Biomedical subjects

R Mayeux

Publications and source records attributed to R Mayeux.

At least 19 recordsLinked to original sources

PubMed2006

Familial Alzheimer disease in Latinos: interaction between APOE, stroke, and estrogen replacement.

BACKGROUND: Factors that modify risk related to APOE variants have been examined primarily in unrelated patients and controls, but seldom in family-based studies. Stroke, vascular risk factors, estrogen replacement therapy (ERT), head injury (HI), and smoking have been reported to influence risk of sporadic but not familial Alzheimer disease (AD). OBJECTIVES: To examine the potential relationship between these risk factors and APOE, the authors used a family study design in a population in which the APOE-epsilon4 variant is strongly associated with risk of AD. METHODS: Latino families primarily from the Caribbean Islands in which two or more living relatives had dementia were identified in the New York City metropolitan area, the Dominican Republic, and Puerto Rico. A total of 1,498 participants from 350 families underwent a clinical interview, medical and neurologic examinations, neuropsychological testing, and APOE genotyping. Diagnosis was made by consensus using research criteria for AD. RESULTS: APOE-epsilon4 was associated with a nearly twofold increased risk of AD. A history of stroke was also associated with a fourfold increased risk. A statistical interaction between APOE-epsilon4 and stroke was observed. Women with an APOE-epsilon4 who took ERT did not have an increased risk of AD, but in women with a history of stroke ERT was a deleterious effect modifier. CONCLUSIONS: APOE-epsilon4 and stroke independently increase risk of familial Alzheimer disease (AD) among Latinos, and may interact to further increase AD risk. Among women, the risk of AD associated with APOE-epsilon4 may be attenuated by a history of ERT.

Aged↗

PubMed2005

Decline in cognitive and functional skills increases mortality risk in nondemented elderly.

OBJECTIVE: To investigate the relation between rate of decline in cognitive and functional/physical abilities and risk of death in nondemented elderly. METHODS: Data were included from individuals participating in a prospective study of aging and dementia in Medicare recipients, 65 years and older, residing in northern Manhattan. The authors included 878 members of the cohort who had measures of memory, cognitive, language, or functional scores over three study intervals, excluding all participants who were demented or had more than one problem in activity of daily living (ADL) skills at baseline. Participants were classified as showing no decline, slow, medium, or rapid rate of decline, based on the slope of change in cognitive and functional/physical factors. The authors used survival methods to examine the relation of rate of decline in cognitive and functional performance to subsequent mortality in younger and older nondemented elderly and across three ethnic groups, adjusting for potential confounders. RESULTS: Nondemented elderly with preserved ADL skills who showed rapid rates of decline on measures of visuospatial reasoning/cognitive, language, ADL, and instrumental ADL functions were approximately twice as likely to die as nondemented elderly who showed no decline or slower rates of decline, while rate of decline in memory or in measures of extremity mobility was not related to risk of death. The association of the rate of decline to risk of death was stronger in relatively young (< or =75 years) than in older participants. CONCLUSIONS: Rate of decline in cognitive and functional skills predicts mortality in nondemented elderly.

Age Factors↗

PubMed2005

Aggregation of vascular risk factors and risk of incident Alzheimer disease.

BACKGROUND: The prevalence of Alzheimer disease (AD) is increasing in the elderly, and vascular risk factors may increase its risk. OBJECTIVE: To explore the association of the aggregation of vascular risk factors with AD. METHODS: The authors followed 1,138 individuals without dementia at baseline (mean age 76.2) for a mean of 5.5 years. The presence of vascular risk factors was related to incident possible and probable AD. RESULTS: Four risk factors (diabetes, hypertension, heart disease, and current smoking) were associated with a higher risk of AD (p < 0.10) when analyzed individually. The risk of AD increased with the number of risk factors (diabetes + hypertension + heart disease + current smoking). The adjusted hazards ratio of probable AD for the presence of three or more risk factors was 3.4 (95% CI: 1.8, 6.3; p for trend < 0.0001) compared with no risk factors. Diabetes and current smoking were the strongest risk factors in isolation or in clusters, but hypertension and heart disease were also related to a higher risk of AD when clustered with diabetes, smoking, or each other. CONCLUSIONS: The risk of Alzheimer disease (AD) increased with the number of vascular risk factors. Diabetes and current smoking were the strongest risk factors, but clusters including hypertension and heart disease also increased the risk of AD. These associations are unlikely to be explained by misclassification of the outcome, given strong associations when only probable AD is considered.

