Alzheimer's disease and its related dementias in US Native Americans: A major public health concern.

Alzheimer's disease (AD) and Alzheimer's related dementias (ADRD) are growing public health concerns in aged populations of all ethnic and racial groups. AD and ADRD are caused by multiple factors, such as genetic mutations, modifiable and non-modifiable risk factors, and lifestyle. Studies of postmortem brains have revealed multiple cellular changes implicated in AD and ADRD, including the accumulation of amyloid beta and phosphorylated tau, synaptic damage, inflammatory responses, hormonal imbalance, mitochondrial abnormalities, and neuronal loss. These changes occur in both early-onset familial and late-onset sporadic forms. Two-thirds of women and one-third of men are at life time risk for AD. A small proportion of total AD cases are caused by genetic mutations in amyloid precursor protein, presenilin 1, and presenilin 1 genes, and the APOE4 allele is a risk factor. Tremendous research on AD/ADRD, and other comorbidities such as diabetes, obesity, hypertension, and cancer has been done on almost all ethnic groups, however, very little biomedical research done on US Native Americans. AD/ADRD prevalence is high among all ethnic groups. In addition, US Native Americans have poorer access to healthcare and medical services and are less likely to receive a diagnosis once they begin to exhibit symptoms, which presents difficulties in treating Alzheimer's and other dementias. One in five US Native American people who are 45 years of age or older report having memory issues. Further, the impact of caregivers and other healthcare aspects on US Native Americans is not yet. In the current article, we discuss the history of Native Americans of United States (US) and health disparities, occurrence, and prevalence of AD/ADRD, and shedding light on the culturally sensitive caregiving practices in US Native Americans. This article is the first to discuss biomedical research and healthcare disparities in US Native Americans with a focus on AD and ADRD, we also discuss why US Native Americans are reluctant to participate in biomedical research.

A blood screening tool for detecting mild cognitive impairment and Alzheimer's disease among community-dwelling Mexican Americans and non-Hispanic Whites: A method for increasing representation of diverse populations in clinical research.

INTRODUCTION: Representation of Mexican Americans in Alzheimer's disease (AD) clinical research has been extremely poor. METHODS: Data were examined from the ongoing community-based, multi-ethnic Health & Aging Brain among Latino Elders (HABLE) study. Participants underwent functional exams, clinical labs, neuropsychological testing, and 3T magnetic resonance imaging of the brain. Fasting proteomic markers were examined for predicting mild cognitive impairment (MCI) and AD using support vector machine models. RESULTS: Data were examined from n = 1649 participants (Mexican American n = 866; non-Hispanic White n = 783). Proteomic profiles were highly accurate in detecting MCI (area under the curve [AUC] = 0.91) and dementia (AUC = 0.95). The proteomic profiles varied significantly between ethnic groups and disease state. Negative predictive value was excellent for ruling out MCI and dementia across ethnic groups. DISCUSSION: A blood-based screening tool can serve as a method for increasing access to state-of-the-art AD clinical research by bridging between community-based and clinic-based settings.

Alzheimer's Disease and Related Dementia in Indigenous Populations: A Systematic Review of Risk Factors.

BACKGROUND: There remains a lack of information and understanding of the prevalence and incidence of Alzheimer's disease and related dementia in Indigenous populations. Little evidence available suggests that Indigenous peoples may have disproportionately high rates of Alzheimer's disease and related dementia (ADRD). OBJECTIVE: Given this information, this study systematically explores what risk factors may be associated with ADRD in Indigenous populations. METHODS: A search of all published literature was conducted in October 2016, March 2018, and July 2019 using Medline, Embase, and PsychINFO. Subject headings explored were inclusive of all terms related to Indigenous persons, dementia, and risk. All relevant words, phrases, and combinations were used. To be included in this systematic review, articles had to display an association of a risk factor and ADRD. Only studies that reported a quantifiable measure of risk, involved human subjects, and were published in English were included. RESULTS: Of 237 articles originally identified through database searches, 45 were duplicates and 179 did not meet a priori inclusion criteria, resulting in 13 studies eligible for inclusion in this systematic review. CONCLUSION: The large number of potentially modifiable risk factors reported relative to non-modifiable risk factors illustrates the importance of socioeconomic context in the pathogenesis of ADRD in Indigenous populations. The tendency to prioritize genetic over social explanations when encountering disproportionately high disease rates in Indigenous populations can distract from modifiable proximal, intermediate, and distal determinants of health.

