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PubMed2004

Cognitive decline in high-functioning older persons is associated with an increased risk of hospitalization.

OBJECTIVES: To examine hospital use for patients with evidence of cognitive decline indicative of early cognitive impairment. DESIGN: Medicare Part A hospital utilization data were linked to data from the MacArthur Research Network on Successful Aging Community Study to examine the association between baseline cognition and decline in cognitive function over a 3-year period and any hospitalization over that same period. SETTING: New Haven, Connecticut, and East Boston, Massachusetts. PARTICIPANTS: Subjects (N=598) were from two sites of the MacArthur Research Network on Successful Aging Community Study, a 7-year cohort study of community-dwelling older persons with high physical and cognitive functioning. MEASUREMENTS: Multivariate logistic regression was used to determine the association between any hospitalization over 3 years (1988-91) as the outcome variable and baseline cognitive function and decline in cognition over 3 years as primary predictor variables. Decline was based upon repeated (1988 and 1991) measures of delayed verbal recall and the Short Portable Mental Status Questionnaire (SPMSQ). RESULTS: Of 598 subjects, 48 died between 1988 and 1991. No baseline (1988) delayed recall scores or change in recall scores (1988-91) were associated with hospitalization. Although 48.2% declined on verbal memory scores, decline was not associated with risk of hospitalization. Of 494 subjects with complete 3-year data, 31.2% declined at least one point on the SPMSQ, and 4.7% declined more than two points. Among individuals aged 75 and older at baseline, the adjusted odds ratio for hospitalization for those who declined more than 2 points compared with those who declined less was 7.8 (95% confidence interval=2.0-30.8). CONCLUSION: Although specific memory tests were not associated with hospitalization, high-functioning older persons who experienced decline in overall cognitive function were more likely to be hospitalized. Variation in baseline cognitive function in this high-functioning cohort did not affect hospitalization, but additional research is needed to evaluate associations with other healthcare costs.

Activities of Daily Living↗

PubMed2002

CSF tau protein phosphorylated at threonine 231 correlates with cognitive decline in MCI subjects.

In this longitudinal study of 77 patients with mild cognitive impairment (MCI), the authors analyzed whether levels of tau protein phosphorylated at threonine 231 (p-tau(231)) in CSF correlate with progression of cognitive decline. High CSF p-tau(231) levels at baseline, but not total tau protein levels, correlated with cognitive decline and conversion from MCI to AD. Independently, old age and APOE-epsilon 4 carrier status were predictive as well. Our data indicate that an increased p-tau(231) level is a potential risk factor for cognitive decline in patients with MCI.

Adult↗

PubMed2005

Antioxidant nutrient intake and supplements as potential moderators of cognitive decline and cardiovascular disease in obstructive sleep apnea.

Cognitive deficits and cardiovascular disease (CVD) are comorbid conditions frequently associated with obstructive sleep apnea (OSA). Oxygen free radical release and its differential regulation of cytokine synthesis and immune modulation resulting from OSA-related hypoxic events have been hypothesized as the underlying mechanism(s) for the cognitive deficits and CVD in OSA. A number of studies have suggested that increased levels of oxidative stress and/or antioxidant deficiencies may also be risk factors in cognitive decline and CVD. The influence of antioxidant nutrients and supplements, such as Vitamins B6, B12, C, E, folic acid, alpha-lipoic acid and Coenzyme Q(10) on cognitive decline and CVD have been investigated. The influence of antioxidant nutrients or supplements on OSA remains to be investigated. Even if dietary or supplemental antioxidants do not prove to be effective therapies for OSA, dietary assessment and prescription to increase dietary intake of neuro- and cardio-protective nutrients may make it possible to reduce some of the cognitive and cardiovascular sequelae associated with OSA.

Antioxidants↗

PubMed1999

Cognitive decline and Japanese culture in a cohort of older Japanese Americans in King County, WA: the Kame Project.

