共查询到20条相似文献，搜索用时 31 毫秒
1.
Jessica Tulloch Lesley Leong Sunny Chen C. Dirk Keene Steven P. Millard Andrew Shutes-David Oscar L. Lopez Julia Kofler Jeffrey A. Kaye Randy Woltjer Peter T. Nelson Janna H. Neltner Gregory A. Jicha Douglas Galasko Eliezer Masliah James B. Leverenz Chang-En Yu Debby Tsuang 《Alzheimer's & dementia》2018,14(7):889-894
Introduction
Inheritance of the ε4 allele of apolipoprotein E (APOE) increases a person's risk of developing both Alzheimer's disease (AD) and Lewy body dementia (LBD), yet the underlying mechanisms behind this risk are incompletely understood. The recent identification of reduced APOE DNA methylation in AD postmortem brains prompted this study to investigate APOE methylation in LBD.Methods
Genomic DNA from postmortem brain tissues (frontal lobe and cerebellum) of neuropathological pure (np) controls and npAD, LBD + AD, and npLBD subjects were bisulfite pyrosequenced. DNA methylation levels of two APOE subregions were then compared for these groups.Results
APOE DNA methylation was significantly reduced in npLBD compared with np controls, and methylation levels were lowest in the LBD + AD group.Discussion
Given that npLBD and npAD postmortem brains shared a similar reduction in APOE methylation, it is possible that an aberrant epigenetic change in APOE is linked to risk for both diseases. 相似文献2.
Niklas Mattsson Colin Groot Willemijn J. Jansen Susan M. Landau Victor L. Villemagne Sebastiaan Engelborghs Mark M. Mintun Alberto Lleo José Luis Molinuevo William J. Jagust Giovanni B. Frisoni Adrian Ivanoiu Gaël Chételat Catarina Resende de Oliveira Karen M. Rodrigue Johannes Kornhuber Anders Wallin Aleksandra Klimkowicz-Mrowiec Rik Ossenkoppele 《Alzheimer's & dementia》2018,14(7):913-924
Introduction
Apolipoprotein E (APOE) ε4 is the major genetic risk factor for Alzheimer's disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid β (Aβ) pathology.Methods
We included 3451 Aβ+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE ε4 prevalence in relation to age, sex, education, and geographical location.Results
The APOE ε4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in Aβ+ cognitively normal and Aβ+ mild cognitive impairment (P < .05) but not in Aβ+ AD dementia (P = .66). The prevalence was highest in Northern Europe but did not vary by sex or education.Discussion
The APOE ε4 prevalence in AD was higher than that in previous studies, which did not require presence of Aβ pathology. Furthermore, our results highlight disease heterogeneity related to age and geographical location. 相似文献3.
Usman Saeed Saira S. Mirza Bradley J. MacIntosh Nathan Herrmann Julia Keith Joel Ramirez Sean M. Nestor Qinggang Yu Jo Knight Walter Swardfager Steven G. Potkin Ekaterina Rogaeva Peter St. George-Hyslop Sandra E. Black Mario Masellis 《Alzheimer's & dementia》2018,14(9):1137-1147
Introduction
Although the apolipoprotein E ε4-allele (APOE-ε4) is a susceptibility factor for Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), its relationship with imaging and cognitive measures across the AD/DLB spectrum remains unexplored.Methods
We studied 298 patients (AD = 250, DLB = 48; 38 autopsy-confirmed; NCT01800214) using neuropsychological testing, volumetric magnetic resonance imaging, and APOE genotyping to investigate the association of APOE-ε4 with hippocampal volume and learning/memory phenotypes, irrespective of diagnosis.Results
Across the AD/DLB spectrum: (1) hippocampal volumes were smaller with increasing APOE-ε4 dosage (no genotype × diagnosis interaction observed), (2) learning performance as assessed by total recall scores was associated with hippocampal volumes only among APOE-ε4 carriers, and (3) APOE-ε4 carriers performed worse on long-delay free word recall.Discussion
These findings provide evidence that APOE-ε4 is linked to hippocampal atrophy and learning/memory phenotypes across the AD/DLB spectrum, which could be useful as biomarkers of disease progression in therapeutic trials of mixed disease. 相似文献4.
