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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Psychol Aging. 2015 Feb 9;30(1):74–82. doi: 10.1037/pag0000013

Conscientiousness, Dementia Related Pathology, and Trajectories of Cognitive Aging

Robert S Wilson 1, Patricia A Boyle 2, Lei Yu 3, Eisuke Segawa 4,5, Joel Sytsma 6, David A Bennett 7
PMCID: PMC4361241  NIHMSID: NIHMS659484  PMID: 25664558

Abstract

The study aim was to determine the contribution of dementia related pathologies to the association of conscientiousness with late-life cognitive health. At enrollment in 2 longitudinal clinical-pathologic cohort studies, 309 older persons without cognitive impairment completed a standard conscientiousness measure. Annually thereafter, they completed a battery of 17 cognitive tests. Upon death, they underwent a uniform neuropathologic examination from which measures of neurofibrillary tangles, Lewy bodies, chronic gross cerebral infarction, and hippocampal sclerosis were derived. The relation of conscientiousness and the neuropathologic markers to cognitive decline was assessed in mixed-effects change point models to accommodate nonlinear cognitive decline. During a mean of 10.7 years of follow-up, annual decline on a composite measure of global cognition (baseline mean=0.082, SD = 0.499) was gradual (estimated mean = −0.036, 95% confidence interval [CI]: −0.046, −0.025) until a mean of 3.2 years before death (95% CI: −3.6, −2.8) when it accelerated to a mean annual loss of 0.369-unit (95% CI: −0.426,−0.317), a tenfold increase. Higher conscientiousness (baseline mean = 33.6, SD = 5.1) was associated with slower terminal decline (estimate=0.064, 95% CI: 0.024, 0.103) but not preterminal decline (estimate =0.005, 95% CI: −0.003, 0.013). After adjustment for neuropathologic burden, conscientiousness was still related to terminal decline (estimate = 0.057, 95% CI: 0.019, 0.094) and accounted for 4% of the variance in terminal slopes. In addition, the association of neocortical Lewy bodies with terminal cognitive decline was attenuated in those with higher conscientiousness. The results suggest that higher conscientiousness is protective of late-life cognitive health.

Keywords: conscientiousness, terminal cognitive decline, Lewy bodies

Introduction

Conscientiousness, a personality trait denoting goal directedness and self-control (Roberts, Lejuez, Krueger, Richards, & Hill, 2014) is related to cognitive health in old age, with lower level of the trait predicting more rapid cognitive decline (Wilson, Schneider, Arnold, Bienias, & Bennett, 2007; Chapman et al., 2012) and higher risk of dementia (Wilson et al., 2007; Duberstein et al., 2011; Terracciano et al., 2014). The factors underlying this association are not known. Because dementia is usually preceded by a decade or more of cognitive slippage (Amieva et al., 2008; Wilson, Leurgans, Boyle & Bennett, 2011) and conscientiousness declines as individuals develop mild cognitive impairment (Donati et al., 2013) and dementia (Robins Wahlin & Byrne, 2011; Duchek, Balota, Storandt, & Larsen, 2007), one hypothesis is that low conscientiousness predicts cognitive loss because it is an early sign of its occurrence rather than a true risk factor (Duberstein et al., 2011). However, in previous analyses of data from the Religious Orders Study, there was no evidence that conscientiousness was associated with dementia related pathology as predicted by a reverse causality hypothesis (Wilson et al., 2007).

Much of the association of conscientiousness with noncognitive health outcomes appears to be mediated by social environmental factors and health related behaviors (Bogg & Roberts, 2004), but it is difficult to imagine how conscientiousness could influence cognitive health without somehow affecting the brain. Because personality traits are enduring dispositions to think, act, and feel in particular ways, and because experience dependent neuroplastic changes are well documented in animal (Markham & Greenough, 2004; Barnes & Finnerty, 2010) and human (Draganski et al., 2006; Woollett & Maguire, 2011) research, it is likely that traits do influence brain organization and function over the life span. For example, conscientiousness and related traits have been associated with functional (Brown, Manuck, Flory, & Harris, 2006) and volumetric (Jackson, Balota, & Head, 2011) variation in prefrontal cortex. In old age, therefore, a high level of conscientiousness might help support cognitive aging independently of dementia related pathologic burden, modify the impact of pathology on cognitive aging, or both. Understanding the bases of the association of conscientiousness with late-life change in cognitive function may suggest novel strategies for maintaining cognitive health in old age, but knowledge is limited because few studies have the requisite antemortem and postmortem data.