OBJECTIVES: The prevalence of Alzheimer's disease in studies of Japanese show generally lower rates when compared with those of Caucasians. We hypothesized that among a cohort of Japanese Americans lifestyle differences would act to modify progression of the Alzheimer pathologic process over many years, resulting in a slower cognitive decline among persons whose lifestyle is more characteristically Japanese. METHODS: One thousand, eight hundred and thirty-six nondemented persons were screened with the Cognitive Abilities Screening Instrument (CASI) at baseline, and 1,604 were rescreened 2 years later. Baseline questions included migration status, exposure to Japanese culture in early life and maintenance of such culture in adulthood, and other risk factors. Cognitive decline was defined as a 2-year loss of > or = 5.15 points/100 on CASI. RESULTS: In multivariable logistic regression, variables relating to reading, writing, and speaking Japanese, being born or having lived in Japan in early life, and having friends who are only/mostly Japanese were inversely associated with cognitive decline (odds ratios ranged between 0.28 and 0.64, with p < .05). Two factors emerged in a factor analysis of these variables. The strongest explained 49% of the variance for acculturation and loaded heavily on knowledge of the Japanese language and having spent one's early years in Japan. When this factor was dichotomized into the top 20th percentile, it predicted cognitive decline with an odds ratio of 0.12 (95% CI 0.03-0.49). DISCUSSION: These results show that a Japanese lifestyle may decrease the risk of expressing cognitive decline over a 2-year follow-up period. Lower cardiovascular disease rates among Japanese may also predispose them to lower rates of cognitive decline. The greater social support characteristic of Japanese culture as well as the role that Japanese language and culture may play in neural connectivity during brain development and/or in mental stimulation in adult life may also explain our findings.

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PubMed1999

Impaired olfaction as a marker for cognitive decline: interaction with apolipoprotein E epsilon4 status.

OBJECTIVE: To determine whether olfactory status predicts cognitive decline (CD) over a 2-year follow-up period. METHODS: The authors enrolled individuals in a community-based longitudinal study of memory and aging in the Japanese-American community in King County, WA, between 1992 and 1994. At baseline they screened 1,985 persons using the Cognitive Abilities Screening Instrument (CASI) and the 12-item Cross-Cultural Smell Identification Test (CC-SIT). Of these 1,985 people, 1,836 were found not to be demented. Two years later the authors rescreened 1,604 participants with the CASI. They defined CD as a 2-year loss of > or =5.15 points/100 on the CASI. They genotyped 69% of the 1,604 people completing both examinations for apolipoprotein E (apoE). RESULTS: After adjusting for age, CASI score at baseline, education, smoking, sex, and follow-up time, the authors determined an odds ratio (OR) for CD of 0.90 (95% CI, 0.84 to 0.97) for an increase in each correct point on the CC-SIT (range, 0 to 12). Compared with normosmics, the OR for persons with impaired olfaction (microsmics) was 1.25 (95% CI, 0.83 to 1.89) and for anosmics the OR was 1.92 (95% CI, 1.06 to 3.47). Persons who were anosmic at baseline and who had at least one APOE-epsilon4 allele had 4.9 times the risk of CD (95% CI, 1.6 to 14.9) compared with normosmics without the epsilon4 allele. The estimated relative risk among women was 9.7 (95% CI, 1.3 to 70.4), and for men the risk was 3.2 (95% CI, 0.8 to 12.6). Receiver operating characteristic (ROC) curves showed that although the area under the curve (AUC) for baseline CASI was only 0.51, the AUC for CC-SIT alone was 0.62. Adding CC-SIT to the ROC model with CASI improved the AUC curve from 0.51 to 0.62. CONCLUSIONS: Unexplained olfactory dysfunction in the presence of one or more APOE-epsilon4 alleles is associated with a high risk of cognitive decline. Cross-Cultural Smell Identification Test classifies people with cognitive decline correctly to a greater degree than a global cognitive test.

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PubMed2006

Identifying patients at high and low risk of cognitive decline using Rey Auditory Verbal Learning Test among middle-aged memory clinic outpatients.