Sonia Moreno–Grau Octavio Rodríguez-Gómez Ángela Sanabria Alba Pérez-Cordón Domingo Sánchez-Ruiz Carla Abdelnour Sergi Valero Isabel Hernández Maitée Rosende-Roca Ana Mauleón Liliana Vargas Asunción Lafuente Silvia Gil Miguel Ángel Santos-Santos Montserrat Alegret Ana Espinosa Gemma Ortega Marina Guitart A. Vivas 《Alzheimer's & dementia》2018,14(5):634-643
Introduction
Subjective cognitive decline (SCD) has been proposed as a potential preclinical stage of Alzheimer's disease (AD). Nevertheless, the genetic and biomarker profiles of SCD individuals remain mostly unexplored.Methods
We evaluated apolipoprotein E (APOE) ε4's effect in the risk of presenting SCD, using the Fundacio ACE Healthy Brain Initiative (FACEHBI) SCD cohort and Spanish controls, and performed a meta-analysis addressing the same question. We assessed the relationship between APOE dosage and brain amyloid burden in the FACEHBI SCD and Alzheimer's Disease Neuroimaging Initiative cohorts.Results
Analysis of the FACEHBI cohort and the meta-analysis demonstrated SCD individuals presented higher allelic frequencies of APOE ε4 with respect to controls. APOE dosage explained 9% (FACEHBI cohort) and 11% (FACEHBI and Alzheimer's Disease Neuroimaging Initiative cohorts) of the variance of cerebral amyloid levels.Discussion
The FACEHBI sample presents APOE ε4 enrichment, suggesting that a pool of AD patients is nested in our sample. Cerebral amyloid levels are partially explained by the APOE allele dosage, suggesting that other genetic or epigenetic factors are involved in this AD endophenotype. 相似文献5.
Cerebral amyloid angiopathy in Down syndrome and sporadic and autosomal-dominant Alzheimer's disease
María Carmona-Iragui Mircea Balasa Bessy Benejam Daniel Alcolea Susana Fernández Laura Videla Isabel Sala María Belén Sánchez-Saudinós Estrella Morenas-Rodriguez Roser Ribosa-Nogué Ignacio Illán-Gala Sofía Gonzalez-Ortiz Jordi Clarimón Frederick Schmitt David K. Powell Beatriz Bosch Albert Lladó Michael S. Rafii Juan Fortea 《Alzheimer's & dementia》2017,13(11):1251-1260
Introduction
We aimed to investigate if cerebral amyloid angiopathy (CAA) is more frequent in genetically determined than in sporadic early-onset forms of Alzheimer's disease (AD) (early-onset AD [EOAD]).Methods
Neuroimaging features of CAA, apolipoprotein (APOE), and cerebrospinal fluid amyloid β (Aβ) 40 levels were studied in subjects with Down syndrome (DS, n = 117), autosomal-dominant AD (ADAD, n = 29), sporadic EOAD (n = 42), and healthy controls (n = 68).Results
CAA was present in 31%, 38%, and 12% of cognitively impaired DS, symptomatic ADAD, and sporadic EOAD subjects and in 13% and 4% of cognitively unimpaired DS individuals and healthy controls, respectively. APOE ε4 genotype was borderline significantly associated with CAA in sporadic EOAD (P = .06) but not with DS or ADAD. There were no differences in Aβ040 levels between groups or between subjects with and without CAA.Discussion
CAA is more frequently found in genetically determined AD than in sporadic EOAD. Cerebrospinal fluid Aβ40 levels are not a useful biomarker for CAA in AD. 相似文献6.
