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PubMed1999

Total homocysteine and cognitive decline in a community-based sample of elderly subjects: the Rotterdam Study.

Homocysteine has been associated with an increased risk of cardiovascular disease. Cardiovascular diseases have been related to cognitive decline. The authors investigated the association of homocysteine with concurrent cognitive impairment and subsequent cognitive decline in a random sample of 702 community-dwelling respondents aged 55 years or over to the prospective Rotterdam Study in 1990-1994. Multiple logistic regression was used to calculate odds ratios and 95 percent confidence intervals for the association between total homocysteine levels and cognitive impairment (Mini-Mental State Examination (MMSE) score <26) and cognitive decline (drop in MMSE score of >1 point/year). Mean duration of follow-up was 2.7 years. After adjustment for age, sex, and education, there was no relation between total homocysteine and cognitive impairment (highest vs. lowest tertile: odds ratio (OR) = 1.30, 95% confidence interval (CI): 0.50, 3.38) or cognitive decline (middle vs. lowest tertile: OR = 1.14, 95% CI: 0.67, 1.93; highest vs. lowest tertile: OR = 0.91, 95% CI: 0.52, 1.58). Subjects who were lost to follow-up due to death or nonresponse had slightly higher age-adjusted homocysteine levels and lower MMSE scores at baseline. Sensitivity analyses showed that selective loss to follow-up was not a likely explanation for the absence of an association in the participants. Although a relation between homocysteine and reduced cognitive function is biologically plausible, this study suggests no such association in a community-based sample of the elderly.

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PubMed2005

Lipid lowering agents are associated with a slower cognitive decline in Alzheimer's disease.

BACKGROUND: Data from epidemiological studies and animal models imply that disturbances in cholesterol metabolism are linked to Alzheimer's disease susceptibility. Lipid lowering agents (LLAs) may have implications for the prevention of Alzheimer's disease. OBJECTIVE: To investigate whether LLAs are associated with a slower cognitive decline in Alzheimer's disease. METHODS: An observational study in 342 Alzheimer patients followed in a memory clinic for 34.8 months (mean age 73.5 years, mini-mental state examination score (MMSE) 21.3 at entry); 129 were dyslipaemic treated with LLAs (47% with statins), 105 were untreated dyslipaemic, and 108 were normolipaemic. The rate of cognitive decline was calculated as the difference between the first and last MMSE score, divided by the time between the measurements, expressed by year. Patients were divided into slow and fast decliners according to their annual rate of decline (lower or higher than the median annual rate of decline in the total population). RESULTS: Patients treated with LLAs had a slower decline on the MMSE (1.5 point/year, p = 0.0102) than patients with untreated dyslipaemia (2.4 points/year), or normolipaemic patients (2.6 points/year). Patients with a slower decline were more likely to be treated with LLAs. Logistic regression analysis, with low annual cognitive decline as the dependent variable, showed that the independent variable LLA (treated with or not) was positively associated with the probability of lower cognitive decline (odds ratio = 0.45, p = 0.002). CONCLUSIONS: LLAs may slow cognitive decline in Alzheimer's disease and have a neuroprotective effect. This should be confirmed by placebo controlled randomised trials in patients with Alzheimer's disease and no dyslipaemia.

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PubMed2001

A gender difference in the association between APOE genotype and age-related cognitive decline.