In this paper, we examine the associations among conscientiousness, cognitive aging, and postmortem pathologic markers linked to dementia. Participants are 309 older individuals without cognitive impairment at enrollment in the Religious Orders Study or Rush Memory and Aging Project, longitudinal clinical-pathologic cohort studies with nearly identical protocols. At study baseline, participants completed a standard self report measure of conscientiousness. Cognitive function was assessed annually for a mean of 10.7 years. At death, there was a uniform neuropathologic examination to assess 4 common lesions associated with dementia and cognitive decline. In a series of mixed-effects change point models that allowed cognitive decline to accelerate in the last years of life, we tested 3 non-mutually exclusive hypotheses about the association of conscientiousness and late-life cognitive health: that conscientiousness is associated with dementia related pathology; that conscientiousness modifies the relation of pathology to cognitive decline; and that conscientiousness is associated with residual variability in cognitive trajectories not attributable to dementia related pathologies.

Methods

Participants

All data are from older individuals who participated in one of two ongoing clinical-pathologic studies initiated in the 1990s. In the Religious Orders Study, Catholic nuns, priests, and monks were recruited from sites across the United States (Wilson, Bienias, Evans, & Bennett, 2004; Bennett, Schneider, Arvanitakis, & Wilson, 2012), and in the Rush Memory and Aging Project, lay persons were recruited from the Chicago metropolitan region (Bennett, Schneider, Buchman, Mendes de Leon, & Wilson, 2005; Bennett et al., 2012). Eligibility for each study required the absence of a dementia diagnosis prior to enrollment, age at baseline >50, and agreement to annual examinations and brain autopsy at death. Participants signed an informed consent and anatomical gift act. The institutional review board of Rush University Medical Center approved each study.

At the time of these analyses, 2,040 persons had personality data. To minimize error in measuring conscientiousness, we excluded 518 individuals with cognitive impairment at the time of personality assessment (438 with mild cognitive impairment, 80 with dementia). This left 1,522 individuals at baseline. There were 155 persons ineligible for follow-up due to death in the first study year (n=43) or enrollment within the past study year (n=112). Follow-up data were available on 1,347 of the remaining 1,367 individuals (98.5 %), and 961 had completed at least 5 annual cognitive assessments, which we required to adequately capture nonlinear cognitive change. Of 365 who died in this latter group, 351 (96.2 %) underwent a brain autopsy, and a uniform neuropathological examination had been completed on the first consecutive 338 individuals. We excluded 19 persons without complete pathologic data and 10 persons who did not complete a cognitive assessment within 2 years of death. This left 309 individuals eligible for analyses and they had a mean of 10.7 years of annual cognitive testing (SD=4.0). Because the Rush Memory and Aging Project began later than the Religious Orders Study and personality assessment was introduced after study baseline, most individuals (n=302) were from the Religious Orders Study. The participants died at a mean age of 87.6 (SD = 6.8) which was a mean of 0.6 year since the last clinical evaluation (SD = 0.4); they had completed an average of 18.2 years of formal schooling (SD =3.4); 109 (35.3 %) were men.

Assessment of Personality and Affect

The 12-item measures of conscientiousness and neuroticism from the NEO Five-Factor Inventory (Costa & McCrae, 1992) were administered once in each study. This was the baseline evaluation of the Religious Orders Study but a later evaluation in the Rush Memory and Aging Project, which for the purposes of these analyses was treated as baseline. Agreement with each item was rated on a 5-point scale. Item scores ranged from 0 to 4 and were added to yield a total score for each trait that ranged from 0 to 48. Cronbach's coefficient alpha was 0.82 for conscientiousness and 0.80 for neuroticism, indicating adequate internal consistency. Based on prior research (Saucier, 1998), we created scores for 3 conscientiousness facets (orderliness, goal striving, dependability) and 2 neuroticism facets (negative affect, self reproach). Because the facets do not have the same number of items, we used mean items scores in facet analyses. Depressive symptoms were assessed at baseline with a 10-item Center for Epidemiological Studies Depression Scale (Kohout, Berkman, Evans, & Cornoni-Huntly, 1993). For each of 10 symptoms (e.g., “I felt sad”), participants were asked if they had felt that way much of the past week. The score, which is the number symptoms endorsed, has previously been associated with cognitive decline (Wilson, Mendes de Leon, Bennett, Bienias, & Evans, 2004) and mortality (Wilson, Bienias, Mendes de Leon, Evans, & Bennett, 2003).