Luciano A. Sposato Estefanía Ruíz Vargas Patricia M. Riccio Jon B. Toledo John Q. Trojanowski Walter A. Kukull Lauren E. Cipriano Antonia Nucera Shawn N. Whitehead Vladimir Hachinski 《Alzheimer's & dementia》2017,13(7):770-777
Introduction
Heart failure (HF) and atrial fibrillation (AF) have been associated with a higher risk of Alzheimer's disease (AD). Whether HF and AF are related to AD by enhancing AD neuropathological changes is unknown.Methods
We applied network analyses and multiple logistic regression models to assess the association between HF and AF with severity of AD neuropathology in patients from the National Alzheimer's Coordinating Center database with primary neuropathological diagnosis of AD.Results
We included 1593 patients, of whom 129 had HF and 250 had AF. HF and AF patients were older and had milder AD pathology. In the network analyses, HF and AF were associated with milder AD neuropathology. In the regression analyses, age (odds ratio [OR] 0.94, 95% confidence interval [CI] 0.93–0.95 per 1-year increase in age, P < .001) and the interaction term HF × AF (OR 0.61, 95% CI 0.40–0.91, P = .014) were inversely related to severe AD pathology, whereas APOE ε4 genotype showed a direct association (OR 1.68, 95% CI 1.31–2.16). Vascular neuropathology was more frequent in patient with HF and AF patients than in those without.Discussion
HF and AF had milder AD neuropathology. Patients with milder AD lived longer and had more exposure to vascular risk factors. HF and AF patients showed a higher frequency of vascular neuropathology, which could have contributed to lower the threshold for clinically evident dementia. 相似文献7.
Alison C. Burggren Zanjbeel Mahmood Theresa M. Harrison Prabha Siddarth Karen J. Miller Gary W. Small David A. Merrill Susan Y. Bookheimer 《Alzheimer's & dementia》2017,13(7):739-748
Introduction
The translocase of outer mitochondrial membrane 40 (TOMM40), which lies in linkage disequilibrium with apolipoprotein E (APOE), has received attention more recently as a promising gene in Alzheimer's disease (AD) risk. TOMM40 influences AD pathology through mitochondrial neurotoxicity, and the medial temporal lobe (MTL) is the most likely brain region for identifying early manifestations of AD-related morphology changes.Methods
In this study, we examined the effects of TOMM40 using high-resolution magnetic resonance imaging in 65 healthy, older subjects with and without the APOE ε4 AD-risk variant.Results
Examining individual subregions within the MTL, we found a significant relationship between increasing poly-T lengths of the TOMM40 variant and thickness of the entorhinal cortex only in subjects who did not carry the APOE ε4 allele.Discussion
Our data provide support for TOMM40 variant repeat length as an important contributor to AD-like MTL pathology in the absence of APOE ε4. 相似文献8.
Karen Ritchie Isabelle Carrière Li Su John T. O&#x;Brien Simon Lovestone Katie Wells Craig W. Ritchie 《Alzheimer's & dementia》2017,13(10):1089-1097
Introduction
Although biomarker studies of late-onset Alzheimer's disease suggest pathology to be present decades before diagnosis, little is known about cognitive performance at this stage.Methods
A sample of 210 adults (aged 40–59) of whom 103 have a parent diagnosed with dementia (family history subgroup) underwent computerized cognitive testing. Apolipoprotein E (apoE) status was determined, and 193 subjects had magnetic resonance imaging. Distance from dementia onset was estimated in relation to age of parental diagnosis, and Cardiovascular Risk Factors, Aging, and Incidence of Dementia Risk Scores were calculated.Results
Lower hippocampal volumes (P = .04) were associated with poorer spatial location recall and higher Dementia Risk Scores with poorer visual recognition (P = .0005), and lower brain and hippocampal volume (P < .0001, P = .04, respectively). Family history subgroup participants closer to dementia onset had lower scores on visual working memory (P = .05), whereas those with an APOE ε4 allele performed better on form perception (P = .005).Discussion
Middle-aged adults at risk of dementia show evidence of poorer cognitive performance, principally in visuospatial functions. 相似文献9.
James D. Stefaniak Li Su Elijah Mak Nasim Sheikh-Bahaei Katie Wells Karen Ritchie Adam Waldman Craig W. Ritchie John T. O&#x;Brien 《Alzheimer's & dementia》2018,14(2):253-258
Introduction
Cerebral small vessel disease (CSVD) is associated with late-onset Alzheimer's disease (LOAD) and might contribute to the relationship between apolipoprotein E ε4 (APOE ε4) and LOAD, in older people. However, it is unclear whether CSVD begins in middle age in individuals genetically predisposed to LOAD.Methods
We assessed the relationship between radiological markers of CSVD, white matter hyperintensities and microbleeds, and genetic predisposition to LOAD in a cross-sectional analysis of cognitively normal subjects aged 40–59 years recruited from the PREVENT Dementia study.Results
Microbleed prevalence was 14.5%, and mean ± standard deviation white matter hyperintensity percentage of total brain volume was 0.41 ± 0.28%. There was no significant association between APOE ε4 carrier status or history of parental dementia and white matter hyperintensity volume (P = .713, .912 respectively) or microbleeds (P = .082, .562 respectively) on multiple regression.Discussion
Genetic predisposition to LOAD, through APOE genotype or AD family history, is not associated with CSVD in middle age. 相似文献10.
