Prevalence of prodromal Alzheimer disease

Prevalence of prodromal Alzheimer disease

Orul Presentation: Epidemiology S203 II MID-LIFE SMOKING AND LATE-LIFE ALZHEIMER’S EASE: THE HONOLULU-ASIA AGING STUDY Suzznne L Tyas, Univ of Ma...

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Orul

Presentation:

Epidemiology

S203

II

MID-LIFE SMOKING AND LATE-LIFE ALZHEIMER’S EASE: THE HONOLULU-ASIA AGING STUDY Suzznne L Tyas, Univ of Manitoba, Veteran’s

Affairs,

Honolulu,

Bethesda,

MD;

J Lamer,

National

HI;

Len R White, Pacific Institute

Winnipeg,

MB Canadu;

Richard

J Havlik,

Health

Research

on Aging.

Bethesda,

George

National Institute.

DIS-

W Ross, Dcpt

Institute Honolulu,

of

on Aging, HI: Lmow

DIETARY ANTI-OXIDANTS THE ROTTERDAM STUDY. Marianne

J En&hurt,

Witteman,

Albert

Muw

THE INCIDENCE OF ALZHEIMER’S DISEASE DOES NOT VARY BY GENDER IN ROCHESTER, MN

D Edland, C/in.

Walter

Rochrstrr.

A Roccn,

Ronald

C Prtersm,

Ruth H Cha, Emre

Kokmun.

MN

Incidence rates of AlTheimer’\ dl\ease are higher in women than men m several recent ctudies. although contrary findings have been reported. It remains uncertain whether this gender pattern holds across all populations. We determined age and gender specific incidence rates among the population of at rlak persons aged 50 and over residing in Rochester, MN during the 1985 to 1989 quinquenmum. Cases were ascertained through the medical records linkage system of the Rochester Epidemiology Project that encompasses records of essentially all medical care provided to the elderly residents of Rochester. Computer indices of clinical diagnoses, histological diagnoses, and medical procedurea were reviewed for indications of dementia. All medical records for each so identified person were examined by a trained nurse abstractor. A neurologist confirmed the presence of dementia, established a differential diagnosis by DSM-IV critena, and estimated the date of onset. A total of 356 inadent Alzheimer cases were identified. Incidence rates increased exponentially with age, and there was no clear pattern of differential rivk by gender (Table). Data are consistent with rates obwrved during the 1975.1979 and 1980-1984 quinquennia for this geographically defined population [Rocca, of ~1.. AJE 1998;148:51-621, suggesting that this is a stable finding. In Rochester, MN, the largest population for which incident cabeb have been enumerated to date, gender is not a significant predictor of riqk of incident Alzheimer’s disease.

Table Incidence rates of Alzheimer’s disease by age and gender (per 1,000 person-years; DSM-IV criteria) Age (in years) 5&54

55-59

6&64

65-69

70-74

John

M B Breteler,

C Swieten, Erasmus

Jacqueline

Med

Ctr,

C M

Rotterdam

Netherlands

Oxidative stress may play a role in the etiology of Alzheimer’s disease. Moreover, oxidation may be an important step in atherogenesis and vascular risk factors and atherosclerosis have been associated with both Alzheimer’s disease and vascular dementia. We examined whether the dietary intake of anti-oxidants, and fruit and vegetables as sources of anti-oxidants, is related to risk of (subtypes) of dementia. The rtudy was conducted in the Rotterdam Study, a prospective population-based study among 7983 subjects aged 55 years and over. Complete data on daily dietary intake was obtained from 5407 dementia-free non-institutionalised subjects at baseline (1990.1993). Follow-up examinations took place in 1993-1994 and 1997.1999. In addition, the cohort was continuously monitored for incident mortahty and morbidity. The association between daily dietary intake of anti-oxidants (p-carotene, flavonoids, selenium, vitamin E and vitamin C) and fruit and vegetables and risk of (subtypes of) dementia was examined by Cox proportional hazards regression with adjustment for age, sew, education and energy-intake. Relative riska (RR) were calculated per standard deviation increase in intake. After a mean follow-up of 6.0 years 199 subjects developed dementia (149 Alzheimer’s disease and 28 vascular dementia). High intake of vitamin E, vitamin C and vegetable5 decreased the risk of total dementia (RR (95% Cl) 0.83 (0.70-0.99). 0.91 (95%CI 0.78-1.05) and 0.81 (0.68. 0.97) respectively), as well as the risk of Alzheimer’s disease (RR (95% Cl) 0.81 (0.66.0.99), 0.82 (0.68-0.98) and 0.82 (0.67-1.00) respectively). No relation was found between intake of p-carotene, flavonoids, selenium and fruit and the risk of dementia. Our findings suggest that high daily dietary intake of vitamin E, vitamin C and vegetables may protect against dementia and Alzheimer’s disease.