Aged↗

PubMed2005

Impact of plasma lipids and time on memory performance in healthy elderly without dementia.

OBJECTIVE: To examine the association of plasma lipid levels to changes in cognitive function in elderly subjects without dementia. METHODS: The authors examined changes in performance in tests of memory, visuospatial/cognitive, and language abilities in 1,147 elderly individuals without dementia or cognitive impairment at baseline followed for 7 years using generalized estimating equations. RESULTS: Performance in all cognitive domains declined significantly over time, while there was no association between levels of any plasma lipid or lipid lowering treatment and memory, cognitive/visuospatial, or language performance at any interval. Higher age at baseline was related to lower scores in all three domains at each interval, while higher education and white ethnicity were associated with higher scores in all domains. Analyses relating plasma lipids to performance in color trails tests using proportional hazards regression showed no association. In subsequent analyses excluding subjects with incident dementia, memory performance declined over time, while cognitive/visuospatial and language performance did not. Higher plasma high density lipoprotein and total cholesterol were associated with higher scores in language performance at baseline; this domain declined faster among individuals with higher total cholesterol, but this result was not significant after taking multiple comparisons into account. Plasma triglycerides, low density lipoprotein, or treatment with lipid lowering agents were not associated with changes in cognitive performance. CONCLUSIONS: Plasma lipid levels or treatment with lipid lowering agents in the elderly were not associated with changes in cognitive function.

Aged↗

PubMed2005

Association between mild parkinsonian signs and mild cognitive impairment in a community.

BACKGROUND: Mild parkinsonian signs (MPS) are associated with prevalent and incident dementia but it is not known whether they are associated with mild cognitive impairment (MCI). OBJECTIVE: To determine whether MPS and specific MPS (changes in axial function, rigidity, tremor) are associated with MCI in nondemented community-dwelling older people in northern Manhattan, NY. METHODS: Participants underwent neurologic assessment, including a modified motor portion of the Unified Parkinson Disease Rating Scale. MCI was diagnosed in nondemented participants who had cognitive impairment based on neuropsychological testing and no functional impairment. Participants with MCI were classified as having MCI with memory impairment (MCI+M) vs MCI without memory impairment (MCI-M). RESULTS: MCI was present in 608 (27.3%) of 2,230 participants, including 255 participants with MCI+M and 353 with MCI-M; 1,622 participants did not have MCI. MPS were present in 369 (16.5%) of 2,230 participants. In a univariate logistic regression model, odds of MCI+M (vs no MCI) were 51% higher in participants with MPS compared to those with no MPS (OR = 1.51, 95% CI = 1.09 to 2.09, p = 0.01). Multivariate models yielded similar results (OR = 1.45, 95% CI = 1.03 to 2.05, p = 0.03). Rigidity was present in a higher proportion of participants with MCI+M compared to participants without MCI. CONCLUSIONS: Mild parkinsonian signs, especially rigidity, are associated with amnestic mild cognitive impairment. Mild parkinsonian signs and mild cognitive impairment may share similar pathogeneses. Whether this involves Alzheimer-type pathology, Lewy bodies, or vascular changes in the basal ganglia or basal ganglia circuitry deserves further investigation in postmortem studies.

Age Factors↗

PubMed2004

Plasma homocysteine levels and risk of Alzheimer disease.