Katrine Laura Rasmussen Børge Grønne Nordestgaard Ruth Frikke-Schmidt Sune Fallgaard Nielsen 《Alzheimer's & dementia》2018,14(12):1589-1601
Introduction
We tested the hypothesis that low plasma complement C3 is observationally and genetically associated with high risk of Alzheimer's disease (AD).Methods
We studied 95,442 individuals enrolled in the Copenhagen General Population Study. In genetic analyses, we further included 8367 individuals from the Copenhagen City Heart Study. In the two studies, 1189 and 35 developed AD during median 8 years follow-up.Results
The multifactorially adjusted hazard ratio for risk of AD for a one standard deviation lower levels of complement C3 was 1.11 (95% confidence interval: 1.04–1.19) in all individuals and 1.66 (1.33–2.07) in APOE ε44 carriers. In Mendelian randomization, the corresponding genetic estimates were 1.66 (1.05–2.63) overall and 1.99 (0.52–7.65) in APOE ε44 carriers.Discussion
Low baseline levels of complement C3 were associated with high risk of AD. The risk was amplified in APOE ε44 highly susceptible individuals, and these findings were substantiated by a Mendelian randomization approach, potentially implying causality. Based on these findings, we present and thoroughly discuss an updated Alzheimer hypothesis incorporating low complement C3 levels. 相似文献11.
Introduction
The etiologies of dementia are complex and influenced by genetic and environmental factors including medical conditions.Methods
We used Cox regression model to estimate the individual and joint effects of physical activity (PA), apolipoprotein E (APOE) ε4, and diabetes status on risk of dementia and cognitive impairment without dementia (CIND) among 1438 cognitively intact Mexican American elderly who were followed up to 10 years.Results
The risk of developing dementia/CIND was increased more than threefold in APOE ε4 carriers or diabetics with low levels of PA compared with ε4 noncarriers or nondiabetics who engaged in high PA (ε4: hazard ratio [HR] = 3.44, 95% confidence interval [CI] = 1.85–6.39; diabetes: HR = 3.11, 95% CI = 1.87–5.18); the presence of all three risk factors increased risk by nearly 10-fold (HR = 9.49, 95% CI = 3.57–25.3).Discussion
PA in elderly Hispanics protects strongly against the onset of dementia/CIND, especially in APOE ε4 carriers and those who have diabetes. 相似文献12.
Raffaele Cacciaglia José Luis Molinuevo Carles Falcón Anna Brugulat-Serrat Gonzalo Sánchez-Benavides Nina Gramunt Manel Esteller Sebastián Morán Carolina Minguillón Karine Fauria Juan Domingo Gispert 《Alzheimer's & dementia》2018,14(7):902-912
Introduction
Apolipoprotein E (APOE)-ε4 is the major genetic risk factor for Alzheimer's disease. However, the dose-dependent impact of this allele on brain morphology of healthy individuals remains unclear.Methods
We analyzed gray matter volumes (GMvs) in a sample of 533 healthy middle-aged individuals with a substantial representation of ε4-carriers (207 heterozygotes and 65 homozygotes).Results
We found APOE-ε4 additive GMv reductions in the right hippocampus, caudate, precentral gyrus, and cerebellar crus. In these regions, the APOE genotype interacted with age, with homozygotes displaying lower GMv after the fifth decade of life. APOE-ε4 was also associated to greater GMv in the right thalamus, left occipital gyrus, and right frontal cortex.Discussion
Our data indicate that APOE-ε4 exerts additive effects on GMv in regions relevant for Alzheimer's disease pathophysiology already in healthy individuals. These findings elucidate the mechanisms underlying the increased Alzheimer's disease risk in ε4-carriers, suggesting a dose-dependent disease vulnerability on the brain structure level. 相似文献13.