Risk Factors for Alzheimer's Disease and Related Dementia Diagnoses in American Indians.

The burden of Alzheimer's disease and related dementias (ADRD) has increased substantially in the United States, particularly in health disparity populations. Little is known about the epidemiology of ADRD in American Indian (AI) adults, although they have a high prevalence of ADRD risk factors including hypertension, diabetes, obesity, and smoking. Using electronic health records from a large health care organization during 2016-18, we describe characteristics of AI patients aged ≥55 years with and without an ADRD diagnosis, assess ADRD risk factors and contrast findings with results from age- and sex-matched non-Hispanic White (NHW) patients. To identify factors associated with ADRD diagnoses, we estimated population-averaged prevalence rate ratios to approximate relative risk (RR) using generalized estimating equations models adjusted for age, sex, and marital and rural residency status. The age-adjusted prevalence of ADRD diagnosis was 6.6% of AI patients, compared with 4.4% in NHW patients. Patient age and diagnosis of hypertension, depression, hyperlipidemia, or diabetes were significantly associated with higher risk of ADRD diagnosis in AIs (RR range: 1.1-2.8) whereas female sex or being married/having a partner were associated with lower risk of ADRD diagnosis (each RR=.7). ADRD risk factors were generally similar between AI and NHW patients, except for sex and marital status. However, the adjusted risk of ADRD was approximately 49% higher in AI patients. To our knowledge, our study is the first to examine ADRD diagnoses and comorbidities in AIs across a large geographical region in southwest United States. Future efforts to confirm our findings in diverse AI communities are warranted.

Gamma glutamyltransferase and risk of dementia in prediabetes and diabetes.

Diabetes is associated with cognitive impairment and greater risk for dementia, but the role of gamma-glutamyltransferase (γ-GT) in dementia has not been elucidated. We determined incident dementia including Alzheimer's disease and vascular dementia, analyzing data from participants aged 40 years or older in the National Health Insurance Database, collected by the National Health Insurance Service in Korea, from January 2009 to December 2015. During a median follow-up of 7.6 years, 272,657 participants were diagnosed as having dementia. Higher serum γ-GT was associated with increased risk of dementia (HR = 1.22, 95% CI = 1.20-1.24), and had a strong positive association with early onset dementia (HR = 1.32, 95% CI = 1.24-1.40). An additive impact of higher γ-GT on dementia was observed regardless of glycemic status, and prevalent diabetes with the highest γ-GT quartile had a 1.8-fold increased dementia risk (HR = 1.82, 95% CI = 1.78-1.85). This effect of γ-GT concentration in diabetes was more prominent in individuals with vascular dementia (HR = 1.94, 95% CI = 1.84-2.04). In subgroup analysis, young age, male sex, and relatively healthy subjects with a higher γ-GT quartile had more increased dementia risk. In conclusion, γ-GT concentration as well as glycemic status could be a future risk factor for dementia in the general population.

Intention to Screen for Alzheimer's Disease by Residential Locale.

A random digit dialing sample from Missouri (USA) was used to compare associations between psychosocial factors and Alzheimer's disease (AD) screening intention based on residential locale. Linear regression associations between demographics and five psychosocial constructs (dementia knowledge, perceived screening benefits, preventive health behaviors, perceived susceptibility, and self-efficacy) and screening intention were compared by residential locale. Participants (n = 932) had a mean age of 62 years (urban: n = 375; suburban: n = 319, rural: n = 238). African Americans more often lived in urban than suburban/rural neighborhoods, and more urban than suburban/rural residents reported insufficient income. Preventative health behaviors (e.g., dentist visits) were higher in urban and suburban versus rural participants. AD screening intention did not differ by residential locale. Among urban participants, self-efficacy to get screened was associated with screening intention. Among rural participants, dementia knowledge was associated with screening intention. Perceived screening benefits and perceived susceptibility to AD were associated with screening intention regardless of locale. Unlike urban participants, rural participants demonstrated greater screening intention with greater dementia knowledge. Our findings suggest that psychosocial factors associated with AD screening intention differ depending on residential locale. Strategies to increase dementia screening may need to account for regional variations to be maximally effective.