OBJECTIVE: To explore the association between high homocysteine levels and risk of Alzheimer disease (AD) in the Washington Heights-Inwood Columbia Aging Project (WHICAP). METHODS: The authors obtained fasting plasma samples in 909 elderly subjects chosen at random from a cohort of Medicare recipients; there was longitudinal data in 679 subjects without dementia at baseline who were followed for 3,206 person-years. Prevalent and incident dementia and its subtypes were diagnosed using standard methods. RESULTS: There were 128 persons with prevalent AD and 109 with incident AD in 3,206 person-years of follow-up. The adjusted OR of prevalent AD for the highest quartile of homocysteine compared to the lowest was 1.3 (95% CI = 0.7, 2.3; p for trend = 0.25). In longitudinal analyses, the authors found that the adjusted hazard ratio of AD for the highest quartile of homocysteine was 1.4 (95% CI = 0.8, 2.4; p for trend = 0.31). The authors also found that high homocysteine levels were not related to a decline in memory scores over time. Age was a significant confounder in all the analyses. The study had 80% power to detect a hazard ratio of 1.3 in the longitudinal analyses. CONCLUSION: High homocysteine levels were not associated with AD and were not related to a decrease in memory scores over time.

Age Factors↗

PubMed2004

Genetic influences on memory performance in familial Alzheimer disease.

OBJECTIVE: To investigate the heritability of memory and other cognitive measures in families with multiple individuals with Alzheimer disease (AD) to determine if neuropsychological measures can be used to better understand genetic contributions to AD. METHODS: The genetic contributions to the variation in declarative memory, attention, abstract reasoning, language, and visuospatial function using a variance component method were estimated. For memory scores, the proportion of genetic contribution was estimated, controlling for APOE. RESULTS: The unadjusted heritability estimates for the declarative memory tasks ranged from 0.47 for delayed recall to 0.25 for delayed recognition, where a heritability estimate of 1 indicates that genetic factors explain all of the phenotypic variance and a heritability score of 0 indicates that genetic factors explain none. When adjusted for sex, age, education, and general intelligence, the heritability estimates increased to 0.60 for delayed recall and 0.41 for delayed recognition. None of the other cognitive tests showed heritability estimates as high as that observed for memory. When the influence of APOE was taken into account, the heritability estimates changed modestly for delayed recall and consistent long-term retrieval, whereas the estimates for other memory scores did not change, suggesting that APOE contributes little to these memory scores. CONCLUSIONS: Declarative memory in familial AD is under strong genetic influence, only part of which is attributable to APOE. Memory performance should prove to be a useful phenotypic component in the investigation of the genetic basis of AD.

Aged↗

PubMed2004

Fine mapping of 10q and 18q for familial Alzheimer's disease in Caribbean Hispanics.

Familial Alzheimer's disease (AD [MIM 104300]) has been a focus of intense investigation, primarily in Caucasian families from Europe and North America families. Although the late-onset form of familial AD, beginning after age 65 years, has been linked to regions on chromosomes 10q and 12p, the specific genetic variants have not yet been consistently identified. Using a unique cohort of families of Caribbean Hispanics ancestry, we screened the genome using 340 markers on 490 family members from 96 families with predominantly late-onset AD. We observed the strongest support for linkage on 18q (LOD=3.14). However, 17 additional markers (chromosomes 1-6, 8, 10, 12, and 14) exceeded a two-point LOD score of 1.0 under the affecteds-only autosomal dominant model or affected sibpair model. As we previously reported the fine-mapping effort on 12p showing modest evidence of linkage, we focused our fine-mapping efforts on two other candidate regions in the current report, namely 10q and 18q. We added 31 family members and eight additional Caribbean Hispanic families to fine map 10q and 18q. With additional microsatellite markers, the evidence for linkage for 18q strengthened near 112 cM, where the two-point LOD score for D18S541 was 3.37 and the highest NPL score in that region was 3.65 (P=0.000177). This narrow region contains a small number of genes expressed in the brain. However, at 10q (134-138 cM), the NPL score decreased from 3.15 (P=0.000486) to 2.1 (P=0.0218), but two broad peaks remained overlapping with previously reported peaks. Our results provide modest support for linkage on 10q and 12p in this cohort of Caribbean Hispanic families with familial Alzheimer's disease, and strong evidence for a new locus on 18q.