OBJECTIVE: To determine whether the APOE epsilon4 allele is associated with age-related intellectual decline in a community-dwelling sample of Danes. METHODS: A sample of 189 subjects who did not have dementia was tested with the Wechsler Adult Intelligence Scale (WAIS) at the ages of 50 and 80 years. Of these subjects, 163 (84 women and 79 men) completed all WAIS subtests at both assessments and 139 completed the digit symbol and block design subtests at the ages of 50, 60, 70, and 80 years. RESULTS: Cognitive decline from the age of 50 to the age of 80 years was substantial and larger for the performance subtests than for the verbal subtests (the declines were 18.40 for the performance IQ and 8.39 for the verbal IQ). APOE genotype was unrelated to the observed WAIS results of the 80-year assessment, but there was a significant interaction between APOE genotype and sex for decline scores in the performance IQ and three performance subtests (digit symbol, block design, and object assembly). In women, 26 epsilon4 carriers showed larger decline than 58 noncarriers, whereas there was no significant relation between APOE genotype and cognitive decline in men. The association in women between APOE genotype and cognitive decline was significant only for decline in the decade from age 70 to age 80 years. The interaction between sex and APOE genotype remained significant when education was included as a covariate. CONCLUSION: The APOE epsilon4 allele is associated with normal age-related decline in cognitive functions in women only. This finding may be supportive of recent evidence suggesting sex differences in APOE-associated risk for AD. Thus, the sex difference in the risk of sporadic AD may partly be explained by a sex-specific impact of the APOE epsilon4 allele on age-related cognitive decline.

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PubMed2003

Rate of cognitive decline and mortality in Alzheimer's disease.

BACKGROUND: Alzheimer's disease (AD) is associated with increased mortality, but survival in those with the disease varies widely. It is uncertain how much of the variation in survival is due to individual differences in rate of disease progression. METHODS: During a 4-year period, 354 persons with AD underwent annual clinical evaluations that included administration of 17 cognitive function tests, from which global and specific measures of cognitive function were derived. A growth curve approach was used to assess individual rates of cognitive decline and proportional hazards models adjusted for age, sex, and education to examine the associations of baseline level of cognition and rate of cognitive decline with mortality. RESULTS: During the 4-year study period, 242 persons survived and 112 died. At baseline, the global measure of cognition ranged from -1.68 to 1.36 (mean = 0.03, SD = 0.57), with higher scores indicating better function. Baseline level of cognition was not related to mortality (p = 0.12). Global cognition declined an average of 0.56 unit/year, with substantial heterogeneity (SD = 0.41). To determine mortality risk, persons were divided into quartiles based on rate of cognitive decline and survival contrasted in the quartile with the least decline with survival in each remaining quartile, adjusting for baseline level of cognition. Compared with those with the least decline, risk of death was increased more than threefold in the subgroup with mild decline, more than fivefold in those with moderately rapid decline, and more than eightfold in those with the most rapid decline. Similar results were found after controlling for baseline health and disability and in analyses using specific cognitive function measures. CONCLUSION: Mortality in AD is strongly associated with rate of cognitive decline.

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PubMed2006

Random change point model for joint modeling of cognitive decline and dementia.

We propose a joint model for cognitive decline and risk of dementia to describe the pre-diagnosis phase of dementia. We aim to estimate the time when the cognitive evolution of subjects in the pre-dementia phase becomes distinguishable from normal evolution and to study whether the shape of cognitive decline depends on educational level. The model combines a piecewise polynomial mixed model with a random change point for the evolution of the cognitive test and a log-normal model depending on the random change point for the time to dementia. Parameters are estimated by maximum likelihood using a Newton-Raphson-like algorithm. The expected cognitive evolution given age to dementia is then derived and the marginal distribution of dementia is estimated to check the log-normal assumption.

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PubMed2005

Rapid cognitive decline: searching for a definition and predictive factors among elderly with Alzheimer's disease.

The pattern and rate of cognitive decline in AD patients is far from uniform. In clinical practice, certain patients present episodes of rapid cognitive loss, whereas others deteriorate more progressively. At present time, there is little known about rapid decline in cognitive function in patients with AD, and moreover among older population. The main objective of this review was to elaborate a proposal of definition of rapid cognitive decline in order to facilitate its applicability into ordinary medical practice and to be relevant for clinical-decision making in old patients with AD. After the literature review, our results from longitudinal prospective studies and our clinical practice experience, we propose the following definition of rapid cognitive decline: a four-point or greater loss on the MMSE within six months and the loss of at least one point on the MMSE during the following six months. After ELSA cohort's results, 11% of an AD population of 312 patients were rapid cognitive decliners, complying with our proposed definition. They represent a non-negligible proportion of the population afflicted by AD.