Complex interactions underlie racial disparity in the risk of developing Alzheimer's disease dementia.

INTRODUCTION: We aim to determine racial disparities and their modifying factors in risk for Alzheimer's disease (AD) dementia among cognitively normal individuals 65 years or older. METHODS: Longitudinal data from the National Alzheimer's Coordinating Center Uniform Data Set on 1229 African Americans (AAs) and 6679 whites were analyzed for the risk of AD using competing risk models with death as a competing event. RESULTS: Major AD risk factors modified racial differences which, when statistically significant, occurred only with older age among APOE ε4 negative individuals, but also with younger age among APOE ε4 positive individuals. The racial differences favored AAs among individuals with body mass index (BMI) < 30, but whites among individuals with a high BMI (≥ 30), and were additionally modified by sex, education, hypertension, and smoking status. CONCLUSIONS: The presence, direction, and relative magnitude of racial disparity for AD represent an interactive function of major AD and cerebrovascular risk factors.

The role of social and behavioral risk factors in explaining racial disparities in age-related cognitive impairment: a structured narrative review.

Alzheimer's disease (AD) is a growing public health concern with large disparities in incidence and prevalence between African Americans (AAs) and non-Hispanic whites (NHWs). The aim of this review was to examine the evidence of association between six modifiable risk factors (education, smoking, physical inactivity, obesity, social isolation, and psychosocial stress) and Alzheimer's disease risk in AAs and NHWs. We identified 3,437 studies; 45 met inclusion criteria and were included in this review. Of the examined risks, education provided the strongest evidence of association with cognitive outcomes in AAs and NHWs. This factor may operate directly on Alzheimer's disease risk through the neurocognitive benefits of cognitive stimulation or indirectly through social status.

Discriminative Ability of Montreal Cognitive Assessment Subtests and Items in Racial and Ethnic Minority Groups.

INTRODUCTION: The Montreal Cognitive Assessment (MoCA) is a popular screening tool for Mild Cognitive Impairment (MCI). The psychometric properties of the MoCA have not been widely examined in minority groups. We aimed to analyze the discriminate ability of subtests and items by race and ethnicity given gold-standard clinical diagnosis of cognitive status. METHODS: We analyzed data from the National Alzheimer Coordinating Center Uniform Data Set March 2018 data freeze. Stepwise regression was used to determine which subtests predicted cognitive status (normal cognition, MCI, or dementia), by race/ethnicity. Item discrimination and difficulty was calculated by race/ethnicity and cognitive status. RESULTS: In our sample (n=3895), with an average age of 69.7, 80.7% were non-Hispanic white, 15.0% were non-Hispanic black, and 4.2% were Hispanic. Among non-Hispanic whites all subtests, education, and age predicted clinician diagnosis, while visuospatial/executive, attention, language, delayed recall, and orientation subtests were predictive among non-Hispanic blacks and visuospatial/executive, delayed recall, and orientation subtests and education were predictive among Hispanics. Item discrimination and difficulty varied by race/ethnicity and cognitive status. CONCLUSIONS: By understanding the psychometric properties of MoCA subtests, we can focus on subtests that have higher discrimination and more diagnostic utility. Subtests should be further evaluated for use in screening of minority individuals.

A pathogenic PSEN2 p.His169Asn mutation associated with early-onset Alzheimer's disease.