19231PREVALENCE Frederick

75-79

80-84

85-X9 9(&94 95-99

Male

0.3

0.2

0.4

1.0

3.5

9.5

17.7

26.9

48.9

21.7

Female

0.1

0.2

0.3

1.1

2.9

10.1

20. I

34.5

46.1

65.6

W Unverzagt,

Medicine, lbndun

Stevm

Ruitmherg.

Monique

MD

Although recent cohort studies have identified smoking as a risk factor for Alzheimu’s disease (AD), the effect of early patterns and level of smoking on AD is unknown. We examined the dose-response relationship between mid-life smoking levela and late-life risk of dementia in a cohort of Japanese-American men followed since 1965 as part of the Honolulu Heat Program (HHP) and the Honolulu-Asia Aging Study. The men reported their mid-life Emoking history in 1965 and 1974 when they were 45-65 years of age. Dementia was assessed in 1991.93 by a three-step procedure that included screening cognitive function m the full sample (n=3734; 80% of the surviving original~cohort) and conducting a detailed diagostic work-up on a subsample (n=426). Diagnostic criteria used were DSM-III-R for dementia and NINCDS-ADRDA for AD. AD with contributing cerebrovascular disease was classified as mixed dementia. The analyaip is based on the 2014 men who reported ever smoking in the mid-life exam and for whom dementia status was known. We calculated pack-years of smoking and categorized level of smoking as light (deciles l-3, reference group), medium (deciles 4-6). heavy (deciles 7-8) and very heavy (deciles 9-10). We used logistic regression to estimate the relative risk (RR) and 95% confidence intervals (Cl) for dementia by smoking level. Adjusting for age, education, and apolipoprotein ~4, thZ risk of AD increased significantly with pack-years of smoking to a RR of 2. I8 (95% CI= 1.07-4.69) at medium levels and a RR of 2.40 (95% CI= 1.16-5.17) at heavy levels of smoking. Very heavy levels of smoking were not associated with AD (RR= 1.08, 95% CI=O.43-2.63). The findings were similar for mixed dementia. Adjustment for cardiovascular risk factors, wbclinical atherowlerotis, woke, and forced expiratory volume did not significantly change these results. In men with a history of mid-life smokmg, pack-years predicted the risk of late-life AD in a dose-dependent manner up to heavy smoking levels. A strong survivor bias in very heavy smokers may explain the lack of association between AD and very high levels of smoking.

pBiJ

Annemieke

Hofmnn,

AND THE RISK OF DEMENTIA.

Mrdicine.

Indiunupolis,

Nigeria;

Sujum

GUI,

IN: Olusegun

Siu L Hui,

It~dinrmpolis.

OF PRODROMAL

Kathleen

ALZHEIMER DISEASE

ChGtinstinr L Emslry,

Bniyrwu, S Hall,

Adesola Hufih

Indiana

0 Ogunniyi,

C Hmdrir,

Univ

Sch

of

Uni\’ of Ibadan,

Indmnu

Univ Sch of’

IN

Context: Alzheimer diwase (AD) typically begins as an isolated loss of memory, an amnestic disorder, before evolving over time into a global dementia. While the prevalence of the dementia due to AD is well known (i.e., approximately 5% for community-dwelling perwns over age 65 in North America and Europe), less is known about the prevalence of the prodromal. or amnestic. phase of AD. Objective: To determine the prevalence of prodromal AD among community-dwelling, elderly African Americans. Method: 29 contiguous census tracts in Indianapolis were identified which had a high percentage of African American residents. Inclusion criteria were self-reported race as African American and age 65 years or older. Addresses in the target area were randomly sampled. 2,212 of 2,582 eligible subjects agreed to in-home cognitive and functional screenings. A stratified subsample received full clinical assewnent (physician examination, informant interview, neuropsychological testing, and laboratory studies including neuroimaging as needed) and diagnosis. Prodromal AD was defined as medically unexplained, isolated loss of short-term memory causing minima1 to no impairment in activities of daily living. Memory loss was coded as present if noted in any or all of the following: informant-reported memory loss, physician-detected memory loss, or performance below the 7th percentile of same aged peers on neuropsychological tests. Results: The wzened population averaged 73.9 + 7.0 years of age and 9.6 ? 3.1 years of education with 65% being female. A total of 351 persons received full clinical assessment and diagnosis. These subjects averaged 77.8 +- 7.5 years of age and 8.3 -t 3.5 years of education with 59% being female. Of the 351 clinically-assessed subjects, I Xl were diagnosed as normal, 65 as demented, and I05 as cognitively impaired (CI) but not demented. Of the I05 CI, 48 had medically unexplained, isolated memory loss (prodromal AD). Using logistic regression, weighted for the probability of selection for clinical assessment, and controlling for age and gender, the prevalence of prodromal AD was calculated at 12.5%. Conclusion: Prodromal AD, or medically unexplained, isolated memory loss. is quite common. It affects I in 8 communitydwelling African Americans over age 65.