OBJECTIVES: To investigate whether application of cutoff levels in an episodic memory test (Rey Auditory Verbal Learning Test, RAVLT) is a useful method for identifying patients at high and low risk of cognitive decline and subsequent dementia. METHODS: 224 patients with memory complaints (mean age = 60.7 years, mean MMSE = 28.2) followed-up at a memory clinic over approximately 3 years were assigned retrospectively to one of three memory groups from their baseline results in RAVLT [severe (SIM), moderate (MIM) or no impairment (NIM)]. These groups were investigated regarding cognitive decline. RESULTS: Patients assigned to SIM showed significant cognitive decline and progressed to dementia at a high rate, while a normal performance in RAVLT at baseline (NIM) predicted normal cognition after 3 years. Patients with MIM constituted a heterogeneous group; some patients deteriorated cognitively, while the majority remained stable or improved. CONCLUSIONS: The application of cutoff levels in RAVLT at baseline showed that patients with severely impaired RAVLT performance were at a high risk of cognitive decline and progression to dementia, while patients with normal RAVLT results did not show cognitive decline during 3 years. Furthermore, the initial degree of memory impairment was decisive in the cognitive prognosis 3 years later.

Acoustic Stimulation↗

PubMed2003

Hypothesis testing of a change point during cognitive decline among Alzheimer's disease patients.

In this paper, we present a statistical hypothesis test for detecting a change point over the course of cognitive decline among Alzheimer's disease patients. The model under the null hypothesis assumes a constant rate of cognitive decline over time and the model under the alternative hypothesis is a general bilinear model with an unknown change point. When the change point is unknown, however, the null distribution of the test statistics is not analytically tractable and has to be simulated by parametric bootstrap. When the alternative hypothesis that a change point exists is accepted, we propose an estimate of its location based on the Akaike's Information Criterion. We applied our method to a data set from the Neuropsychological Database Initiative by implementing our hypothesis testing method to analyze Mini Mental Status Exam scores based on a random-slope and random-intercept model with a bilinear fixed effect. Our result shows that despite large amount of missing data, accelerated decline did occur for MMSE among AD patients. Our finding supports the clinical belief of the existence of a change point during cognitive decline among AD patients and suggests the use of change point models for the longitudinal modeling of cognitive decline in AD research.

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PubMed1999

Cannabis use and cognitive decline in persons under 65 years of age.

The purpose of this study was to investigate possible adverse effects of cannabis use on cognitive decline after 12 years in persons under age 65 years. This was a follow-up study of a probability sample of the adult household residents of East Baltimore. The analyses included 1,318 participants in the Baltimore, Maryland, portion of the Epidemiologic Catchment Area study who completed the Mini-Mental State Examination (MMSE) during three study waves in 1981, 1982, and 1993-1996. Individual MMSE score differences between waves 2 and 3 were calculated for each study participant. After 12 years, study participants' scores declined a mean of 1.20 points on the MMSE (standard deviation 1.90), with 66% having scores that declined by at least one point. Significant numbers of scores declined by three points or more (15% of participants in the 18-29 age group). There were no significant differences in cognitive decline between heavy users, light users, and nonusers of cannabis. There were also no male-female differences in cognitive decline in relation to cannabis use. The authors conclude that over long time periods, in persons under age 65 years, cognitive decline occurs in all age groups. This decline is closely associated with aging and educational level but does not appear to be associated with cannabis use.

Adult↗

PubMed1999

Cognitive decline after major noncardiac operations: a preliminary prospective study.

BACKGROUND: Cardiac operations frequently are complicated by postoperative cognitive decline. Less common and less studied is postoperative cognitive decline after noncardiac surgery, so we determined its incidence, severity, and possible predictors. METHODS: Twenty-nine patients who had thoracic and vascular procedures were studied. A neurocognitive test battery was administered preoperatively and 6 to 12 weeks postoperatively. A change score (preoperative minus postoperative) was calculated for each measure in each individual. Cognitive deficit (a measure of incidence) was defined as a 20% decrement in 20% or more of the completed tests. The average scores of all tests and the average decline (a measure of severity) were determined. RESULTS: The incidence of cognitive deficit was 44.8%. Overall the severity of the decline was an average of 15% decline. In the 44.8% of patients who had cognitive deficit, the severity was 24.7%. Multivariable predictors of cognitive decline were age (for incidence and severity) and years of education (for severity). CONCLUSIONS: Cognitive decline after noncardiac operations is a frequent complication of surgical procedures. The severity could preclude successful return to a preoperative lifestyle.