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PubMed2002

Volumetric MRI predicts rate of cognitive decline related to AD and cerebrovascular disease.

OBJECTIVE: To examine volumetric MRI correlates of longitudinal cognitive decline in normal aging, AD, and subcortical cerebrovascular brain injury (SCVBI). BACKGROUND: Previous cross-sectional studies examining the relationship between cognitive impairment and dementia have shown that hippocampal and cortical gray matter atrophy are the most important predictors of cognitive impairment, even in cases with SCVBI. The authors hypothesized that hippocampal and cortical gray matter volume also would best predict rate of cognitive decline in cases with and without SCVBI. METHODS: Subjects were recruited for a multicenter study of contributions to dementia of AD and SCVBI. The sample (n = 120) included cognitively normal, cognitively impaired, and demented cases with and without lacunes identified by MRI. Cases with cortical strokes were excluded. Average length of follow-up was 3.0 years. Measures of hippocampal volume, volume of cortical gray matter, presence of subcortical lacunes, and volume of white matter hyperintensity were derived from MRI. Random effects modeling of longitudinal data was used to assess effects of baseline MRI variables on longitudinal change in a measure of global cognitive ability. RESULTS: Cortical gray matter atrophy predicted cognitive decline regardless of whether lacunes were present. Hippocampal atrophy predicted decline only in those without lacunes. Neither lacunes nor white matter hyperintensity independently predicted decline. CONCLUSIONS: Results suggest that cortical atrophy is an index of disease severity in both AD and subcortical cerebrovascular brain injury and consequently predicts faster progression. Hippocampal volume may index disease severity and predict progression in AD. The absence of this effect in cases with lacunes suggests that this group is etiologically heterogeneous and is not composed simply of cases of AD with incidental stroke.

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PubMed2001

The role of apolipoprotein E in cognitive decline after cardiac operation.

BACKGROUND: Recently, Tardiff and colleagues have suggested that the presence of the apolipoprotein E, epsilon4 allele was associated with increased likelihood of cognitive decline after coronary artery bypass grafting. The objective of the current study was to replicate this earlier work using an increased sample size. The increased sample also enabled an analysis by individual genotype in cognitive decline after coronary artery bypass grafting. METHODS: Apolipoprotein E genotyping was performed on 111 individuals undergoing coronary artery bypass grafting. Each participant underwent a battery of nine neuropsychological tests before operation and 4 to 7 weeks after operation. RESULTS: Cognitive decline, assessed by both continuous Z change scores and two categoric measures of cognitive deficit, was not significantly associated with either individual apolipoprotein E genotypes or categorization by the presence or absence of the epsilon4 allele. The examination of potential moderating factors did not alter this finding. CONCLUSIONS: This study suggests that the epsilon4 allele is not associated with cognitive decline in the weeks after coronary artery bypass grafting.

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PubMed2005

Trajectories of cognitive decline and social relations.

We assessed conjoint trajectories of cognitive decline and social relations over 7 years on a representative sample of community-dwelling elderly persons. We analyzed data using repeated measurement models. Social integration, family ties, and engagement with family were associated with cognitive function at advanced ages, controlling for education and introducing depressive symptoms, functional limitations, and chronic conditions as intervening variables. Association of social integration, through participation in community activities, with change in cognitive decline was more significant at advanced ages. Having friends was significantly associated with change in cognitive function in women only. Our findings have important implications for clinical medicine and public health because associations of social relations with cognitive function suggests that they may help to maintain cognitive function in old age.

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PubMed2006

Perspectives on depression, mild cognitive impairment, and cognitive decline.