Assessment of Cognitive Function

A battery of 17 cognitive performance tests was administered annually in each study by trained research assistants. There were 7 episodic memory measures: immediate and delayed story recall (Wilson et al., 2002), Logical Memory Ia and IIa (Wechsler, 1987), and Word List Memory, Word List Recall, and Word List Recognition (Welsh et al., 1994). Semantic memory was assessed with a 15-item version (Welsh et al., 1994) of the Boston Naming Test (Kaplan, Goodglass. & Weintraub, 1983), a verbal fluency test involving naming examples of animals and vegetables in separate 1 minute trials (Welsh et al., 1994; Wilson et al., 2002), and a 15-item word reading test (Wilson et al., 2002). Working memory was assessed with Digit Span Forward and Backward (Weschler, 1987) and Digit Ordering (Wilson et al., 2002). Perceptual speed was assessed with the oral form of the Symbol Digit Modalities Test (Smith, 1982) and a modified version (Wilson et al., 2002) of Number Comparison (Ekstrom, French, Harman, & Kerman). Visuospatial ability was assessed with a 15-item form of Judgment of Line Orientation (Benton, Sivan, Hamsher, Varney, & Spreen, 1994) and a 12-item form of Standard Progressive Matrices (Raven, Court, & Raven, 1992).

To limit floor and ceiling artifacts, composite measures of 2 or more individual tests were used in analyses. Raw test scores were transformed to z scores using the baseline mean and standard deviation for all participants in the parent studies. Each composite measure was the mean of its component z scores. The primary outcome was a composite measure of global cognition based on all 17 tests. We also formed composite measures of episodic memory (using 7 tests), semantic memory (3 tests), working memory (3 tests), perceptual speed (2 tests), and visuospatial ability (2 tests), supported by factor analyses in these (Wilson et al, 2002; Wilson, Barnes, & Bennett, 2003; Wilson et al., 2005) and other (Wilson et al., 2009; Krueger et al., 2009) cohorts.

Neuropathologic Examination

We followed a standard protocol for brain removal, which took place a mean of 8.6 hours after death (SD=6.7), tissue sectioning and preservation, and quantification of pathologic data, with examiners blinded to all clinical information (Schneider et al., 2006; Bennett et al., 2006). One cerebral hemisphere, one cerebellar hemisphere, and the brainstem were fixed in 4% paraformaldehyde and then cut coronally into 1-cm slabs that were examined for gross infarcts. The age, volume, and location of each infarct was noted. In analyses, we excluded infarcts that occurred within 6 months of death, and treated the remaining chronic gross infarcts as present or absent. We measured the density of tau-immunoreactive tangles in 8 brain regions (superior frontal cortex, dorsal lateral prefrontal cortex, anterior cingulate cortex, primary visual cortex, angular/supramarginal gyrus, inferior temporal cortex, entorhinal cortex, hippocampus [subfield 1/subiculum]) with an anti-paired helical filament-tau antibody clone AT8 (1:2,000; ThermoScientific, Rockford, IL) and computer assisted sampling. Regional scores were standardized and averaged to yield a summary index of tangle density (Bennett, Schneider, Wilson, Bienias, & Arnold, 2004). We looked for Lewy bodies in the substantia nigra, 2 limbic sites (entorhinal cortex, anterior cingulate cortex), and 3 neocortical sites (superior or middle temporal cortex, inferior parietal cortex, midfrontal cortex) using a monoclonal phosphorylated antibody to alpha-synuclein (1:20,000; Wako Chemical USA Inc., Richmond, VA) (Schneider et al., 2006; Wilson, Yu, et al., 2011). Lewy bodies were treated as present or absent in primary analyses. In secondary analysis, they were subdivided into 3 mutually exclusive stages using a modified version of the McKeith consensus criteria (McKeith et al., 1996): nigral (confined to substantia nigra), limbic (in anterior cingulate cortex or entorhinal cortex but not neocortex), and neocortical (in temporal, parietal, or frontal cortex). Severe neuronal loss in the pyramidal cell layer of any hippocampal subfield or the subiculum was classified as hippocampal sclerosis (Wilson et al., 2014).

