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Depressive symptomatology and incident cognitive decline in an elderly community sample.

BACKGROUND: It is not known whether depression is a cause or consequence of progressive cognitive decline. We assessed the relationship between depressive symptoms and subsequent cognitive decline in the community-dwelling elderly population. METHODS: Data were from a population-based cohort study that enrolled 2812 noninstitutionalized elderly residents of New Haven, Conn, and followed them with in-home visits in 1982, 1985, 1988, and 1994. Cognitive function was assessed with the Short Portable Mental Status Questionnaire (SPMSQ). Response to the SPMSQ was scored as high, medium, and low, and cognitive decline was defined as a transition to a lower category. Depressive symptoms were measured with the Center for Epidemiological Studies Depression Scale. RESULTS: An elevated level of depressive symptoms was associated with an increased risk of incident cognitive decline among medium SPMSQ performers (3-year odds ratio [OR], 1.72; 95% confidence interval [CI], 1.04-2.82, P=.03; 6-year OR, 2.40; 95% CI, 1.33-4.34; P=.004; 12-year OR, 1.65; 95% CI, 0.62-4.38; P=.31) but not among high performers (3-year OR, 0.93; 95% CI, 0.62-1.39; P=.71; 6-year OR, 1.03; 95% CI, 0.67-1.58; P=.90; 12-year OR, 1.26; 95% CI, 0.59-2.71; P=.55), after adjustment for age, sex, race, education, income, housing type, functional disability, cardiovascular profile, and alcohol use. CONCLUSIONS: Depressive symptoms, particularly dysphoric mood, presage future cognitive losses among elderly persons with moderate cognitive impairments. However, the data do not provide support for the hypothesis that depressive symptoms are associated with the onset or rate of cognitive decline among cognitively intact elderly persons.

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Cognitive decline is faster in Lewy body variant than in Alzheimer's disease.

OBJECTIVES: To quantify the rate of cognitive decline on the Mini-Mental State Examination (MMSE) in autopsy-diagnosed Lewy body variant (LBV) of Alzheimer's disease (AD) cases. We hypothesized that LBV patients would have a faster cognitive decline and shorter survival compared with patients with pure AD. BACKGROUND: Prior reports have shown extrapyramidal signs to be associated with a poorer prognosis in AD. It has been suggested that LBV is often characterized by a rapidly progressive course. Few data are available regarding the rate of cognitive decline in autopsy-confirmed LBV dementia cases. METHODS: We searched the databases of the University of California-San Diego Alzheimer's Disease Research Center and the Consortium to Establish a Registry in Alzheimer's Disease (CERAD) for dementia cases with 1) an autopsy diagnosis of definite or probable AD (CERAD criteria) with concomitant Lewy bodies and 2) longitudinal MMSE assessments. This resulted in a series of 40 LBV cases and 148 AD cases without Lewy bodies, with comparable baseline MMSE scores, age, and education. The rate of cognitive decline was calculated as the baseline MMSE -- final MMSE. Methods were devised to reduce floor effects on the MMSE. RESULTS: The average rate of cognitive decline was -5.8 +/- 4.5 points/y in LBV and -4.1 +/- 3.0 points/y in AD (t-test, p < 0.01). The LBV group declined a similar amount on the MMSE (means, -10.0 versus -9.6 points) over a significantly shorter time interval (1.9 versus 2.7 years; p = 0.005) than did AD patients. At baseline, the mean MMSE scores were nearly identical (18.2 in LBV; 17.8 in AD), but on follow-up examinations approximately 1, 2, and 3 years later, there were intergroup mean differences of 1.8 points (two-tailed p = 0.19), 4.2 points (p = 0.04), and 5.6 points (p = 0.03), respectively. The LBV cases had shorter survival time from the onset of cognitive symptoms (7.7 +/- 3.0 years versus 9.3 +/- 3.5 years; p = 0.007) and a shorter mean survival after entry/baseline, which was of marginal significance (3.6 versus 4.1 years; p = 0.11). CONCLUSIONS: This study demonstrates that LBV is characterized by a faster cognitive decline and accelerated mortality compared with AD.