Adult↗

PubMed1999

[Arterial hypertension and cognitive decline].

Arterial hypertension is the leading risk factor for all stroke subtypes. However, its relationship with cognitive decline and dementia is more complex than a simple causal relationship. Cognitive functions are worse in patients with arterial hypertension, especially when the level of education is lower, age higher and arterial hypertension more severe. Arterial hypertension is an independent factor of cognitive decline. It also leads to white matter changes which contribute to the cognitive decline. Longitudinal studies have shown that a higher blood pressure at the age of 70 years is associated with an increased risk of dementia (vascular or Alzheimer) 10 to 15 years later, but blood pressure spontaneously decreases as dementia occurs. Treatments of arterial hypertension decrease the incidence of stroke, but clinical trials are still necessary to determine if they also decrease the incidence of dementia. Preliminary results obtained in elderly subjects with systolic arterial hypertension, support this hypothesis.

Alzheimer Disease↗

PubMed2002

Long-term benzodiazepine use and cognitive decline in the elderly: the Epidemiology of Vascular Aging Study.

Several cross-sectional studies have found cognitive impairment in subjects taking benzodiazepines for long periods. However, it is not known whether long-term use of benzodiazepines accelerates cognitive decline in the elderly. The authors addressed this issue in a follow-up study of 1,389 people aged 60 to 70 years recruited from the electoral rolls of the city of Nantes (Epidemiology of Vascular Aging study). Data on cognitive functioning (five cognitive tests), depressive symptoms (Center for Epidemiologic Studies-Depression Scale), anxiety symptoms (Spielberger Inventory Scale), use of psychotropics and other drugs, and tobacco and alcohol consumption were collected at baseline, 2-year, and 4-year examinations. People reporting to take benzodiazepines at one, two and three examinations were classified as episodic, recurrent, and chronic users, respectively. Among the 1,176 subjects (85%) who participated in the three examinations, the proportions of episodic, recurrent, and chronic users were 10%, 6%, and 7%, respectively. Chronic users of benzodiazepines had a significantly higher risk of cognitive decline in the global cognitive test (Mini Mental State Examination) and the two attention tests than nonusers (Mini Mental State Examination: odds ratio [OR] [95% confidence interval (CI)] = 1.9 [1.0-3.5]; Digit Symbol Substitution test: OR [95% CI] = 2.7 [1.6-4.7]; Trail Making test, part B: OR [95% CI] = 2.1 [1.2-3.7]). Overall, episodic and recurrent users had lower cognitive scores than nonusers, but differences were not statistically significant. These results were independent of age, sex, education, alcohol and tobacco use, anxiety and depression scores, and use of psychotropic drugs other than benzodiazepines. The findings suggest that long-term use of benzodiazepines is risk factor of increased cognitive decline in the elderly.

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PubMed2005

Socioeconomic differences in cognitive decline and the role of biomedical factors.

PURPOSE: This study examines the association between socioeconomic status and cognitive decline in a community-based cohort of well-functioning older adults and seeks to determine whether this link could be explained by biomedical factors. METHODS: Data are from 2574 men and women aged 70 to 79 years from Pittsburgh, PA, and Memphis, TN, participating in the Health, Aging and Body Composition study (Health ABC). Three indicators of socioeconomic status were used: education, income, and ownership of financial assets. Cognitive decline over 4 years was defined as a decrease of five points or more in the Modified Mini-Mental State Examination (3MS) score. Biomedical factors measured at baseline, included heart disease, cerebrovascular disease, diabetes, hypertension, poor pulmonary function, and high serum levels of inflammatory markers. RESULTS: Adjusted odds ratios were significantly higher in those with low education, low income, and few assets. Odds ratios ranged from 1.51 to 2.16 in the lowest socioeconomic groups. Additional adjustment for biomedical factors reduced the odds ratios of cognitive decline by an average of 2% for education, 5% for income, and 8% for the number of assets. CONCLUSIONS: Low socioeconomic status predicts a decline in cognitive function in older adults and this relationship is not mediated by biomedical factors.