Statistical Analysis

We analyzed change in cognition in mixed-effects change point models (Laird & Ware, 1982) employing a Bayesian Monte Carlo Markov Chain approach (Gelman, Carli, Stern, & Robin, 2004) with Open BUGS software (Lunn, Spiegelhalter, Thomas, & Best, 2009). Time was treated as years before death. Rate of cognitive decline was permitted to increase at some variable point to allow for terminal acceleration in cognitive decline (Wilson, Beckett, Bienias, Evans & Bennett, 2003; Sliwinski et al., 2006; Thorvaldsson et al., 2008; Wilson, Segawa, Hizel, Boyle, & Bennett, 2012). Thus, each person's cognitive trajectory has 4 components, including a preterminal slope, an inflection or change point, a terminal slope, and an intercept that indicates level of function proximate to death. The change point indicates the onset of terminal decline. Each component of the cognitive trajectory including the change point is parameterized as a linear function of covariates of interest, such as conscientiousness and the neuropathologic markers. The interaction of a covariate with a trajectory component indicates the modifying effect of the covariate on that part of the cognitive trajectory, taking into account its association with other trajectory components. To accommodate variability in cognitive trajectories, random effects were included for the intercept, preterminal slope, change point, and terminal slope. Each analysis had terms to account for age at death, sex, and education. The first model included terms for the association of conscientiousness with each cognitive trajectory component. Subsequent analyses had terms for neuroticism; depressive symptoms; neuroticism facets alone; neuropathologic markers; conscientiousness and neuropathologic markers; conscientiousness, neuropathologic markers, and conscientiousness x neuropathologic markers (with separate models for each marker); conscientiousness, neuropathologic markers, and conscientiousness x Lewy body stage (with separate models for each stage); and conscientiousness facets (analyzed separately) and neuropathologic markers. The primary outcome was a composite measure of global cognition. The model with terms for conscientiousness and neuropathologic markers was repeated using measures of specific cognitive functions in separate analyses.

Results

Conscientiousness and Cognition

Level of conscientiousness, assessed at study baseline, ranged from a low of 11 to a high of 48 (mean = 33.6, SD = 5.1, skewness = −0.5). Conscientiousness was not related to age at baseline (r= −0.07, p=0.217), age at death (r = −0.03, p=0.617), education (r=0.08, p=0.138), or sex (t[180.1]=1.0, p=0.326).

At baseline, scores on the composite measure of global cognition were approximately normally distributed (mean=0.082, SD=0.499, skewness = −0.7). Participants were annually followed for a mean of 10.7 years (SD=4.0) with a mean of 0.6 year from the final assessment to death (SD = 0.4).

We analyzed change in the global cognitive measure in a mixed-effects model that allowed rate of cognitive decline to increase at a variable point before death. This and all subsequent models controlled for age at death, sex, and education. In the initial analysis (Table 1, model A), the terminal acceleration in global cognitive decline began a mean of 3.2 years before death. Cognitive decline was gradual before this point with a mean loss of 0.036-unit per year on the global cognitive measure, which represents 7% of the baseline SD (0.036/0.499). After the change point, the global cognitive score declined a mean of 0.369-unit per year, which represents 74% of the baseline SD (0.369/0.499), a tenfold increase.

Table 1.