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Clinical and radiological determinants of prestroke cognitive decline in a stroke cohort.

OBJECTIVES: Stroke seems to be related to dementia more often than previously assumed and vascular factors are also related to Alzheimer's disease. The pathophysiology of poststroke dementia includes ischaemic changes in the brain, a combination of degenerative and vascular changes, and changes only related to Alzheimer's disease. Some cognitive decline recognised after a stroke may be due to pre-existing cognitive decline. The aim of this study was to determine the clinical and radiological determinants of prestroke cognitive decline. METHODS: The study group comprised 337 of 486 consecutive patients aged 55 to 85 years who 3 months after ischaemic stroke completed a comprehensive neuropsychological test battery; structured medical, neurological, and mental status examination; interview of a knowledgeable informant containing structured questions on abnormality in the cognitive functions; assessment of social functions before the index stroke; and MRI. RESULTS: Frequency of prestroke cognitive decline including that of dementia was 9.2% (31/337). The patients with prestroke cognitive decline were older, more often had less than 6 years of education, and had history of previous stroke. Vascular risk factors did not differ significantly between these two groups. White matter changes (p=0.004), cortical entorhinal, hippocampal, and medial temporal atrophy (p<0.001), cortical frontal atrophy (p=0.008); and any central atrophy (p<0.01), but not the frequencies or volumes of old, silent, or all infarcts on MRI differentiated those with and without prestroke cognitive decline. The correlates of prestroke cognitive decline in logistic regression analysis were medial temporal cortical atrophy (odds ratio (OR) 7.5, 95% confidence interval (95%CI) 3.2-18.2), history of previous ischaemic stroke (OR 4.4, 95% CI 1.8-10.6), and education (OR 0.9, 95% CI 0.8-0.9). CONCLUSIONS: History of previous stroke, but not volumes or frequencies was found to correlate with prestroke cognitive decline. Other associating factors were rather those usually associated with degenerative dementia: white matter changes and cerebral atrophy; and in multiple models medial temporal cortical atrophy and education. The possible overlap between two or more underlying diseases must be remembered in diagnosis and treatment of patients with vascular cognitive impairment.

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Psychotropic drug use and cognitive decline among older men and women.

This epidemiological study focuses on cognitive change related to psychotropic drug use in a population-based sample of subjects aged 65 and over. Cognitive functioning was assessed in 1982 and 1988 by the Short Portable Mental Status by Pfeiffer, and cognitive decline was defined as an increase of more than 2 errors in 1988 relative to the 1982 assessment. Psychotropic drugs were classified into benzodiazepines and non-benzodiazepines. For both medications, four patterns of intake were considered: no use reported at both interviews, continuous use at both interviews, temporary use at the 1982 interview and new use at the 1988 interview. Depressive symptomatology was assessed by the Center for Epidemiologic Studies Depression Scale. The analysis was performed on 1200 subjects with no or minimal impairment at baseline for whom complete data were available. Univariate analyses showed cognitive decline associated with gender, level of education and new medical condition; it was also related to depressive symptomatology and psychotropic drug use. These two factors were the most strongly associated with decrease in performance in multivariate analyses. Cognitive decline differed according to class of psychotropic drugs and pattern of use: benzodiazepine temporary users exhibited a lower risk compared with never users (OR = 0.23, p = 0.056), non-benzodiazepine new users a higher risk (OR = 5.02, p < 0.001). Despite the simple measures of cognitive functioning and psychopathology, and the approximation in pattern of psychotropic drug use, these results emphasize the importance of considering psychotropic drugs in studies of cognitive decline in elderly subjects.

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Physical activity in relation to cognitive decline in elderly men: the FINE Study.