Aged↗

PubMed2003

Plasma A[beta]40 and A[beta]42 and Alzheimer's disease: relation to age, mortality, and risk.

BACKGROUND: Plasma amyloid [beta]-peptide (A[beta]) 40 and A[beta]42 levels are increased in persons with mutations causing early-onset familial Alzheimer's disease (AD). Plasma A[beta]42 levels were also used to link microsatellite genetic markers to a putative AD genetic locus on chromosome 10 and were observed in patients with incipient sporadic AD. METHODS: The authors measured plasma A[beta]40 and A[beta]42 levels using a sandwich ELISA after the initial examination of 530 individuals participating in an epidemiologic study of aging and dementia. Participants were examined at 18-month intervals, and plasma A[beta]40 and A[beta]42 levels were repeated in 307 subjects 3 years after baseline. RESULTS: Compared with individuals who never developed AD, patients with AD at baseline and those who developed AD during the follow-up had significantly higher A[beta]42, but not A[beta]40, plasma levels. The risk of AD in the highest quartile of plasma A[beta]42 was increased by more than twofold over that in the lowest quartile. The highest plasma A[beta]42 levels were observed in patients with AD who died during the follow-up. Plasma A[beta]42, but not A[beta]40, levels decreased over time in patients with newly acquired AD. CONCLUSIONS: Plasma A[beta]40 and A[beta]42 increase with age and are strongly correlated with each other. Plasma A[beta]40 and A[beta]42 levels are elevated in some patients before and during the early stages of AD but decline thereafter. High plasma A[beta]42 levels may also be associated with mortality in patients with AD.

Age Distribution↗

PubMed2003

The impact of comorbid disease and injuries on resource use and expenditures in parkinsonism.

BACKGROUND: Persons with parkinsonism have high rates of both associated and unrelated prevalent comorbid conditions. A better understanding of patterns of care and expenditures may aid in designing programs to enhance functioning, lengthen independent living, and manage costs. METHODS: The authors linked national survey data of 24,831 elderly to nearly 1.9 million Medicare claims. Persons with parkinsonism (n = 791) were identified from survey or Medicare encounters for paralysis agitans. Comorbid disease risk was measured using age-adjusted OR with 95% CI. Comorbidity cost ratios (ratio of average per person per year charges for parkinsonism alone vs with comorbid conditions) were developed to describe incremental costs of comorbidities. RESULTS: Patients with parkinsonism were older (78.5 +/- 7.6 vs 75.1 +/- 8.3 years, p < 0.0001) and had more injuries resulting in broken bones (35.6% vs 19.5%, p < 0.0001), including broken hips (15.9% vs 5.8%, p < 0.0001), during the 5-year study. Broken hips were more prevalent among men (OR 3.4, 95% CI 2.5 to 4.8) and women (OR 2.5, 95% CI 2.1 to 3.1) with than without parkinsonism. Among those with parkinsonism, comorbidity cost ratios demonstrated two- to threefold higher charges for dementia, broken bones, broken hip, and diabetes. CONCLUSIONS: Comorbidity associated with parkinsonism is an under-recognized contribution to higher resource use and expenditures. Further study of injuries, dementia, and diabetes is required to assess whether public health interventions could reduce excess morbidity and expenditures associated with parkinsonism.

Aged↗

PubMed2002

Primary care expenditures before the onset of Alzheimer's disease.

OBJECTIVE: To investigate primary care expenditures in the period before diagnosis of AD. METHODS: In a population-based sample of Medicare enrollees in New York City, person-level 1996 Medicare claims, summed over primary care encounters, were examined for people who developed AD in 1997 to 1998 and those who did not. RESULTS: People who developed AD were more likely to use Medicare outpatient and ambulatory care 1 to 2 years before diagnosis. Compared with respondents who did not develop AD, the excess cost for men was $1,167 (85% higher) and for women $239 (26% higher). Among elderly people > or = 75 years in the United States, the prodromal period of AD was associated with an excess Medicare-based primary care cost of $128.5 to $194.7 million. CONCLUSION: In addition to huge costs associated with AD after diagnosis, prediagnosis costs are an unrecognized source of expenditures related to the disease.