CONTEXT: The public health implications of depression and cognitive impairment in late life are enormous. Cognitive impairment and late-life depression are associated with increased risk for subsequent dementia; however, investigations of these phenomena appear to be proceeding along separate tracks. OBJECTIVES AND DATA SOURCE: The National Institute of Mental Health organized the conference "Perspectives on Depression, Mild Cognitive Impairment, and Cognitive Decline" to consider how the varied perspectives might be better integrated to examine the associations among depression, mild cognitive impairment, and cognitive decline and to illuminate the common or distinct mechanisms involved in these associations. DATA SYNTHESIS: The following 2 broad questions were addressed: (1) What gaps in our knowledge have the greatest public health significance? (2) Can we more efficiently use our research dollars and participant resources to fill these gaps? Meeting participants included grantees from the National Institute of Mental Health and the National Institute on Aging and program staff from the National Institute of Mental Health, the National Institute on Aging, and the National Institute of Neurological Disorders and Stroke. CONCLUSIONS: One of the most important recommendations to emerge from the meeting discussions is for increased collaboration among clinical and epidemiological investigators whose work focuses in the area of depression with those working primarily in the area of memory disorders. Directions for future research were identified.

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PubMed2003

Silent brain infarcts and the risk of dementia and cognitive decline.

BACKGROUND: Silent brain infarcts are frequently seen on magnetic resonance imaging (MRI) in healthy elderly people and may be associated with dementia and cognitive decline. METHODS: We studied the association between silent brain infarcts and the risk of dementia and cognitive decline in 1015 participants of the prospective, population-based Rotterdam Scan Study, who were 60 to 90 years of age and free of dementia and stroke at base line. Participants underwent neuropsychological testing and cerebral MRI at base line in 1995 to 1996 and again in 1999 to 2000 and were monitored for dementia throughout the study period. We performed Cox proportional-hazards and multiple linear-regression analyses, adjusted for age, sex, and level of education and for the presence or absence of subcortical atrophy and white-matter lesions. RESULTS: During 3697 person-years of follow-up (mean per person, 3.6 years), dementia developed in 30 of the 1015 participants. The presence of silent brain infarcts at base line more than doubled the risk of dementia (hazard ratio, 2.26; 95 percent confidence interval, 1.09 to 4.70). The presence of silent brain infarcts on the base-line MRI was associated with worse performance on neuropsychological tests and a steeper decline in global cognitive function. Silent thalamic infarcts were associated with a decline in memory performance, and nonthalamic infarcts with a decline in psychomotor speed. When participants with silent brain infarcts at base line were subdivided into those with and those without additional infarcts at follow-up, the decline in cognitive function was restricted to those with additional silent infarcts. CONCLUSIONS: Elderly people with silent brain infarcts have an increased risk of dementia and a steeper decline in cognitive function than those without such lesions.

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PubMed2004

Dietary niacin and the risk of incident Alzheimer's disease and of cognitive decline.

BACKGROUND: Dementia can be caused by severe niacin insufficiency, but it is unknown whether variation in intake of niacin in the usual diet is linked to neurodegenerative decline. We examined whether dietary intake of niacin was associated with incident Alzheimer's disease (AD) and cognitive decline in a large, prospective study. METHODS: This study was conducted in 1993-2002 in a geographically defined Chicago community of 6158 residents aged 65 years and older. Nutrient intake was determined by food frequency questionnaire. Four cognitive tests were administered to all study participants at 3 year intervals in a 6 year follow up. A total of 3718 participants had dietary data and at least two cognitive assessments for analyses of cognitive change over a median 5.5 years. Clinical evaluations were performed on a stratified random sample of 815 participants initially unaffected by AD, and 131 participants were diagnosed with 4 year incident AD by standardised criteria. RESULTS: Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. In a logistic regression model, relative risks (95% confidence intervals) for incident AD from lowest to highest quintiles of total niacin intake were: 1.0 (referent) 0.3 (0.1 to 0.6), 0.3 (0.1 to 0.7), 0.6 (0.3 to 1.3), and 0.3 (0.1 to 0.7) adjusted for age, sex, race, education, and ApoE e4 status. Niacin intake from foods was also inversely associated with AD (p for linear trend = 0.002 in the adjusted model). In an adjusted random effects model, higher food intake of niacin was associated with a slower annual rate of cognitive decline, by 0.019 standardised units (SU) per natural log increase in intake (mg) (p = 0.05). Stronger associations were observed in analyses that excluded participants with a history of cardiovascular disease (beta = 0.028 SU/year; p = 0.008), those with low baseline cognitive scores (beta = 0.023 SU/year; p = 0.02), or those with fewer than 12 years' education (beta = 0.035 SU/year; p = 0.002) CONCLUSION: Dietary niacin may protect against AD and age related cognitive decline.