Relation of Conscientiousness to Late-life Change in Global Cognition

Model term Model A Model B
Estimate 95% CI Estimate 95% CI
Preterminal slope −0.036 −0.046, −0.025 −0.024 −0.035, −0.012
Change point −3.190 −3.558, −2.838 −2.849 −3.229, −2.462
Terminal slope −0.369 −0.422 −0.317 −0.317 −0.382, −0.255
Conscientiousness × preterminal slope 0.005 −0.003, 0.013 0.002 −0.005, 0.010
Conscientiousness × change point −0.015 −0.243, 0.218 −0.098 −0.309, 0.110
Conscientiousness × terminal slope 0.064 0.024, 0.103 0.057 0.019, 0.094
Random effects
    Var(intercept) 2.213 1.790, 2.511 1.491 1.246, 1.783
    Var(preterminal slope) 0.003 0.002, 0.004 0.002 0.0018, 0.003
    Var(change point) 3.314 2.539, 3.820 2.219 1.744, 2.788
    Var(terminal slope) 0.060 0.045, 0.079 0.053 0.038, 0.072
    Cov(intercept, preterminal slope) 0.049 0.036, 0.064 0.028 0.018, 0.038
    Cov(intercept, change point) 2.037 1.656, 2.476 1.309 1.025, 1.637
    Cov(intercept, terminal slope) 0.218 0.162, 0.286 0.182 0.134, 0.241
    Cov(preterminal slope, change point) 0.051 0.034, 0.068 0.021 0.007, 0.034
    Cov(preterminal slope, terminal slope) 0.002 0.0001, 0.005 0.002 −0.0002, 0.004
    Cov(change point, terminal slope) 0.045 −0.025, 0.111 0.027 −0.030, 0.081
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Note. From 2 mixed-effects change point models with terms for age at death, sex, and education; model B also had terms for neurofibrillary tangles, Lewy bodies, gross cerebral infarcts, and hippocampal sclerosis. CI, confidence interval.

To test for the hypothesized association of conscientiousness with cognitive decline, the model included terms for the association of conscientiousness with cognitive trajectory components (Table 1, model A). Conscientiousness was not associated with the change point. Higher conscientiousness was associated with slower rate of cognitive decline, but the association was only significant for cognitive decline after the change point. Conscientiousness accounted for 6.2% of the variability in rates of terminal decline in global cognition.

Because the neuroticism trait was associated with conscientiousness (r=−0.25, p<0.001) and has previously been related to cognitive decline [2], we repeated the model with terms added for neuroticism (mean=16.5, SD=5.6, skewness=0.6). In this analysis, neuroticism was not related to any trajectory component and the association of conscientiousness with terminal cognitive decline persisted (estimate=0.070, 95% confidence interval [CI]: 0.030, 0.111). Results were similar after controlling depressive symptoms at baseline (estimate = 0.067, 95% CI: 0.027, 0.106.). Facets of negative affect (mean item score = 1.50, SD=0.59, skewness = 0.5, coefficient alpha = 0.65) and self reproach (mean item score = 1.28, SD=0.49, skewness =0.8, coefficient alpha=0.74) can be derived from the 12-item neuroticism scale (Saucier, 1998). Neither facet was related to any trajectory component.

Conscientiousness, Neuropathologic Burden, and Cognition

On neuropathologic examination, the composite measure of tau tangle density ranged from 0.0 to 54.9 (mean=5.4, SD=6.6, skewness=2.8). There were 67 individuals (21.7%) with Lewy bodies, 97 (31.4%) with 1 or more chronic gross cerebral infarcts, and 21 (6.8 %) with hippocampal sclerosis.

In a linear regression model, conscientiousness was not related to Lewy bodies (estimate = −0.934, SE = 0.725, p = 0.200), gross cerebral infarcts (estimate = 0.004, SE = 0.643, p = 0.995), hippocampal sclerosis (estimate = 0.351, SE = 1.190, p = 0.768), or tangle density (estimate = −0.078, SE = 0.046, p = 0.087) though the latter association was nearly significant. In a mixed-effects change point model, 3 neuropathologic markers were related to preterminal cognitive decline (tangle estimate = −0.023, 95% CI: −0.033, −0.014; Lewy body estimate = −0.023, 95% CI: −0.040, −0.005; hippocampal sclerosis estimate = −0.035, 95% CI: −0.065, −0.004) and together accounted for 25.9% of the variability in preterminal decline not attributable to age at death, sex, or education. Two markers were related to terminal cognitive decline (Lewy body estimate = −0.192, 95% CI: −0.295, −0.095; infarct estimate = −0.123, 95% CI: −0.210, −0.040) and together accounted for 13.2% of variability in terminal decline. When conscientiousness was added to this model, higher conscientiousness continued to be associated with slower rate of terminal decline (estimate = 0.057, 95% CI: 0.019, 0.094) and accounted for 4.0% residual variability in terminal cognitive decline not attributable to demographic variables or common dementia related pathology.