BACKGROUND: Autosomal dominant early-onset Alzheimer's disease (EOAD) is genetically heterogeneous and has been associated with mutations in 3 different genes, coding for amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2). Most frequent cases are associated with mutations in the PSEN1 gene, whereas mutations in the APP and PSEN2 genes are rare. METHODS: Patient who presented progressive memory decline in her 50s was enrolled in this study. A broad battery of neuropsychological tests and neuroimaging was applied to make the diagnosis. Genetic tests were performed in the patient to evaluate possible mutations using next-generation sequencing (NGS). The pathogenic nature of missense mutation and its 3D protein structure prediction were performed by in silico prediction programs. RESULTS: A pathogenic mutation in the PSEN2 gene in a Korean patient associated with EOAD was identified. Targeted Next-generation sequencing and Sanger sequencing revealed a heterozygous C to A transition at position 505 (c.505C>A), resulting in a probably missense mutation at codon 169 (p.His169Asn) in PSEN2. PolyPhen-2 and SIFT software analyses predicted this mutation to be a probable damaging variant. This hypothesis was supported by the results of 3D in silico modelling analyses that predicted the p.His169Asn may result in major helix torsion due to histidine to asparagine substitution. Mutation may cause additional stresses with hydrophobic residues on the surface that interact inside the transmembrane domain III, which is a conserved domain in PSEN2 His169. CONCLUSION: These findings revealed that the p.His169Asn might be an important residue in PSEN2, which may alter the functions of PSEN2, suggesting its potential involvement with AD phenotype. Future functional studies are needed to evaluate the role of PSEN2 p.His169Asn mutation in AD disease progression.

Cerebral Amyloid Angiopathy: Similarity in African-Americans and Caucasians with Alzheimer's Disease.

Cerebral amyloid angiopathy (CAA) of the Aß type is variably present in the brains of patients with Alzheimer's disease (AD). CAA contributes to cognitive decline and increases the risk of lobar hemorrhage; because both AD-typical dementia and lobar hemorrhage are more common in African-Americans than in Caucasians, we postulated that African-Americans with AD might be particularly susceptible to CAA. To test this hypothesis, we analyzed CAA histopathologically in the large vessels and capillaries of autopsy-derived frontal, temporal, parietal, and occipital cortical samples from African-Americans (n = 18) and Caucasians (n = 19) with end-stage AD. In the combined cohort of 37 subjects, 22% of the subjects had severe CAA in large vessels, and 11% had severe CAA in capillaries. However, the prevalence and histopathologic characteristics of CAA were similar in the African-Americans and Caucasians. This conclusion was substantiated in an independent sample from the National Alzheimer's Coordinating Center database, in which the degree of CAA was comparable in 1,554 Caucasians and 68 African-Americans with end-stage AD. These findings support a growing consensus that the fundamental histopathologic features of AD are largely impartial to the race of the afflicted.

APOE ε4 allele elevates the expressions of inflammatory factors and promotes Alzheimer's disease progression: A comparative study based on Han and She populations in the Wenzhou area.

OBJECTIVE: This study aimed to investigate the impact of apolipoprotein E 4 (APOE4) gene polymorphisms on the expressions of inflammatory factors and the progression of Alzheimer's disease (AD). METHODS: A total of 185 AD patients (the case group, 130 cases from the Han ethnic group and 55 cases from the She ethnic group) and 190 healthy individuals (the control group, 130 cases from the Han ethnic group and 60 cases from the She ethnic group) were recruited for our study. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was conducted to detect APOE4 genotype and allele frequency. Enzyme-linked immunosorbent assay (ELISA) was used to determine the expressions of inflammatory factors in plasma. RESULTS: In both Han and She populations, the frequency of ε3/4 and ε4/4 genotypes and the ε4 allele was significantly higher in the case group than that in the control group. ε3/4 and ε4/4 genotypes and the ε4 allele were the risk factors for AD. In both Han and She populations, the ε2/4, ε3/4 and ε4/4 carriers showed increased levels of TNF-α, IL-6, and IL-1ß when compared with the ε2/2 + ε2/3 + ε3/3 carriers. The TNF-α, IL-6, and IL-1ß levels were higher in the ε4/4 carriers than those in the ε2/4 and ε3/4 carriers, and ε2/4, ε3/4 and ε4/4 carriers in the case group exhibited increased levels of TNF-α, IL-6, and IL-1ß when compared with the control group (P<0.05). Logistic regression analysis indicated that the ε3/4 genotype and TNF-α, IL-6, and IL-1ß levels were associated with the susceptibility to AD in the Han population, while ε3/4 and ε4/4 genotypes and TNF-α, IL-6, and IL-1ß levels were related to the susceptibility to AD in the She population. CONCLUSIONS: The APOE4 ε4 allele may enhance susceptibility to AD and promotes the expressions of inflammatory factors in AD.