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PubMed2003

The menopause and HRT. HRT and cognitive decline.

It is biologically plausible that hormone replacement therapy (HRT) would be protective against cognitive decline and Alzheimer's disease (AD). We review observational and randomized trials to determine whether HRT might protect against cognitive decline in cognitively unimpaired and demented women. We also address issues of clinical relevance, including duration and type of treatment and patient characteristics, including type of menopause (surgical versus natural), age, education and menopausal symptoms. Differences in participant characteristics and testing methods limit the ability to draw conclusions across randomized studies of HRT in non-demented women. The available evidence suggests no detrimental effect of HRT on cognitive function and inconsistent benefits on verbal memory and reasoning, frontal functions and speeded attention. Meta-analyses of observational trials suggest that HRT protects against the development of AD, but randomized trials indicate no long-lasting benefit in patients with AD. Evidence is insufficient to recommend HRT to maintain cognitive function.

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PubMed1997

The progress of cognitive decline in multiple sclerosis. A controlled 3-year follow-up.

The purpose of this study was to illustrate how cognitive functioning evolves over time in patients with multiple sclerosis. We followed the evolution of cognitive performances in two clinically and demographically similar multiple sclerosis groups, the 'cognitively preserved' (n = 20) and the 'cognitively mildly deteriorated' (n = 22), and in healthy controls (n = 34). We conducted the follow-up examination using the Mild Deterioration Battery, the Mini-Mental State Examination, and a set of additional neuropsychological measures after an interval of 3 years. The drop-out rate in our study was only 5%. The 'cognitively preserved' multiple sclerosis group showed substantial neuropsychological stability by performing as well as the controls both at baseline and at follow-up. By contrast, the initially 'cognitively mildly deteriorated' group demonstrated progressive cognitive decline on many neuropsychological tests. The intermediate-length screening battery, the Mild Deterioration Battery, was sensitive to this decline, whereas the briefer Mini-Mental State Examination was not. The progressive cognitive decline could not be predicted from other disease variables. The study demonstrated that intact cognitive functioning in multiple sclerosis may remain stable, whereas incipient cognitive decline seems to be widespread and progressive in nature. Thus, progressive cognitive deterioration should be considered as one of the characteristics of multiple sclerosis.

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PubMed2006

Cognitive decline in older Mexican Americans with diabetes.

OBJECTIVE: To examine social, demographic and health factors associated with cognitive decline over a seven-year period among older Mexican Americans with diabetes. METHODS: A population-based sample of 808 noninstitutionalized Mexican Americans aged >65 years with diabetes who had a Mini-Mental State Examination (MMSE) >17 at baseline from the Hispanic Established Population for the Epidemiological Study of the Elderly (H-EPESE). Measurements included sociodemographics, diabetic treatment received (oral hypoglycemic or insulin), self-reported medical conditions, self-reported diabetes-related complications, high depressive symptoms and ADL limitations. RESULTS: The mean MMSE score at baseline was 25.3 + (SD=3.7). The rate of decline in cognitive function (MMSE) during the follow-up period was 0.37 point per year. Using general linear mixed models, we found that being male, and having high depressive symptoms and diabetic complications (kidney impairment, circulation problems or limb amputation) were factors significantly associated with greater declines in MMSE score over time. CONCLUSION: Circulation problems, kidney impairment and depression are the major factors associated with cognitive decline in older Mexican Americans with diabetes.

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PubMed1988

AIDS-related dementia: a case report of rapid cognitive decline.