BACKGROUND: Physical activity may be associated with better cognition. OBJECTIVE: To investigate whether change in duration and intensity of physical activity is associated with 10-year cognitive decline in elderly men. METHODS: Data of 295 healthy survivors, born between 1900 and 1920, from the Finland, Italy, and the Netherlands Elderly (FINE) Study were used. From 1990 onward, physical activity was measured with a validated questionnaire for retired men and cognitive functioning with the Mini-Mental State Examination (maximum score 30 points). RESULTS: The rates of cognitive decline did not differ among men with a high or low duration of activity at baseline. However, a decrease in activity duration of >60 min/day over 10 years resulted in a decline of 1.7 points (p < 0.0001). This decline was 2.6 times stronger than the decline of men who maintained their activity duration (p = 0.06). Men in the lowest intensity quartile at baseline had a 1.8 (p = 0.07) to 3.5 (p = 0.004) times stronger 10-year cognitive decline than those in the other quartiles. A decrease in intensity of physical activity of at least half a standard deviation was associated with a 3.6 times stronger decline than maintaining the level of intensity (p = 0.003). CONCLUSIONS: Even in old age, participation in activities with at least a medium-low intensity may postpone cognitive decline. Moreover, a decrease in duration or intensity of physical activity results in a stronger cognitive decline than maintaining duration or intensity.

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The incidence of cognitive decline after (not) undergoing coronary artery bypass grafting: the impact of a controlled definition.

BACKGROUND: After coronary artery bypass grafting (CABG), 20-30% of patients are reported to suffer from cognitive decline. Studies reporting these high incidences, however, have not included an appropriate control group. METHODS: We repeatedly administered a series of neuropsychological tests to 112 healthy middle-aged volunteers not undergoing surgery, and applied two widely used definitions of cognitive decline to their test results. In addition, we re-analysed the neuropsychological test data of 281 CABG patients with a definition of cognitive decline that takes into account the natural variability of test performance that was found in the volunteers. RESULTS: Three months after their first assessment, 14-28% of the volunteers suffered from cognitive decline according to the definitions of cognitive decline after CABG. Using the controlled definition of cognitive decline that takes the natural variability in test performance into account, we found that only 7.7% of the CABG patients suffered from cognitive decline at 3 months after their operation. CONCLUSION: These data suggest that the incidence of cognitive dysfunction after CABG has previously been greatly overestimated.

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The rate of cognitive decline and risk of reaching clinical milestones in Alzheimer disease.

BACKGROUND: Previous studies revealed that cognitive test scores were related to functional outcome in Alzheimer disease (AD). However, the relationship between the rate of cognitive decline at the initial disease phase and the risk of reaching clinical milestones in subsequent years has not yet been examined. OBJECTIVE: To examine whether the rate of cognitive decline predicts the risk of reaching functional milestones in patients with probable AD. DESIGN: A 5-year prospective study was conducted at 3 sites. SETTING: Outpatient research and treatment centers. PARTICIPANTS: Patients diagnosed with probable AD (N = 236; mean age, 73 years; 59% women; mean years of education, 13). MAIN OUTCOME MEASURES: Modified Mini-Mental State Examination (mMMSE) scores were used to assess the rate of cognitive decline over time. Total dependence score and 2 clinical milestones: (1) the need to be dressed, groomed, and washed and (2) receiving a level of care equivalent to a placement in a health-related facility, were derived from the Dependence Scale. RESULTS: General estimating equation analyses revealed that the rate of cognitive decline during the entire follow-up period was positively related to an increase in total dependence scores. Cox analyses showed that a fast rate of decline during the first year was related to an increase in the risk of reaching clinical milestones in subsequent years. Analyses controlled for age, sex, education, and baseline mMMSE scores. CONCLUSION: A fast rate of cognitive decline was associated with increasing risk of reaching clinical milestones in AD.

Activities of Daily Living↗

Left ventricular hypertrophy and blood pressure as predictors of cognitive decline in old age.

