O2-01-03

O2-01-03

S182 Oral O2-01-02: Primary Prevention and Risk 3 Methods: In 1992-1994, we administered a risk factor questionnaire to 1,836 dementia-free individu...

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S182

Oral O2-01-02: Primary Prevention and Risk 3

Methods: In 1992-1994, we administered a risk factor questionnaire to 1,836 dementia-free individuals, who represented the Japanese American population aged 65 and over in King County, WA. Part of this baselineevaluation included the administration of the 3RT, a computer-assisted test of reaction time (n⫽1,646), the NART, and questions about age, gender, education. DSM-IV criteria were used to diagnose dementia over the following 10 years. We used Cox Proportional Hazards regression with follow-up as the time axis in models including age at entry, gender and education. Results: 173 subjects were diagnosed with incident dementia; 147 had CRT data. The HR for dementia associated with education (1-year increase) was 0.96 (95% CI⫽0.91-0.99, p⫽0.029). When CRT median (of 32 trials) was added to the model, each 10 milliseconds (ms) increase in time was associated with a 0.7% increase in risk for dementia (95% CI⫽1.002-1.012, p⫽0.007) and the association with education was lost (p⫽.127). Among a subset of 694 subjects with NART data, an increase in 10ms in the CRT measure increased the risk for dementia by 3.6% (95% CI⫽1.009-1.064, p⫽0.009). In models including both CRT and NART, both were independently significant [HR associated with CRT⫽1.034 per 10 ms (95% CI⫽1.007-1.062, p⫽0.014); HR associated with estimated IQ score⫽0.95 per point (95% CI⫽0.91-0.99, p⫽0.0199)] with education losing significance in all models that included either CRT or NART. Conclusions: The relation between education and dementia is confounded by reaction time and estimated IQ score. Choice reaction time and NART measure different phenomena that contribute independently to the risk of dementia over a 10-year follow-up period. O2-01-02

ANTIOXIDANT VITAMIN INTAKE AND DEMENTIA IN THE OLDEST-OLD: THE 90ⴙ STUDY

Maria M. Corrada1, Claudia H. Kawas1, Annlia Paganini-Hill2, 1 University of California Irvine, Irvine, CA, USA; 2University of Southern California, Los Angeles, CA, USA. Contact e-mail: [email protected] Background: Several studies have suggested that antioxidant vitamin intake may protect against the development of dementia. Few studies, however, have been able to investigate this association in the oldest-old. Objective: To determine if intake of antioxidant vitamins is associated with dementia in 90⫹ year-olds. Methods: The Leisure World Cohort Study is a population-based prospective study of nearly 14,000 residents of a California retirement community who completed a postal health survey in the early 1980s. The questionnaire included details on use of vitamin A, C, and E supplements and dietary intake of foods containing vitamins A and C. Vitamin intake was categorized using tertiles for the whole cohort. Those alive and aged 90 or older on 1/1/2003 (n⫽1151) were recruited into The 90⫹ Study. Dementia was determined by a neurological exam (DSM-IV criteria), a MMSE ⬍24, a telephone CASI-short score ⬍26, or an informant questionnaire. Logistic regression was used to calculate odds ratios for dementia. Results: We determined cognitive status in 911 of 941 participants in The 90⫹ Study. Average age of participants when the health survey was completed was 72 years (range: 68-87) and 94 years (range: 90-106) when evaluated as part of The 90⫹ Study. Most participants (77%) were female. Dementia was identified in 41% of participants. It was determined by in-person examination (neurological exam or MMSE) in 46% of participants, telephone CASI in 18%, and by information provided by an informant in 36%. After adjusting for age and sex, dementia in 90⫹ year-olds was not related to supplemental intake of vitamins A, C, or E nor to total (supplemental plus dietary) intake of vitamin A. Moderate total intake of vitamin C was associated with dementia (OR⫽1.59, 95%CI⫽1.13 - 2.23). Further adjustment for education, smoking, body mass index, or alcohol intake did not change the results. Conclusions: Antioxidant vitamin intake measured decades before the determination of dementia is not related to dementia in a cohort of participants who survived to age 90⫹. Our finding of increased risk of dementia in those consuming moderate amounts of vitamin C is counterintuitive to the expected protective effect of antioxidants on dementia development.