To test whether conscientiousness modified the relation of pathology to cognitive decline, we repeated the previous analysis with terms added for the interaction of conscientiousness and each pathologic measure with the cognitive trajectory components (Table 2). There was a marginally significant but probably spurious interaction between conscientiousness and tangles such that the association of tangle density with terminal cognitive decline was stronger at higher levels of conscientiousness. There was a more robust association of conscientiousness with Lewy bodies such that the association of Lewy bodies with terminal cognitive decline was reduced at higher levels of conscientiousness (Figure 1, teal line) compared to lower levels of the trait (Figure 1, red line). We conducted additional analyses to see if the interaction with conscientiousness emerged at a specific stage of Lewy body disease. As shown in Table 3, conscientiousness modified the association of neocortical Lewy body disease with terminal cognitive decline.

Table 2.

Interaction of Conscientiousness and Neuropathology Conditions with Late-life Change in Global Cognition

Model term Estimate 95% CI
Conscientiousness × tangles × preterminal slope −0.038 −0.110, 0.029
Conscientiousness × tangles × change point −0.336 −1.851, 1.218
Conscientiousness × tangles × terminal slope −0.276 −0.510, −0.051
Conscientiousness × Lewy bodies × preterminal slope 0.013 −0.029, 0.054
Conscientiousness × Lewy bodies × change point 0.659 −0.602, 1.892
Conscientiousness × Lewy bodies × terminal slope 0.284 0.079, 0.490
Conscientiousness × infarcts × preterminal slope −0.016 −0.070, 0.039
Conscientiousness × infarcts × change point 0.885 −0.539, 2.369
Conscientiousness × infarcts × terminal slope −0.017 −0.258, 0.225
Conscientiousness × hippocampal sclerosis × preterminal slope −0.011 −0.065, 0.038
Conscientiousness × hippocampal sclerosis × change point 1.503 −0.067, 2.921
Conscientiousness × hippocampal sclerosis × terminal slope −0.094 −0.304, 0.107
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Note. From 4 mixed-effects change point models with terms for age at death, sex, education, neurofibrillary tangles, Lewy bodies, gross cerebral infarcts, and hippocampal sclerosis. CI, confidence interval.

Figure 1.

Figure 1

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Rates of terminal decline in global cognitive function in persons without Lewy bodies (green line) and persons with Lewy bodies and high (teal line, 90thpercentile), medium (blue line, 50th percentile), and low (red line, 10th percentile) levels of conscientiousness, adjusted for age at death, sex, education, tangles, gross cerebral infarcts, and hippocampal sclerosis.

Table 3.

Interaction of Conscientiousness and Lewy Body Disease with Late-life Change in Global Cognition

Model term Estimate 95% CI
Conscientiousness × nigral stage × preterminal slope −0.003 −0.062, 0.057
Conscientiousness × nigral stage × change point 0.347 −1.511, 2.391
Conscientiousness × nigral stage × terminal slope −0.076 −0.496, 0.595
Conscientiousness × limbic stage × preterminal slope −0.044 −0.097, 0.006
Conscientiousness × limbic stage × change point 1.529 −0.116, 3.254
Conscientiousness × limbic stage × terminal slope −0.131 −0.398, 0.156
Conscientiousness × neocortical stage × preterminal slope 0.030 −0.004, 0.065
Conscientiousness × neocortical stage × change point −0.061 −1.028, 0.927
Conscientiousness × neocortical stage × terminal slope 0.280 0.116, 0.448
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Note. From 3 mixed-effects change point models with terms for age at death, sex, education, neurofibrillary tangles, gross cerebral infarcts, and hippocampal sclerosis. CI, confidence interval.

Domains of Conscientiousness and Cognition

Conscientiousness is a broadly defined trait composed of multiple facets. The 12-item measure used in this study includes brief measures of 3 facets of the trait (Saucier, 1998): orderliness (mean item score = 2.72, SD=0.56, skewness = −0.9, coefficient alpha = 0.70), goal striving (mean item score = 2.79, SD = 0.54, skewness = −0.5, coefficient alpha = 0.66), and dependability (mean item score = 2.89, SD = 0.44, skewness = −0.1, coefficient alpha = 0.60). To determine whether the facets were differentially related to terminal decline, we analyzed each one separately. As shown in Table 4, higher level of each facet was associated with slower rate of terminal decline in global cognition.

Table 4.

