Influence of education on the pattern of cognitive deterioration in AD patients: The cognitive reserve hypothesis

INSERM U.593, Université Victor Ségalen, Bordeaux, France.
Brain and Cognition (Impact Factor: 2.48). 04/2005; 57(2):120-6. DOI: 10.1016/j.bandc.2004.08.031
Source: PubMed


The cognitive reserve hypothesis proposes that a high educational level could delay the clinical expression of Alzheimer's disease (AD) although neuropathologic changes develop in the brain. Therefore, some studies have reported that when the clinical signs of the disease emerge, high-educated patients may decline more rapidly than low-educated patients because the neuropathology is more advanced. However, these studies have only investigated the decline of global cognition or an isolated cognitive process. To study the differential deterioration pattern of several cognitive processes according to education, the performance of 20 AD patients with a high educational level and a low educational level were compared with the performance of 20 control subjects on a neuropsychological battery. The results showed that cognitive deterioration of AD patients is different according to education, although the global performance was similar in AD patients. The high-educated patients exhibited greater impairment of abstract thinking whereas the low-educated patients showed greater impairment of memory and attentional function. This confirms that some cognitive processes, such as abstract thinking, decline more rapidly in high-educated patients whereas others seem to evolve more slowly if compared to low-educated patients. In this latter case, high-educated patients may still benefit from cognitive reserve after the diagnosis of the dementia.