The Association of MME microRNA Binding Site Polymorphism with the Risk of Late Onset Alzheimer's Disease in Northern Han Chinese.

BACKGROUND: Although ß-amyloid (Aß) degradation has been normally implicated in the pathogenesis of late-onset Alzheimer's disease (LOAD) through cellular biological studies, the genetic studies linking Aß degradation and LOAD are still scarce. Neprilysin (NEP), one of the most crucial Aß-degrading enzymes in AD, is the metalloendopeptidase which particularly participates in the monomeric Aß species degradation. MicroRNAs (miRNAs) exert post-transcriptional dysregulation and their target sequence on the 3' untranslated regions (3'UTR) may be regulated by single nucleotide polymorphisms (SNPs). OBJECTIVE: To investigate the potential risk of common locus within NEP gene (MME) with LOAD in Northern Han Chinese population. METHOD: We screened a locus (rs6665) in 3' UTR of NEP gene (MME) which sequence was specially regulated by miRNA-187, and further investigated its possible association with LOAD onset in a large case-control study (984 LOAD patients and 1354 healthy controls) in Northern Han Chinese. RESULTS: The distribution of rs6665 genotype (P=0.003) and allele A/C (P=0.001) showed significant difference between LOAD and controls (Odds Ratio (OR) =1.255, 95% Confidence Interval (CI) =1.102-1.429). After adjusting for age, gender and Apolipoprotein (ApoE) ε4 status, the minor C allele of rs6665 showed significant association with LOAD in all three genotypic models (Dominant: P=0.003, OR=1.291, 95%CI=1.092-1.526; Recessive: P=0.030, OR =1.425, 95%CI =1.035- 1.961; Additive: P=0.001, OR=1.249,95%CI=1.093-1.427). After stratifying by ApoE ε4 status, rs6665 polymorphism was found to elevate the LOAD risk in ApoE ε4 carriers (P=0.002, OR=1.846, 95%CI=1.264-2.697). CONCLUSION: Our study firstly confirmed the association of MME miRNA binding site polymorphism with the risk of LOAD. However, the association results warrant further validation.

Two novel loci, COBL and SLC10A2, for Alzheimer's disease in African Americans.

INTRODUCTION: African Americans' (AAs) late-onset Alzheimer's disease (LOAD) genetic risk profile is incompletely understood. Including clinical covariates in genetic analyses using informed conditioning might improve study power. METHODS: We conducted a genome-wide association study (GWAS) in AAs employing informed conditioning in 1825 LOAD cases and 3784 cognitively normal controls. We derived a posterior liability conditioned on age, sex, diabetes status, current smoking status, educational attainment, and affection status, with parameters informed by external prevalence information. We assessed association between the posterior liability and a genome-wide set of single-nucleotide polymorphisms (SNPs), controlling for APOE and ABCA7, identified previously in a LOAD GWAS of AAs. RESULTS: Two SNPs at novel loci, rs112404845 (P = 3.8 × 10-8), upstream of COBL, and rs16961023 (P = 4.6 × 10-8), downstream of SLC10A2, obtained genome-wide significant evidence of association with the posterior liability. DISCUSSION: An informed conditioning approach can detect LOAD genetic associations in AAs not identified by traditional GWAS.

INPP5D rs35349669 polymorphism with late-onset Alzheimer's disease: A replication study and meta-analysis.

Inositol polyphosphate-5-phosphatase (INPP5D) was reported to be associated with Alzheimer's disease (AD) through modulating the inflammatory process and immune response. A recent genome-wide association study discovered a new locus single nucleotide polymorphism (SNP, rs35349669) of INPP5D which was significantly associated with susceptibility to late-onset Alzheimer's disease (LOAD) in Caucasians. In this study, we investigated the relations between the INPP5D polymorphism rs35349669 and LOAD in Han Chinese population comprising 984 LOAD cases and 1352 healthy controls being matched for age and gender. Our results showed no obvious differences in the genotypic or allelic distributions of rs35349669 polymorphism between LOAD cases and healthy controls (genotype: p = 0.167; allele: p = 0.094). Additionally, when these data were stratified by APOEε4 status, there are still no evident differences in the genotypic or allelic distributions in APOEε4 carriers (p > 0.05). Furthermore, meta-analysis of 81964 individuals confirmed that rs35349669 was significantly associated with the risk for LOAD (OR=1.08, 95%CI=1.06-1.11), but the results remained negative in Chinese subgroup (OR=0.77, 95%CI=0.53-1.13). Overall, the current evidence did not indicate that INPP5D rs35349669 polymorphism play a role in the genetic predisposition to LOAD in Chinese population.