Black or African American↗

PubMed2002

The relationship of hypertension in the elderly to AD, vascular dementia, and cognitive function.

BACKGROUND: Hypertension at the age of 45 to 50 years may predispose to AD later in life. It is not known whether hypertension after age 65 years also contributes to AD risk, and its effect on cognitive function is also not fully understood. METHODS: Data were analyzed from 1,259 Medicare recipients free of dementia in a longitudinal study covering a 7-year period (1991 to 1998). The effect of hypertension was first examined in relationship to the risk for incident AD and then to incident vascular dementia (VaD) using Cox proportional hazards models. Changes in performance over time on tasks of memory, language, and visuospatial/cognitive function were compared in those with and without hypertension using generalized estimating equations. RESULTS: Of the 1,259 subjects, 731 (58.1%) had a history of hypertension associated with diabetes, stroke, and heart disease. A history of hypertension was not associated with an increased risk for AD (rate ratio [RR] 0.9, 95% CI 0.7 to 1.3) but was associated with an increased risk for VaD (1.8 [1.0 to 3.2]). Hypertension was not associated with changes in memory, language, and general cognitive function in normal individuals over time. Compared with individuals with neither hypertension nor heart disease, those with hypertension or heart disease alone had no increase in risk for VaD. However, when both were present, there was a threefold increase in risk for VaD. A sixfold increase in risk was observed when both hypertension and diabetes were present. CONCLUSIONS: Hypertension after age 65 years is not associated with AD and does not adversely affect memory, language, or general cognitive function. A history of hypertension may be an antecedent to VaD, particularly in the presence of heart disease or diabetes.

Aged↗

PubMed2002

Smoking and Parkinson's disease in twins.

OBJECTIVE: To test the hypothesis that cigarette smoking protects against the development of PD. BACKGROUND: Smoking has been inversely associated with PD in many studies, but whether this reflects a biologic effect on the underlying disease process or merely confounding or selection bias remains uncertain. METHODS: The authors compared smoking histories in male twin pairs identified from the National Academy of Sciences--National Research Council World War II Veteran Twins Cohort. The amount of cigarettes smoked (in pack-years) was collected until the time of PD onset in the affected twin or until the time of death for the unaffected twin, whichever came first. Differences in pack-years smoked until PD onset and until 10 and 20 years before onset were compared using paired t-tests. Comparisons were made overall and stratified by zygosity and concordance for PD. To assess the role of shared environment, correlation for smoking behaviors was compared between pairs concordant and discordant for PD. RESULTS: Detailed smoking histories were available for 113 twin pairs in which at least one twin had PD (discordant pairs: 43 monozygotic [MZ], 50 dizygotic [DZ]; concordant pairs: 10 MZ, 10 DZ). Within-pair correlation for ever smoking was high in MZ pairs (phi = 0.47, p = 0.001) but not in DZ pairs (phi = 0.007, p = 0.96). In 33 discordant MZ pairs and 39 discordant DZ pairs in which at least one twin had smoked, the twins without PD smoked more than their brothers smoked (32.5 vs. 22.7 pack-years, p = 0.026). This was more marked in the MZ pairs (37.1 vs. 25.3 pack-years, p = 0.077) than in the DZ pairs (28.6 vs. 20.5 pack-years, p = 0.17). A similar relationship was seen when smoking dose was calculated only until 10 years before PD onset, suggesting that the lower dose of smoking in the twin with PD was not the result of early, undiagnosed disease. CONCLUSION: Within twin pairs, risk of PD is inversely correlated with the dose (in pack-years) of cigarette smoking. This effect is most pronounced in MZ twins, despite the high correlation for smoking. Because MZ twins are genetically identical and are similar behaviorally, this difference is unlikely to result from either genetic factors or environmental confounders. These results are compatible with a true biologic protective effect of cigarette smoking.