Little is known psychometrically about the pattern of cognitive decline associated with acquired immunodeficiency syndrome (AIDS)-related dementia. Pre- and posttest results are presented to illustrate a case example of rapid cognitive decline. Increased psychometric assessment is recommended with additional examination of inconsistent results, which may be dismissed mistakenly as related to psychiatric symptoms. Implications for clinical practice and the role of the psychologist are discussed.

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PubMed1999

Orthostatic hypotension and cognitive decline in older people.

OBJECTIVES: To establish the role of orthostatic hypotension (OH) as a risk factor for cognitive decline among home-dwelling and institutionalized older people and to describe other predictors of cognitive decline. DESIGN: Follow-up study with two clinical examinations. SETTING: A community-based setting in northern Finland. PARTICIPANTS: All of the 1159 people aged 70 or more living in five rural municipalities around the town of Oulu in Northern Finland in 1991. At the time of the follow-up examination, 2.5 years later, 884 of the original participants were alive and 651 were re-examined. MEASUREMENTS: In 1991, 907 people (78.3% of the total population) were tested for orthostatic hypotension, and their cognitive capacity was assessed with the Mini-Mental State Examination (MMSE). The calculation/spelling tasks were excluded from the final version used in the statistical analysis. The re-assessment of cognitive capacity was made on 651 subjects (73.6% of those alive) who had participated in the first examination. The data were analyzed using polychotomous and linear regression analysis models. RESULTS: The prevalence of OH was 28.7%, with no age or sex differences. The mean sum score for the shortened MMSE in 1991 was 21.6 (+/-3.98) for persons with OH and 21.1 (+/-4.08) for non-OH persons. During the follow-up, the sum score declined in the OH group by .44 (+/-2.81) points and in the non-OH group by .83 (+/-3.61) points. No type of OH (systolic or diastolic 1- or 3-minute values or their combination) predicted cognitive decline; the only predictors were old age and low level of formal education. CONCLUSIONS: Orthostatic hypotension is a common clinical condition that affects every fourth person aged 70 years or older. By temporarily inducing cerebral hypoperfusion, it may cause or exacerbate cognitive dysfunction. In an unselected population, OH was not associated with cognitive deterioration, nor did it predict cognitive decline during a 2-year follow-up.

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PubMed2006

Nitrous oxide does not change the incidence of postoperative delirium or cognitive decline in elderly surgical patients.

BACKGROUND: Postoperative delirium and cognitive decline are common in elderly surgical patients after non-cardiac surgery. Despite this prevalence and clinical importance, no specific aetiological factor has been identified for postoperative delirium and cognitive decline. In experimental setting in a rat model, nitrous oxide (N(2)O) produces neurotoxic effect at high concentrations and in an age-dependent manner. Whether this neurotoxic response may be observed clinically has not been previously determined. We hypothesized that in the elderly patients undergoing non-cardiac surgery, exposure to N(2)O resulted in an increased incidence of postoperative delirium than would be expected for patients not receiving N(2)O. METHODS: Patients who were >or=65 yr of age, undergoing non-cardiac surgery and requiring general anaesthesia were randomized to receive an inhalational agent and either N(2)O with oxygen or oxygen alone. A structured interview was conducted before operation and for the first two postoperative days to determine the presence of delirium using the Confusion Assessment Method. RESULTS: A total of 228 patients were studied with a mean (range) age of 73.9 (65-95) yr. After operation, 43.8% of patients developed delirium. By multivariate logistic regression, age [odds ratio (OR) 1.07; 95% confidence interval (CI) 1.02-1.26], dependence on performing one or more independent activities of daily living (OR 1.54; 95% CI 1.01-2.35), use of patient-controlled analgesia for postoperative pain control (OR 3.75; 95% CI 1.27-11.01) and postoperative use of benzodiazepine (OR 2.29; 95% CI 1.21-4.36) were independently associated with an increased risk for postoperative delirium. In contrast, the use of N(2)O had no association with postoperative delirium. CONCLUSIONS: Exposure to N(2)O resulted in an equal incidence of postoperative delirium when compared with no exposure to N(2)O.

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