Relation of Conscientiousness Facets to Late-life Change in Global Cognition

Facet Model term Estimate 95% CI
Orderliness Preterminal slope 0.003 −0.005, 0.010
Change point −0.011 −0.228, 0.194
Terminal slope 0.049 0.012, 0.086
Goal striving Preterminal slope 0.003 −0.005, 0.010
Change point −0.139 −0.340, 0.068
Terminal slope 0.048 0.009, 0.086
Dependability Preterminal slope 0.000 −0.007, 0.008
Change point −0.165 −0.394, 0.061
Terminal slope 0.047 0.007, 0.087
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Note. From 3 mixed-effects change point models with terms for age at death, sex, education, neurofibrillary tangles, Lewy bodies, gross cerebral infarcts, and hippocampal sclerosis. CI, confidence interval.

To determine whether conscientiousness was related to terminal decline in some cognitive domains but not others, we conducted separate analyses using measures of specific forms of cognitive function (Table 5). Higher conscientiousness was associated with slower terminal decline in episodic, semantic, and working memory but not in perceptual speed or visuospatial ability.

Table 5.

Relation of Conscientiousness to Late-life Change in Different Cognitive Domains

Cognitive domain Model term Estimate 95% CI
Episodic memory Preterminal slope 0.002 −0.009, 0.013
Change point 0.012 −0.199, 0.222
Terminal slope 0.065 0.019, 0.112
Semantic memory Preterminal slope 0.005 −0.003, 0.013
Change point −0.067 −0.240, 0.119
Terminal slope 0.094 0.029, 0.162
Working memory Preterminal slope −0.004 −0.010, 0.006
Change point −0.013 −0.225, 0.229
Terminal slope 0.049 0.000, 0.096
Perceptual speed Preterminal slope 0.010 −0.002, 0.022
Change point 0.063 −0.234, 0.365
Terminal slope −0.004 −0.044, 0.033
Visuospatial ability Preterminal slope 0.007 −0.004, 0.018
Change point −0.199 −0.538, 0.159
Terminal slope −0.006 −0.045, 0.032
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Note. From 5 mixed-effects change point models with terms for age at death, sex, education, neurofibrillary tangles, Lewy bodies, gross cerebral infarcts, and hippocampal sclerosis. CI, confidence interval.

Discussion

Conscientiousness was assessed in a group of more than 300 cognitively healthy older persons who subsequently completed annual cognitive testing for a mean of more than a decade, died, and underwent a neuropathologic examination. Conscientiousness was not associated with dementia related pathology, but higher level of conscientiousness was associated with less rapid cognitive decline, even after controlling for neuropathologic burden, and this association was stronger for terminal cognitive decline than preterminal cognitive decline. The results support the idea that higher level of conscientiousness enhances late-life cognitive health.

Higher level of conscientiousness has previously been associated with slower rate of cognitive decline (Wilson et al., 2007; Chapman et al., 2012) and lower risk of dementia (Wilson et al., 2007; Duberstein et al., 2011; Terracciano et al., 2014). The present data are consistent with these observations and build on them in several ways. The finding that the association of conscientiousness with cognitive decline persists after controlling for dementia related pathology runs contrary to the reverse causality hypothesis that low conscientiousness predicts cognitive decline because it is an early sign of the underlying conditions that drive late-life cognitive decline (Duberstein et al., 2011). Although prior work suggests that conscientiousness declines as individuals develop mild cognitive impairment (Donati et al., 2013) and dementia (Robins et al., 2011; Duchek et al., 2007), this research is mainly based on informant report. It is not clear that self report of low conscientiousness is a common or early sign of cognitive impairment.

We also found that conscientiousness was associated with terminal decline in cognitive function but not with preterminal cognitive decline. To our knowledge, this is the first evidence that conscientiousness or any personality trait is associated with terminal cognitive decline. Although personality and lifestyle are usually assumed to influence the initial development of cognitive symptoms more than the rate at which these symptoms worsen, these and previous (Wilson, Leurgans, Boyle, Schniederi, & Bennet, 2010; Boyle et al., 2013) analyses indicate that dementia related pathology accounts for less variability in terminal than preterminal cognitive decline, suggesting that terminal cognitive decline is at least partially modifiable. It may be that movtivational aspects of conscientiousness such as will and goal-directedness play an important role in late-life cognitive functioning (Forstmeier & Maercker, 2008) and that this contribution increases with increasing pathologic burden in neural systems that primarily support cognition. On the other hand, given previous evidence that conscientiousness predicts incident mild cognitive impairment (Wilson et al., 2007), we think it is likely that conscientiousness is also related to preterminal cognitive decline and that we lacked the power to detect it due to the relatively small number of participants and the relatively large number of trajectory components in the change point model.