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    • "The publisher shall not be liable for any loss, actions, claims, proceedings, demand, or costs or damages whatsoever or howsoever caused arising directly or indirectly in connection with or arising out of the use of this material. may reduce the progression of memory decline and deterioration both in Alzheimer's disease (Koepsell et al., 2008; Le Carret et al., 2005; Stern, Albert, Tang, & Tsai, 1999) and in vascular dementia (Lane, Paul, Moser, Fletcher, & Cohen, 2011); may reduce the risk for dementia during aging (Stern et al., 1994; Valenzuela & Sachdev, 2006); and may explain cognitive performance variability in subjects with WMC (Schmidt et al., 2011) or with cognitive impairment and dementia (Vemuri et al., 2011). Those measures, such as reading ability, vocabulary, mental stimulation, and occupational attainment, which reflect lifetime experiences, have therefore been used as surrogate markers of the construct of cognitive reserve (Jones et al., 2011; Siedlecki et al., 2009). "
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    ABSTRACT: The present study aims to investigate the protective effect of formal education on age-related changes in different cognitive domains with the hypothesis that it may attenuate the rate of decline. Individuals aged 50 years or older attending primary care physicians without known brain disease (431 participants, mostly [60.3%] female with 66.3 [±9.1] years of age and 7.7 [±4.1] years of education, on average), were evaluated with a neuropsychological battery including 28 cognitive measures. Cognitive domains identified by factor analysis were subject to repeated multiple regression analyses to determine the variance explained by age and education controlling for gender, depressive symptoms, and vascular risk factors. The slope of the regression equation was compared between two educational groups with an average of 4 years and 11 years of education, respectively. Factors identified corresponded to processing ability (Factor 1), memory (Factor 2), and acquired knowledge (Factor 3). Although education improved performance in Factors 1 and 3, it did not change the slope of age-related decline in any factor. This study suggests that in culturally heterogeneous groups, small increments in education enhance cognition but do not modify the rate of decline of executive functioning with age. These results contradict some clinical findings and need to be confirmed in longitudinal studies.
    Applied Neuropsychology 10/2012; 19(4):287-98. DOI:10.1080/09084282.2012.670145 · 1.97 Impact Factor
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    • "Roe et al. (2008) suggest that cognitive reserve, as reflected in education, may have a stronger or earlier effect on specific cognitive processes such as the abstract reasoning, compared with other cognitive processes. An inverse correlation was found in the study by Le Carret et al. (2005). "
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    ABSTRACT: We sought to longitudinally evaluate the potential association of educational level with performance on verbal and nonverbal tasks in individuals with mild cognitive impairment (MCI). We evaluated patients with MCI, age >50 years, no medication intake, absent vascular risk factors, and no lesions on brain magnetic resonance imaging (MRI). Each patient underwent a clinical assessment packet and a series of neuropsychological tests of the language and constructional praxis subtests of Cambridge Cognitive Examination (CAMGOG) and the Boston naming test (BNT), at baseline, 6 months, and 12 months. Educational levels were defined taking into account the total years of education, the school level, and diplomas. MCI patients with low education level showed a stepwise reduction in scores of naming objects (NO; P = 0.009), definition (DF; P = 0.012), language (LT; P = 0.021), constructional praxis (CD; P = 0.022), confrontation naming skills (BXB; P = 0.033), phonemic help (BFB; P = 0.041), and BNT (P = 0.002). Analysis of covariance, controlling for baseline scores, showed that education was associated with NO score (P = 0.002), DF score (P = 0.005), LT (P = 0.008), CD score (P = 0.008), BXB score (44.36 ± 1.84, P = 0.0001), BFB (P = 0.022), and BNT (P = 0.004). Our findings indicate that education appeared to affect verbal and nonverbal task performance in MCI patients. Despite the fact that higher educated patients are more acquainted with the tasks, slower deterioration in consecutive follow-up examinations could be explained by the cognitive reserve theory. The potential association of this protective effect with delayed onset of symptoms deserves further investigation.
    Brain and Behavior 09/2012; 2(5):620-7. DOI:10.1002/brb3.88 · 2.24 Impact Factor
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    • "The studies that have investigated the effect of cognitive reserve on the rate of decline in Alzheimer's disease (i.e. after onset of dementia) support the hypothesis that although cognitive reserve may delay the onset of dementia, after the onset of dementia the rate of cognitive decline differs based on the subjects' cognitive reserve. Some authors have found that subjects with higher cognitive reserve decline much faster (Unverzagt et al., 1998; Stern et al., 1999; Andel et al., 2006; Hall et al., 2007; Bruandet et al., 2008; Roselli et al., 2009) while others have found that subjects with higher cognitive reserve decline more slowly (Fritsch et al., 2001, 2002; Bennett et al., 2003; Manly et al., 2003; Le Carret et al., 2005) when compared to subjects with low cognitive reserve . In addition, there was also evidence that the rate of decline is the same in both the groups (Del Ser et al., 1999; Paradise et al., 2009). "
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    ABSTRACT: The objective of this study was to investigate how a measure of educational and occupational attainment, a component of cognitive reserve, modifies the relationship between biomarkers of pathology and cognition in Alzheimer's disease. The biomarkers evaluated quantified neurodegeneration via atrophy on magnetic resonance images, neuronal injury via cerebral spinal fluid t-tau, brain amyloid-β load via cerebral spinal fluid amyloid-β1-42 and vascular disease via white matter hyperintensities on T2/proton density magnetic resonance images. We included 109 cognitively normal subjects, 192 amnestic patients with mild cognitive impairment and 98 patients with Alzheimer's disease, from the Alzheimer's Disease Neuroimaging Initiative study, who had undergone baseline lumbar puncture and magnetic resonance imaging. We combined patients with mild cognitive impairment and Alzheimer's disease in a group labelled 'cognitively impaired' subjects. Structural Abnormality Index scores, which reflect the degree of Alzheimer's disease-like anatomic features on magnetic resonance images, were computed for each subject. We assessed Alzheimer's Disease Assessment Scale (cognitive behaviour section) and mini-mental state examination scores as measures of general cognition and Auditory-Verbal Learning Test delayed recall, Boston naming and Trails B scores as measures of specific domains in both groups of subjects. The number of errors on the American National Adult Reading Test was used as a measure of environmental enrichment provided by educational and occupational attainment, a component of cognitive reserve. We found that in cognitively normal subjects, none of the biomarkers correlated with the measures of cognition, whereas American National Adult Reading Test scores were significantly correlated with Boston naming and mini-mental state examination results. In cognitively impaired subjects, the American National Adult Reading Test and all biomarkers of neuronal pathology and amyloid load were independently correlated with all cognitive measures. Exceptions to this general conclusion were absence of correlation between cerebral spinal fluid amyloid-β1-42 and Boston naming and Trails B. In contrast, white matter hyperintensities were only correlated with Boston naming and Trails B results in the cognitively impaired. When all subjects were included in a flexible ordinal regression model that allowed for non-linear effects and interactions, we found that the American National Adult Reading Test had an independent additive association such that better performance was associated with better cognitive performance across the biomarker distribution. Our main conclusions included: (i) that in cognitively normal subjects, the variability in cognitive performance is explained partly by the American National Adult Reading Test and not by biomarkers of Alzheimer's disease pathology; (ii) in cognitively impaired subjects, the American National Adult Reading Test, biomarkers of neuronal pathology (structural magnetic resonance imaging and cerebral spinal fluid t-tau) and amyloid load (cerebral spinal fluid amyloid-β1-42) all independently explain variability in general cognitive performance; and (iii) that the association between cognition and the American National Adult Reading Test was found to be additive rather than to interact with biomarkers of Alzheimer's disease pathology.
    Brain 05/2011; 134(Pt 5):1479-92. DOI:10.1093/brain/awr049 · 9.20 Impact Factor
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