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PubMed2001

The association between depressive symptoms and cognitive decline in community-dwelling elderly persons.

OBJECTIVE: To investigate whether depressive symptoms predict specific types of cognitive decline in order to elucidate the association between late life depression and cognitive decline. BACKGROUND: Mechanisms underlying the association between late life depression and cognitive decline are still unclear. METHOD: Six hundred and forty-one elderly persons of the Longitudinal Aging Study Amsterdam (LASA) aged 70-85 were examined by means of two measurement occasions over a period of 3 years. Depressive symptoms were assessed by means of the CES-D. Various cognitive functions were examined using neuropsychological tests. RESULTS: Depressive symptoms were associated with decline in speed of information processing over a 3-year period, whereas there was no association between depression and increasing memory impairment or global mental deterioration. CONCLUSION: These findings suggest that depressive symptoms are associated with subcortical pathology, most probable white matter lesions.

Aged↗

PubMedDate not supplied

MMSE cross-domain variability predicts cognitive decline in centenarians.

BACKGROUND: Early detection of dementia is one of the key issues in cognitive gerontology. However, so far the detection of early stages in cognitive decline has been rather unreliable. One central limitation of current assessment strategies is that they rely on information about a person's level of performance obtained from a single assessment. OBJECTIVE: In the first part of the present paper, we propose three strategies for overcoming this limitation by using information from several measurement occasions to improve diagnostic reliability. METHODS: In the second part, we present one exemplary empirical analysis of one of these approaches reporting data from the Heidelberg Centenarian Study. RESULTS: In this sample of very old individuals tested at baseline and at a follow-up 18 months later, the intra-individual cross-domain variability across MMSE subscales [1]at baseline predicted cognitive decline (i.e. change in an external cognitive functioning rating from baseline to follow-up) much better than baseline mean MMSE scores. CONCLUSIONS: In conclusion, we discuss the advantage of performance variability as a predictor for cognitive decline.

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PubMed1998

Predicting cognitive decline in patients with hypoxaemic COPD.

The objective was to identify predictors of cognitive decline in patients with hypoxaemic COPD on continuous oxygen therapy. Eighty-four consecutive ambulatory hypoxaemic COPD patients in stable clinical conditions were prospectively studied over the course of 2 yr. Baseline multidimensional assessment included respiratory function tests, blood gas analysis, Mini Mental Status (MMS) test, Geriatric Depression Scale (GDS), Activities of Daily Living (ADLs) and Charlson's index of comorbidity. Reassessments were made 1 yr and 2 yr thereafter. Sequential changes in MMS, GDS and ADLs were assessed by Friedman's ANOVA by rank test. Forty patients completed the study (group A), while 44 died or were lost to follow-up (group B). Group B was characterized by more severe respiratory function impairment and worse performances on ADLs and GDS. In group A, MMS deteriorated from baseline to the 1 yr and 2 yr reassessments (27 +/- 2.9 vs. 25.8 +/- 4.1 and 25.4 +/- 4, P < 0.005), whereas GDS and ADLs did not change significantly; the 23 patients experiencing a decline of MMS had baseline lower percentage predicted FVC (52.3 +/- 17.1 vs. 66.9 +/- 13.4, P < 0.03) and FEV1 (27.2 +/- 8.6 vs. 44 +/- 26.8, P < 0.02) values and better affective status (GDS score: 11.9 +/- 7.7 vs. 16.5 +/- 5.6, P < 0.04). Two-year changes in MMS and in GDS scores were inversely correlated (Spearman's p = -0.32, P = 0.04). Cognitive decline is faster in the presence of severe bronchial obstruction and parallels the worsening of the affective status in COPD patients on oxygen therapy. The onset of depression rather than baseline depressive symptoms seems to be a risk factor for cognitive decline.

Activities of Daily Living↗

PubMed1997

Apolipoprotein E phenotype and cognitive decline in a prospective study of elderly community women.

