuroimage.2013.06.053 · 6.36 Impact Factor
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