Adjusted Odds Ratios for Dementia in The 90⫹ Study* Variable Vitamin Low Med High Vitamin Low Med High Vitamin Low Med High Vitamin Low Med High Vitamin Low Med High

N

Odds Ratio (95%CI)

p-value

479 189 242

1.00 (reference) 0.99 (0.70 - 1.41) 1.01 (0.73 - 1.39)

0.98 0.97

321 334 254

1.00 (reference) 1.23 (0.89 - 1.69) 0.98 (0.69 - 1.38)

0.20 0.90

407 250 252

1.00 (reference) 0.93 (0.67 - 1.29) 0.96 (0.69 - 1.33)

0.65 0.80

284 291 334

1.00 (reference) 0.95 (0.68 - 1.39) 0.99 (0.71 - 1.38)

0.78 0.96

278 309 321

1.00 (reference) 1.59 (1.13 - 2.23) 1.29 (0.92 - 1.81)

0.008 0.15

A Supplements

C Supplements

E Supplements

A Total

C Total

*Adjusted for age and sex; CI is confidence interval

O2-01-03

DEPRESSION IS A RISK FACTOR FOR DEVELOPING IMPAIRMENT IN EXECUTIVE FUNCTION IN A LONGITUDINAL STUDY OF OLDER WOMEN

Paul B. Rosenberg, Michelle M. Mielke, Michelle C. Carlson, Johns Hopkins University, Baltimore, MD, USA. Contact e-mail: [email protected] Background: There is increasing evidence that depressive symptoms are often prodromal to incident Alzheimer’s disease (AD), and mild cognitive impairment (MCI). Similarly, there is evidence suggesting that inflammation is associated with incident AD. Objective: We sought to examine the associations of depression and peripheral inflammation with the development of cognitive impairment similar to MCI in a longitudinal study of elderly women. Methods: A community-acquired sample of 436 elderly women assessed as non-demented at baseline were followed for up to 4 examinations (6 years). Episodic memory was assessed with Hopkins Verbal Learning Test immediate (HVLT-imm) and delayed (HVLT-del) recall, and executive functioning with Trails Making Test-A and B (TMT-A, TMT-B). Participants were characterized as having significant impairment on a cognitive test if their score on a cognitive test fell 1.5 standard deviations below age-education norms for that test. Depression was defined as a score on the Geriatric Depression Scale (30-item) of ⬎⫽8. Serum IL-6 and CRP levels were measured at baseline with standard immunoassays. Multivariate Cox proportional-hazards regressions were performed to determine whether risk factors were associated with the onset of significant cognitive impairment as defined above. Results: Mean age at baseline was 73 years. 14% of the participants were depressed at baseline. Depression increased the risk of developing significant cognitive impairment defined by HVLT-imm, TMT-A, and TMT-B approximately 2-fold. Elevated IL6 serum levels at baseline were associated with increased risk of developing significant cognitive impairment defined by HVLT-imm. Conclusions: Baseline depression was associated with significantly increased risk of developing MCI-like cognitive impairments in immediate recall and executive functioning, suggesting that depressive symptoms are a marker for preclinical MCI and reinforcing prior findings that late-life depression is associated with executive dysfunction. Elevated serum IL6 baseline levels were associated with significant cognitive impairment in immediate recall, suggesting that peripheral inflammation may be a similar marker. The lack of a finding with delayed recall suggests that risk factors for amnestic and non-amnestic MCI may differ. Depression and peripheral may be biomarkers for prodromal AD.