BACKGROUND AND AIMS: The relationships between blood pressure (BP) and cognition are complex and are still partly unclear. The impact of history of hypertension, present BP levels, and left ventricular hypertrophy (LVH) on cognition was investigated in a 10-year follow-up study of an aged population. METHODS: The population-based sample consisted of 75-, 80- and 85-year-old individuals at baseline (N=650). Their history of hypertension was investigated, and present BP values were recorded several times. Echocardiographic examinations were performed twice at 3-year intervals, and electrocardiography (ECG) at entry. Cognitive function was assessed by the Mini-Mental State Examination (MMSE) at baseline and at 10 years, and by the Clinical Dementia Rating (CDR) at baseline, at 1, 5 and 10 years. RESULTS: At baseline, elderly individuals with impaired cognition or dementia had lower BP, but thicker left ventricle posterior wall (LVPW), greater cardiac mass, and more often signs of LVH in ECG than those without cognitive deficits. Echocardiographic LVH, but not BP, predicted cognitive decline in a 5-year follow-up. Patients who died demented within 5 years were characterized by low BP and thin LVPW. Baseline BP and echocardiographic variables were not significantly different between those who had and had not cognitive decline at 10 years, but declining BP tended to precede cognitive deficits. CONCLUSIONS: Results indicate that, the closer cognitive decline, the lower the BP, and suggest that, although LVH is a risk factor of cognitive decline, it loses its predictive value in old age.

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Prediction of cognitive decline after stroke using proton magnetic resonance spectroscopy.

Structural MRI measures have been used to predict cognitive decline in elderly subjects, but few studies have used proton magnetic resonance spectroscopy ((1)H-MRS) for this purpose, particularly after stroke. We studied the potential of (1)H-MRS to predict cognitive decline in patients with stroke or TIA and healthy ageing controls over 12 months and 3 years. Structural MRI and single-voxel (1)H-MRS in the frontal white matter and the occipito-parietal gray matter were performed at the index assessment (3-6 months post-stroke) in 49 stroke/TIA patients and 60 controls. Neuropsychological testing was performed at the index assessment and repeated at 12 months in 30 stroke/TIA patients and 49 controls, and at 3 years in 25 patients and 48 controls. In stroke/TIA patients, frontal NAA/Cr predicted cognitive decline over 12 months and 3 years, and in elderly control subjects frontal NAA predicted cognitive decline over 12 months only. In stroke/TIA patients, the (1)H-MRS measures were better predictors of cognitive decline than structural measures. (1)H-MRS may be useful in assessing early cognitive impairment after stroke/TIA and in normal ageing.

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Cognitive decline is related to education and occupation in a Spanish elderly cohort.

BACKGROUND AND AIMS: The type of education and occupation can sensibly influence cognitive decline. The aim of this study was to examine their impact on cognitive function in a longitudinal study of community-dwelling Spanish people over 65 with low levels of formal education and predominantly unskilled occupations. METHODS: Cognitive function was assessed in 1993 and 1997 using a simple scale including items of memory and orientation that has been previously validated for populations with low levels of formal education. Cognitive score in 1997 and cognitive decline over 4 years (1993-1997) were used as outcomes. Education and occupation were analyzed as determinants of cognitive function using multiple linear regression, and of cognitive decline using logistic and multinomial regressions. RESULTS: Of the 557 subjects who completed the follow-up in 1997, 11% had experienced severe decline and 20.6% mild decline. Overall and mild cognitive decline were predicted by low education and being a farm worker (OR: 2.36, CI 95%: 1.164.81 and OR: 2.37, CI 95%: 1.05-5.37) after controlling for age. CONCLUSIONS: Cognitive decline in the elderly is partially explained by early life events, such as education, and living in a deprived environment over a long period of time. We cannot ascertain whether these effects are direct or mediated by other associated conditions but sample attrition does not account for our results.

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Hypertension and the rate of cognitive decline in patients with dementia of the Alzheimer type.