Diseases in Twins↗

PubMed2001

Chromosome-12 mapping of late-onset Alzheimer disease among Caribbean Hispanics.

Linkage to chromosome 12p for familial Alzheimer disease (AD) has been inconsistent. Using 35 markers near the centromere of chromosome 12, we investigated 79 Caribbean Hispanic families with AD. Two-point linkage analysis using affected sib pairs yielded LOD scores of 3.15 at D12S1623 and 1.43 at D12S1042. The LOD score at D12S1623 decreased to 1.62 in families with late-onset (age >65 years) AD (LOAD), but the LOD score at D12S1042 was unchanged. Among families negative for the apolipoprotein E (APOE-epsilon 4) allele, the LOD score for D12S1623 was lower (1.01), whereas that for D12S1042 increased to 1.73. Among families positive for the APOE-epsilon 4 allele, none of the LOD scores reached 1. Multipoint affected-relative-pair analysis showed peaks at D12S1623 (nonparametric linkage [NPL] score 1.52; P=.028) and near D12S1042, at D12S1057 (NPL score 1.57; P=.027). NPL scores for both D12S1623 and D12S1057 increased in families affected with LOAD, but, in APOE-epsilon 4-negative families, only scores for the region flanking D12S1623 remained elevated (NPL score 1.74; P=.013). This study of Caribbean Hispanics with familial AD extends and provides modest evidence of linkage to loci on chromosome 12p. Linkage varied by age at onset of AD and by the presence or absence of the APOE-epsilon 4 allele.

Adult↗

PubMed2001

A founder mutation in presenilin 1 causing early-onset Alzheimer disease in unrelated Caribbean Hispanic families.

CONTEXT: Genetic determinants of Alzheimer disease (AD) have not been comprehensively examined in Caribbean Hispanics, a population in the United States in whom the frequency of AD is higher compared with non-Hispanic whites. OBJECTIVE: To identify variant alleles in genes related to familial early-onset AD among Caribbean Hispanics. DESIGN AND SETTING: Family-based case series conducted in 1998-2001 at an AD research center in New York, NY, and clinics in the Dominican Republic. PATIENTS: Among 206 Caribbean Hispanic families with 2 or more living members with AD who were identified, 19 (9.2%) had at least 1 individual with onset of AD before the age of 55 years. MAIN OUTCOME MEASURE: The entire coding region of the presenilin 1 gene and exons 16 and 17 of the amyloid precursor protein gene were sequenced in probands from the 19 families and their living relatives. RESULTS: A G-to-C nucleotide change resulting in a glycine-alanine amino acid substitution at codon 206 (Gly206Ala) in exon 7 of presenilin 1 was observed in 23 individuals from 8 (42%) of the 19 families. A Caribbean Hispanic individual with the Gly206Ala mutation and early-onset familial disease was also found by sequencing the corresponding genes of 319 unrelated individuals in New York City. The Gly206Ala mutation was not found in public genetic databases but was reported in 5 individuals from 4 Hispanic families with AD referred for genetic testing. None of the members of these families were related to one another, yet all carriers of the Gly206Ala mutation tested shared a variant allele at 2 nearby microsatellite polymorphisms, indicating a common ancestor. No mutations were found in the amyloid precursor protein gene. CONCLUSIONS: The Gly206Ala mutation was found in 8 of 19 unrelated Caribbean Hispanic families with early-onset familial AD. This genetic change may be a prevalent cause of early-onset familial AD in the Caribbean Hispanic population.

Age of Onset↗

PubMed2001

Mortality and apolipoprotein E in Hispanic, African-American, and Caucasian elders.