FERMT2 rs17125944 polymorphism with Alzheimer's disease risk: a replication and meta-analysis.

A recent meta-analysis of genome-wide association studies (GWAS) in population of Caucasian identified a single nucleotide polymorphism (SNP) rs17125944 in the FERMT2 gene as a new susceptibility locus for late-onset Alzheimer's disease (LOAD). In order to validate the association of the rs17125944 polymorphism with LOAD risk in the northern Han Chinese, we recruited a case-control study of 2338 Han Chinese subjects (984 cases and 1354 age- and gender-matched controls). Our results demonstrated that there was no significant association between the rs17125944 polymorphism and LOAD (genotype: P = 0.953; allele: P = 0.975). Furthermore, no significant differences were observed in alleles and genotypes distribution after stratification by apolipoprotein E (APOE) ε4 and multivariate logistic regression analysis. We also performed a meta-analysis in 81908 individuals. The meta-analysis showed that the C allele is the risk factor for LOAD in Caucasian group (OR = 1.15, 95 % CI = 1.10-1.20) and combined population (OR = 1.13, 95 % CI = 1.08-1.19). While in Chinese population, the C allele is not associated with increased risk of LOAD (OR = 1.07, 95 % CI = 0.89-1.28). In conclusion, our study showed that the rs17125944 polymorphism in FERMT2 gene might not be association with LOAD in northern Han Chinese population.

A Health Profile of Arab Americans in Michigan: A Novel Approach to Using a Hospital Administrative Database.

The objectives of this study were to estimate and compare the prevalence of heart disease, cancer, chronic lower respiratory disease, stroke, Alzheimer's, diabetes, nephrosis, flu/pneumonia, hypertension, and atherosclerosis between Arab Americans and whites attending a large, metropolitan hospital system. The sample included 68,047 patients, 18 years of age or older, who visited the hospital during 2012. Demographic and disease variables were electronically abstracted. Demographic characteristics were compared between Arab Americans and whites using Chi square tests. Sex specific, age-adjusted prevalence ratios (PR) and 95 % confidence intervals were estimated for these two groups using a log-binomial regression model. Compared to white men, Arab American men had a higher prevalence of diabetes (PR 1.40, 95 % CI 1.29-1.52) and hypertension (PR 1.07, 95 % CI 1.04-1.10), and a lower prevalence of chronic lower respiratory disease (PR 0.74, 95 % CI 0.66-0.83). Compared to white women, Arab American women had a higher prevalence of chronic lower respiratory disease (PR 1.12, 95 % CI 1.01-1.25), diabetes (PR 1.49, 95 % CI 1.38-1.60), influenza/pneumonia (PR 1.26, 95 % CI 1.05-1.51) and hypertension (PR 1.04, 95 % CI 1.01-1.08). This study supports previous findings that health disparities exist for Arab Americans, who are classified as "white" in health statistics. Standard inclusion of Arab American as a separate ethnicity category will aid researchers in assessing the health care needs of this growing minority community.

Trends in Disparity by Sex and Race/Ethnicity for the Leading Causes of Death in the United States-1999-2010.