Hypertension has been suspected of being associated with Alzheimer disease (AD). To study this problem, a case-control study investigating the association between hypertension and cognitive decline was conducted as a secondary analysis of data from more than 700 patients diagnosed with AD who had been randomly assigned to the placebo arm of a clinical trial. Additional analyses were undertaken to investigate the effects of baseline disease severity, age, gender, apolipoprotein genotype, and the use of antihypertensive medication in this population. This study found evidence of an association between hypertension and increased cognitive decline in AD patients over a 6-month period. After controlling for baseline disease severity, a pooled odds ratio (OR) was estimated to be 1.6 (95% confidence interval, 1.0-2.7) and found to be statistically significant (p = 0.048). Secondary analyses controlling for gender and apolipoprotein genotype showed no significant effect on the association between hypertension and cognitive decline. With regard to age, patients younger than 65 years with hypertension were more likely to have increased cognitive decline than patients of the same age without hypertension (odds ratio = 6.9, 95% confidence interval, 1.5-31.1; p = 0.005). Treatment with antihypertensives did not appear to provide protection from cognitive decline. Increased cognitive decline among those older than 65 years was comparable for hypertensive and normotensive subjects. This study, examining a large population of patients with AD, provides evidence that the rate in cognitive decline measured over a period of 6 months is accelerated by a state of hypertension in patients younger than 65 years.

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Is diabetes associated with cognitive impairment and cognitive decline among older women? Study of Osteoporotic Fractures Research Group.

BACKGROUND: The long-term effect of type 2 diabetes on cognitive function is uncertain. OBJECTIVE: To determine whether older women with diabetes have an increased risk of cognitive impairment and cognitive decline. DESIGN: Prospective cohort study. SETTING: Four research centers in the United States (Baltimore, Md; Portland, Ore; Minneapolis, Minn; and the Monongahela Valley, Pennsylvania). PARTICIPANTS: Community-dwelling white women 65 years and older (n = 9679). MEASUREMENTS: Physician-diagnosed diabetes and other aspects of health history were assessed by interview. Three tests of cognitive function, the Digit Symbol test, the Trails B test, and a modified version of the Mini-Mental State Examination (m-MMSE), were administered at baseline and 3 to 6 years later. Change in cognitive function was defined by the change in the score for each test. Major cognitive decline was defined as the worst 10th percentile change in the score for each test. RESULTS: Women with diabetes (n = 682 [7.0%]) had lower baseline scores than those without diabetes on all 3 tests of cognitive function (Digit Symbol and Trials B tests, P<.01; m-MMSE, P = .03) and experienced an accelerated cognitive decline as measured by the Digit Symbol test (P<.01) and m-MMSE (P = .03). Diabetes was also associated with increased odds of major cognitive decline as determined by scores on the Digit Symbol (odds ratio = 1.63; 95% confidence interval, 1.20-2.23) and Trails B (odds ratio, 1.74; 95% confidence interval, 1.27-2.39) tests when controlled for age, education, depression, stroke, visual impairment, heart disease, hypertension, physical activity, estrogen use, and smoking. Women who had diabetes for more than 15 years had a 57% to 114% greater risk of major cognitive decline than women without diabetes. CONCLUSION: Diabetes is associated with lower levels of cognitive function and greater cognitive decline among older women.

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Effects of blood pressure lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease.