To investigate whether mortality risk is influenced by apolipoprotein E (APOE) genotype and whether the risk differs by ethnicity, we compared the mortality risk in 2,112 individuals > or = 65 years of age residing in northern Manhattan in New York. Mortality risks associated with the APOE genotype, adjusted for sex, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides, differed significantly by ethnic group. Among Caucasian and Hispanics, the E2/E3 genotype was associated with the lowest mortality risk in the multivariate Cox proportional hazards modeling, adjusted for lipid levels, whereas mortality risk did not differ substantially between the E4/E3 and E3/E3 genotypes. Among African-Americans, the E2/E3 genotype was not associated with the lowest mortality risk, but the E4/E3 genotype was. Adjustment for heart disease, diabetes, and stroke reduced mortality risk associated with each genotype by about 50% for all ethnic groups, but the patterns remained the same. Although we cannot rule out the possibility of a healthy survival bias, our analyses designed to examine healthy survival by comparing risk of mortality in groups who were younger or older at entry do not support this possibility. Our findings suggest that the APOE genotype is associated with mortality and that the genotypic risks differ by ethnic group. Nearly 50% of the mortality risk associated with the APOE genotype appears to act through major chronic diseases, but those diseases only partially explain the mechanism by which the genotypic risk acts. To better understand the observed ethnic differences in mortality risk by genotype, a detailed prospective study is needed to examine the relationships among APOE, other candidate genes, health conditions, and eventual death.

Aged↗

PubMed2001

Diabetes mellitus and risk of Alzheimer's disease and dementia with stroke in a multiethnic cohort.

Research on the relation between diabetes mellitus and dementia has produced conflicting results, and the relation has not been investigated among Blacks and Hispanics. In this study, Cox proportional hazards models were used to analyze longitudinal data from 1,262 elderly subjects without dementia at baseline (1991-1996) who were followed for an average of 4.3 years between 1992 and 1997. Outcomes were incident Alzheimer's disease and dementia associated with stroke. The prevalence of diabetes was 20% at baseline. The adjusted relative risk of Alzheimer's disease among persons with diabetes as compared with those without diabetes was 1.3 (95% confidence interval (CI): 0.8, 1.9). The adjusted relative risk for the composite outcome of Alzheimer's disease and cognitive impairment without dementia (without stroke) in subjects with diabetes was 1.6 (95% CI: 1.2, 2.1). The adjusted relative risk of stroke-associated dementia in persons with diabetes was 3.4 (95% CI: 1.7, 6.9). Among Blacks and Hispanics, approximately one third of the risk of stroke-associated dementia was attributable to diabetes (33% (95% CI: 31, 36) and 36% (95% CI: 33, 37), respectively), as compared with 17% (95% CI: 13, 22) among Whites. The finding of an association between diabetes and the composite outcome of Alzheimer's disease and cognitive impairment without dementia (without stroke) is consistent with prior reports of a modest relation between diabetes and Alzheimer's disease.

Black or African American↗

PubMed2001

Specificity of the fivefold increase in AD in mothers of adults with Down syndrome.

BACKGROUND: In a previous study, the authors found that the risk of AD among mothers who were 35 years or younger when their children with Down syndrome (DS) were born was five times that of mothers of children with other forms of mental retardation. The current study investigated the specificity of the familial aggregation of DS and AD by examining whether mothers who gave birth to children with DS before age 35 are also at increased risk of other age-related neurologic or medical disorders. METHODS: The authors used survival methods to compare cumulative incidence and relative risk of AD, other dementias, and common age-related disorders in parents of 200 adults with DS and parents of 252 adults with other forms of mental retardation. RESULTS: Mothers who were < or =35 years of age when their children with DS were born were four to five times as likely to develop AD as control mothers (rate ratio = 4.8, 95% CI 2.1, 11.2), whereas risk of AD among mothers who were >35 years when their children with DS were born was not significantly increased (rate ratio = 1.8, 95% CI 0.6, 5.1). Risk of AD among fathers of probands with DS was similar to that of control fathers, and did not vary by age at proband birth. Risk of other dementias and of other age-related medical condition was similar among mothers and fathers of probands with DS and control parents, regardless of age at proband birth. CONCLUSION: These findings suggest that the increased risk of AD among mothers who gave birth to children with DS before age 35 appears to represent a specific vulnerability to AD, as opposed to other age-related degenerative disorders.

Adult↗