The factors underlying the association of conscientiousness with late-life cognitive decline are not known. Conscientiousness is associated with health related behaviors, positively with beneficial behaviors such as physical exercise and negatively with risky behaviors such as smoking (Bogg & Roberts, 2004). Thus, some of the association of conscientiousness with cognitive decline may be due to its association with health related behaviors (Bogg & Roberts, 2004) and overall illness burden (Chapman, Roberts, Lyness, & Duberstein, 2013), which in turn may play an important role in terminal cognitive decline. A novel finding in these analyses was that the association of Lewy bodies with rate of terminal cognitive decline was conditional on conscientiousness. Specifically, the association of neocortical Lewy bodies with terminal cognitive decline was reduced in those with higher levels of the conscientiousness trait relative to those with lower levels. It is not clear why conscientiousness might influence Lewy body symptoms in particular, but the disease is characterized by fluctuating cognitive symptoms (Schneider et al., 2012) and passivity (Galvin, Malcom, Johnson, & Morris, 2007), which may be less completely expressed in highly conscientious individuals. In neuroimaging research, higher conscientiousness has been associated with larger regional volumes in prefrontal regions that support planning and self regulation (DeYoung et al., 2010; Jackson Balota, & Head, 2011; Kapogiannis, Sutin, Davatzikos, Costa, & Resnick, 2013), suggesting that years of impulse control and delaying gratification in pursuit of long term goals may enhance structure and function in executive control systems that help maintain cognitive skills in the last years of life.

A counterintuitive finding was that tangles had a marginally stronger association with cognitive decline in those with higher conscientiousness. We previously reported a similar 3-way interaction in the Religious Orders Study between conscientiousness, tangles, and level of cognition proximate to death (Wilson et al., 2007). We have no reasonable explanation for this anomaly. If conscientiousness protects against nonpathological factors with the potential to impair cognition, cognitive-pathological correlations might be somewhat higher among conscientious individuals, but it seems doubtful that this would be a very big effect or that it would apply to some pathological conditions but not others.

The strengths and limitations of these data should be noted. Participants with cognitive impairment at the time of personality assessment were excluded, reducing error in measurement of conscientiousness. Rates of participation in clinical follow-up and brain autopsy each exceeded 95%, making it unlikely that selective attrition biased results. The availability of psychometrically sound cognitive outcomes and a mean of more than 10 years of annual cognitive testing allowed us to reliably capture nonlinear changes in cognitive function. The uniform neuropathologic examination allowed us to control for multiple pathologic influences on cognitive aging. The main limitation is that study participants were selected and so the generalizability of the results is uncertain.

In summary, these results suggest that conscientiousness protects late-life cognitive health partly by blunting the impact of Lewy body disease and partly through mechanisms not associated with dementia related pathologies. Thus, conscientiousness joins a group of experiential variables, including cognitive activity (Wilson et al., 2013) and depressive symptoms (Wilson et al., 2014), that are associated with cognitive aging but not with dementia related pathologies. Understanding the bases of these associations could inform interventions to slow cognitive aging.

Acknowledgments

This research was supported by NIH grants R01AG17917, P30AG10161, R01AG15819, R01AG33678, and R01AG34374, and by the Illinois Department of Public Health. The funding organizations had no role in the design or conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript. The authors thank the many Illinois residents for participating in the Rush Memory and Aging Project and the many Catholic nuns, priests, and brothers for participating in the Religious Orders Study; Traci Colvin, MPH, and Karen Skish, MS, for study coordination; and John Gibbons, MS, and Greg Klein, MS, for data management.

Contributor Information

Robert S. Wilson, Rush Alzheimer's Disease Center, Department of Neurological Sciences, Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL.

Patricia A. Boyle, Rush Alzheimer's Disease Center, Department of Behavioral Sciences, Rush University Medical Center, IL.

Lei Yu, Rush Alzheimer's Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, IL.

Eisuke Segawa, Department of Preventive Medicine, Rush University Medical Center, Chicago, IL; Northwestern University, Evanston, IL..

Joel Sytsma, Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL.

David A. Bennett, Rush Alzheimer's Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, IL..

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