BACKGROUND: High blood pressure and stroke are associated with increased risks of dementia and cognitive impairment. This study aimed to determine whether blood pressure lowering would reduce the risks of dementia and cognitive decline among individuals with cerebrovascular disease. METHODS: The Perindopril Protection Against Recurrent Stroke Study (PROGRESS) was a randomized, double-blind, placebo-controlled trial conducted among 6105 people with prior stroke or transient ischemic attack. Participants were assigned to either active treatment (perindopril for all participants and indapamide for those with neither an indication for nor a contraindication to a diuretic) or matching placebo(s). The primary outcomes for these analyses were dementia (using DSM-IV criteria) and cognitive decline (a decline of 3 or more points in the Mini-Mental State Examination score). RESULTS: During a mean follow-up of 3.9 years, dementia was documented in 193 (6.3%) of the 3051 randomized participants in the actively treated group and 217 (7.1%) of the 3054 randomized participants in the placebo group (relative risk reduction, 12% [95% confidence interval, -8% to 28%]; P =.2). Cognitive decline occurred in 9.1% of the actively treated group and 11.0% of the placebo group (risk reduction, 19% [95% confidence interval, 4% to 32%]; P =.01). The risks of the composite outcomes of dementia with recurrent stroke and of cognitive decline with recurrent stroke were reduced by 34% (95% confidence interval, 3% to 55%) (P =.03) and 45% (95% confidence interval, 21% to 61%) (P<.001), respectively, with no clear effect on either dementia or cognitive decline in the absence of recurrent stroke. CONCLUSIONS: Active treatment was associated with reduced risks of dementia and cognitive decline associated with recurrent stroke. These findings further support the recommendation that blood pressure lowering with perindopril and indapamide therapy be considered for all patients with cerebrovascular disease.

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Cerebrovascular disease, the apolipoprotein e4 allele, and cognitive decline in a community-based study of elderly men.

BACKGROUND AND PURPOSE: Cerebrovascular disease and the apolipoprotein e4 (APOE*4) allele are both important risk factors for cognitive decline. We investigated the combined effect of APOE*4 and cerebrovascular disease on cognitive decline. METHODS: Data are from a cohort of 353 men, aged 69 to 89 years at baseline, living in Zutphen, Netherlands. The 30-point Mini-Mental State Examination (MMSE) was used to measure cognitive decline (drop of > 2 points) from 1990 to 1993 (14% of the sample). Odds ratios (OR [95% confidence interval]) for cognitive decline were adjusted for age, education, and baseline MMSE score. RESULTS: Compared with those without APOE*4 and without a history of cerebrovascular disease, the adjusted OR was 4.7 (1.7 to 12.7) for subjects without APOE*4 but with cerebrovascular disease, 3.3 (1.6 to 6.8) for those with APOE*4 and no cerebrovascular disease, and 17.2 (2.7 to 110.0) for those with both risk factors. The risk for cerebrovascular disease and APOE*4 combined was more than expected from the separate effects. The combined risk of coronary heart disease and APOE*4 was 6.1 (1.7 to 22.3). The analysis of cardiovascular risk factors showed that the risk of cognitive decline was highest in subjects with both APOE*4 and a high cholesterol level, high fibrinogen level, normal blood pressure, or diabetes mellitus. CONCLUSIONS: Cerebrovascular disease and APOE*4 may have a synergistic effect on cognitive decline.

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Does aspirin or other NSAIDs reduce the risk of cognitive decline in elderly persons? Results from a population-based study.

OBJECTIVE: To investigate the protective effect of NSAIDs and aspirin separately on cognitive decline in elderly subjects, controlling for consistent use of these agents over a prolonged period of time. METHODS: The study sample consisted of 1007 subjects, drawn from a population-based random sample of elderly individuals, 62-85 years old, who participated in a 3-year follow-up study. From this sample subjects were selected, who did use NSAIDs and completed all cognitive tests at both measurements (n=137), and subjects who did not use NSAIDs and completed all cognitive tests (n=475). Cognitive tests included the Mini-Mental State Examination (MMSE), tests for episodic memory (Auditory Verbal Learning Test) and information processing speed (coding task). Cognitive decline was computed using Edwards-Nunnally method. Multiple logistic regression analyses were performed to examine the association between NSAID (with and without aspirin) and decline in cognitive performance. Besides, the interaction of NSAIDs with age on cognitive decline was determined. RESULTS: The relative risk estimates of decline in episodic memory (immediate recall) adjusted for age, gender, education, baseline MMSE, vascular diseases, diabetes mellitus and (rheumatoid) arthritis for aspirin users only was more than three times reduced (OR: 0.30, 95% CI: 0.09-0.82). The odds ratio for decline in memory of NSAID use without aspirin, adjusted for age, gender, education, baseline MMSE, vascular diseases, diabetes mellitus and (rheumatoid) arthritis was not significant (OR: 1.00, 95% CI: 0.39-2.93). The effect of aspirin was significant only in persons of 75 years and over (OR: 0.10, 95% CI: 0.01-0.81), not in subjects younger than 75 years (OR: 0.52, 95% CI: 0.14-1.96). NSAIDs did not have benefit on information processing speed. In 92% of aspirin users a low dose of 100mg daily or less was used. CONCLUSION: Low-dose aspirin might be protective for decline in memory in individuals of 75 years and over. The benefit of a low-dose aspirin does not support an anti-inflammatory effect, but suggests an antiplatelet effect. Therefore, a possible protective effect of low-dose aspirin on cognitive decline is likely only in subjects with aspirin use over a prolonged period of time.