OBJECTIVE: To determine whether apolipoprotein E (Apo E) phenotype is associated with cognitive decline in community-dwelling nondemented elderly women. DESIGN: Prospective cohort study. SETTING: A university-affiliated clinic near Pittsburgh, Pa. PATIENTS: A total of 1750 nondemented community-dwelling women, aged 65 years and older, who were enrolled in the Study of Osteoporotic Fractures. MAIN OUTCOME MEASURES: The women completed a baseline interview and performed 3 cognitive tests: the modified Mini-Mental State Examination, Trials B, and Digit Symbol. Serum samples were obtained for Apo E typing. Baseline cognitive scores and repeated scores approximately 6 years after study enrollment were compared in women with and without Apo E epsilon 4. Cognitive decline, defined as the worst 10th percentile change scores, was assessed for each test and by phenotype group. RESULTS: After adjustment for age, education, presence of severe tremor, and depression, baseline scores did not differ by Apo E epsilon 4 status except for lower scores on Trails B in the homozygous epsilon 4 group (mean score, 159.7 compared with 127.7 for the heterozygous epsilon 4 group and 125.4 for the no epsilon 4 group; P = .01). However, repeated test performance on follow-up examination was worse on all tests in those women with 1 or more epsilon 4. Reduction on the modified Mini-Mental State Examination was 0% for no epsilon 4 allele, 1.9% for 1 epsilon 4 allele, and 3.7% for 2 epsilon 4 alleles (P < .001); reduction on Digit Symbol was 6.2% for no epsilon 4 allele, 9.0% for 1 epsilon 4 allele, and 17.5% for 2 epsilon 4 alleles (P = .04); and reduction on Trials B was 5.9% for no epsilon 4 allele, 25.0% for 1 epsilon 4 allele, and 10.9% for 2 epsilon 4 alleles (P = .002). Women with at least 1 epsilon 4 had an odds ratio of 1.6 (95% confidence interval, 1.1-2.3) of having cognitive decline during the study period. CONCLUSION: Apolipoprotein E epsilon 4 is associated with cognitive decline in community-dwelling nondemented women.

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PubMed2006

Telomere length predicts poststroke mortality, dementia, and cognitive decline.

OBJECTIVE: Long-term cognitive development is variable among stroke survivors, with a high proportion developing dementia. Early identification of those at risk is highly desirable to target interventions for secondary prevention. Telomere length in peripheral blood mononuclear cells was tested as prognostic risk marker. METHODS: A cohort of 195 nondemented stroke survivors was followed prospectively from 3 months after stroke for 2 years for cognitive assessment and diagnosis of dementia and for 5 years for survival. Telomere lengths in peripheral blood mononuclear cells were measured at 3 months after stroke by in-gel hybridization. Hazard ratios for survival in relation to telomere length and odds ratios for dementia were estimated using multivariate techniques, and changes in Mini-Mental State Examination scores between baseline and 2 years were related to telomere length using multivariate linear regression. RESULTS: Longer telomeres at baseline were associated with reduced risk for death (hazard ratio for linear trend per 1,000 bp = 0.52; 95% confidence interval, 0.28-0.98; p = 0.04, adjusted for age) and dementia (odds ratio for linear trend per 1,000 bp = 0.19; 95% confidence interval, 0.07-0.54; p = 0.002) and less reduction in Mini-Mental State Examination score (p = 0.04, adjusted for baseline score). INTERPRETATION: Telomere length is a prognostic marker for poststroke cognitive decline, dementia, and death.

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PubMed1997

Allelic variability in D21S11, but not in APP or APOE, is associated with cognitive decline in Down syndrome.

Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome. Molecular genetic and longitudinal neuropsychological analysis was performed for 41 unrelated Caucasian individuals (mean age 48.1 +/- 1.1 years (s.c.m.)) with free trisomy 21. Allele frequencies and genotype distributions were compared among subgroups with or without evidence of cognitive decline. Genetic variability at APOE and APP was not significantly associated with evidence of cognitive decline. However, aged individuals with Down syndrome, without evidence of cognitive decline, demonstrated unusual allelic variability at D21S11. These findings are discussed in the context of current hypotheses of Alzheimer-type dementia in Down syndrome and in the general population.

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