CONTEXT: Temporal trends in disparities in the leading causes of death within and between US demographic subgroups indicate the need for and success of interventions to prevent premature death in vulnerable populations. Studies that report recent trends are limited and outdated. OBJECTIVE: To describe temporal trends in disparities in death rates by sex and race/ethnicity for the 10 leading causes of death in the United States during 1999-2010. DESIGN: We used underlying cause of death data and population estimates from the National Vital Statistics System to calculate age-adjusted death rates for the 10 leading causes of death during 1999-2010. We measured absolute and relative disparities by sex and race/ethnicity for each cause and year of death; we used weighted linear regression to test for significance of trends over time. RESULTS: Of the 10 leading causes of death, age-adjusted death rates by sex and race/ethnicity declined during 1999-2010 for 6 causes and increased for 4 causes. But sex and racial/ethnic disparities between groups persisted for each year and cause of death. In the US population, the decreasing trend during 1999-2010 was greatest for cerebrovascular disease (-36.5%) and the increasing trend was greatest for Alzheimer disease (52.4%). For each sex and year, the disparity in death rates between Asian/Pacific Islanders (API) and other groups varied significantly by cause of death. In 2010, the API-non-Hispanic black disparity was largest for heart disease, malignant neoplasms, cerebrovascular diseases, and nephritis; the API-American Indian/Alaska Native disparity was largest for unintentional injury, diabetes mellitus, influenza and pneumonia, and suicide; and the API-non-Hispanic white disparity was largest for chronic lower respiratory diseases and Alzheimer disease. CONCLUSIONS: Public health practitioners can use these findings to improve policies and practices and to evaluate progress in eliminating disparities and their social determinants in vulnerable populations.

Relationship between the gene polymorphisms of kallikrein-kinin system and Alzheimer's disease in a Hunan Han Chinese population.

This study aimed to determine the connection between polymorphisms of kallikrein kinin system including KLK1 (rs5516), KNG1 (rs710446, rs2304456) and ACE (rs4291, rs4309, rs4343) and late-onset Alzheimer's disease (LOAD). The research was conducted as a case-control study, comprising 201 AD patients in the AD group, and 257 healthy subjects as the control group. PCR amplification and matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF MS) were used to detect the six polymorphisms (rs5516 in KLK1; rs710446, rs2304456 in KNG1; rs4291, rs4309, rs4343 in ACE) from both groups. No statistically significant difference was found between the genotype and allelotype distributions of rs5516, rs710446, rs2304456, rs4291 and rs4343 (P>0.05). The differences between the genotype and allelotype distributions of the rs4309 were statistically significant (P<0.05). Haplotype analysis confirmed the existence of three haplotypes (AG, AT, GT) composed of rs710446/rs2304456, and six haplotypes (ATA, ACA, TCA, TCG, TTA, TTG) composed of rs4291/rs4309/rs4343, among which the distribution of ATA, ACA, TCA between the two groups was statistically significant difference (P<0.05). Our study showed that the polymorphisms of rs5516, rs710446, rs2304456, rs4291 and rs4343 is not related to the incidence of LOAD. The polymorphisms of rs4309 may be related to LOAD, as well as ATA, ACA, and TCA haplotype composed of rs4291/rs4309/rs4343.

Vitamin D levels and cognition in elderly adults in China.

OBJECTIVES: To evaluate the association between vitamin D level and cognitive impairment in individuals aged 60 and older. DESIGN: Cross-sectional cohort study. SETTING: Chinese Longitudinal Healthy Longevity Survey, a community-based cohort study in areas in China where the density of centenarians is exceptionally high. PARTICIPANTS: Individuals with mean age of 84.9 ± 12.7 (N = 2,004). MEASUREMENTS: Participants' cognitive state was evaluated using the Mini-Mental State Examination (MMSE). Vitamin D was measured in plasma using an enzyme-linked immunoassay. RESULTS: The cross-sectional association between quartiles of plasma vitamin D level and cognitive impairment (MMSE score <18) was modeled using logistic regressions. Plasma vitamin D levels were lower in individuals with cognitive impairment (31.9 ± 15.3 nmol/L) than in those without (45.6 ± 19.6 nmol/L). There was a reverse association between plasma vitamin D and cognitive impairment. After adjusting for age, sex, chronic conditions, smoking and drinking habits, outdoor activities, depression, and activity of daily living limitations, the association remained significant. The multivariable-adjusted odds ratio for lowest versus highest vitamin D levels was 2.15 (95% confidence interval (CI) = 1.05-4.41) for cognitive impairment, and the multivariable odds ratio associated with a 1-standard deviation decrement in plasma vitamin D was 1.32 (95% CI = 1.00-1.74) for cognitive impairment. CONCLUSION: Low plasma vitamin D levels were associated with greater odds of cognitive impairment. Further prospective studies in Asian populations are needed to examine the causal direction of this association.