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Age, vascular risk, and cognitive decline in an older, British, African-Caribbean population.

OBJECTIVES: To investigate associations between baseline factors and subsequent cognitive decline in an older African-Caribbean population. DESIGN: Three-year follow-up of a community sample. SETTING: Registration lists for seven primary care services in south London, United Kingdom. PARTICIPANTS: Of 290 Caribbean-born people aged 55 to 75 recruited at baseline, 216 (75%) were reinterviewed after a 3-year period. Sufficient data for analysis were present for 207. MEASUREMENTS: Tests of verbal memory (immediate and delayed), orientation, and attention were administered at baseline and at 3 years. A composite measure of cognitive change was derived through factor analysis. Participants in the lowest quintile were defined as having cognitive decline and were compared with the rest of the sample with respect to baseline characteristics. RESULTS: Cognitive decline was strongly associated with increased age, but not with sex, education, or occupation. It was also not directly associated with hypertension, diabetes mellitus, or exercise, but the age-decline association was significantly stronger in people with diabetes mellitus and was lower in those reporting vigorous physical exercise at baseline. When cognitive decline was investigated separately for individual tests, both these patterns of association were particularly strong for decline in delayed verbal recall. CONCLUSION: The association between increased age and cognitive decline, particularly decline in verbal recall, was stronger in people with diabetes mellitus (but not hypertension) and weaker in people who were more physically active.

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Cognitive decline in adulthood: an 11.5-year follow-up of the Baltimore Epidemiologic Catchment Area study.

OBJECTIVE: The epidemiology of cognitive decline over 11.5 years was investigated in a large community-residing population, with a special emphasis on the relationship between education and cognitive decline. METHOD: The study was an 11.5-year follow-up of a probability sample of the adult household residents of east Baltimore. From the Baltimore cohort of the Epidemiologic Catchment Area study, 1,488 participants completed the Mini-Mental State during three study waves in 1981, 1982, and 1993-1996. For each study participant, the difference in scores on the Mini-Mental State between waves 2 and 3 was calculated. RESULTS: Over a median interval of 11.5 years, the study participants' scores on the Mini-Mental State declined a mean of 1.41 points, and the scores of 68% of the participants declined by at least 1 Mini-Mental State point. With and without adjustment for age, greater declines were associated with having 8 years or less of formal education and with being African American. CONCLUSIONS: Over a long time period, cognitive decline occurred in all age groups. Having more than 8 years of formal education was associated with less decline. However, beyond 9 years, additional education was not associated with a further reduction in cognitive decline. This suggests that a minimal amount of education during early critical periods might confer protection against cognitive decline later in life.

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XE-CT CBF changes during normative aging, cognitive decline and dementia.

Factors accelerating cerebral degenerative changes represent potentially modifiable risks for cognitive decline. Putative risk factors accelerating mild cognitive decline and dementia were correlated with repeated measures of cerebral atrophy, CT densitometry, perfusions and cognitive testing among neurologically and cognitively normative volunteers. TIAs, hypertension, smoking and male gender accelerate cerebral degenerative changes, mild cognitive decline and dementia. Intervention by control of risk factors and cholinesterase inhibitors should prevent cerebral atropho-degenerative changes so that optimal cognitive performance is maintained.

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