Katrine L. Rasmussen Anne Tybjærg-Hansen Børge G. Nordestgaard Ruth Frikke-Schmidt 《Alzheimer's & dementia》2018,14(1):71-80
Introduction
In recent prospective studies, low plasma levels of apolipoprotein E (apoE) are associated with high risk of dementia. Whether this reflects a causal association remains to be established.Methods
Using a Mendelian randomization approach, we studied 106,562 and 75,260 individuals from the general population in observational and genetic analyses, respectively.Results
In observational analyses risk of Alzheimer's disease and all dementia increased stepwise as a function of stepwise lower apoE levels (P for trend, 2 × 10?17 and 9 × 10?21). APOE-weighted allele scores were associated with stepwise decreases in apoE (P for trend, <1 × 10?300). In instrumental variable analysis, the causal risk ratios for a 1 mg/dL genetically determined lower apoE were 1.41 (1.27–1.57) for Alzheimer's disease and 1.33 (1.25–1.43) for all dementia (F-statistics = 3821).Discussion
Genetic and hence lifelong low apoE is associated with high risk of dementia in the general population. The concordance between observational and genetic estimates suggests a potential causal relationship. 相似文献14.
Gyungah R. Jun Jaeyoon Chung Jesse Mez Robert Barber Gary W. Beecham David A. Bennett Joseph D. Buxbaum Goldie S. Byrd Minerva M. Carrasquillo Paul K. Crane Carlos Cruchaga Philip De Jager Nilufer Ertekin-Taner Denis Evans M. Danielle Fallin Tatiana M. Foroud Robert P. Friedland Alison M. Goate Lindsay A. Farrer 《Alzheimer's & dementia》2017,13(7):727-738
Introduction
Genetic loci for Alzheimer's disease (AD) have been identified in whites of European ancestry, but the genetic architecture of AD among other populations is less understood.Methods
We conducted a transethnic genome-wide association study (GWAS) for late-onset AD in Stage 1 sample including whites of European Ancestry, African-Americans, Japanese, and Israeli-Arabs assembled by the Alzheimer's Disease Genetics Consortium. Suggestive results from Stage 1 from novel loci were followed up using summarized results in the International Genomics Alzheimer's Project GWAS dataset.Results
Genome-wide significant (GWS) associations in single-nucleotide polymorphism (SNP)–based tests (P < 5 × 10?8) were identified for SNPs in PFDN1/HBEGF, USP6NL/ECHDC3, and BZRAP1-AS1 and for the interaction of the (apolipoprotein E) APOE ε4 allele with NFIC SNP. We also obtained GWS evidence (P < 2.7 × 10?6) for gene-based association in the total sample with a novel locus, TPBG (P = 1.8 × 10?6).Discussion
Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 相似文献15.
Paul K. Crane Emily Trittschuh Shubhabrata Mukherjee Andrew J. Saykin R. Elizabeth Sanders Eric B. Larson Susan M. McCurry Wayne McCormick James D. Bowen Thomas Grabowski Mackenzie Moore Julianna Bauman Alden L. Gross C. Dirk Keene Thomas D. Bird Laura E. Gibbons Jesse Mez 《Alzheimer's & dementia》2017,13(12):1307-1316
Introduction
There may be biologically relevant heterogeneity within typical late-onset Alzheimer's dementia.Methods
We analyzed cognitive data from people with incident late-onset Alzheimer's dementia from a prospective cohort study. We determined individual averages across memory, visuospatial functioning, language, and executive functioning. We identified domains with substantial impairments relative to that average. We compared demographic, neuropathology, and genetic findings across groups defined by relative impairments.Results
During 32,286 person-years of follow-up, 869 people developed Alzheimer's dementia. There were 393 (48%) with no domain with substantial relative impairments. Some participants had isolated relative impairments in memory (148, 18%), visuospatial functioning (117, 14%), language (71, 9%), and executive functioning (66, 8%). The group with isolated relative memory impairments had higher proportions with ≥ APOE ε4 allele, more extensive Alzheimer's-related neuropathology, and higher proportions with other Alzheimer's dementia genetic risk variants.Discussion
A cognitive subgrouping strategy may identify biologically distinct subsets of people with Alzheimer's dementia. 相似文献16.
Catherine Feart Catherine Helmer Bénédicte Merle François R. Herrmann Cédric Annweiler Jean-François Dartigues Cécile Delcourt Cécilia Samieri 《Alzheimer's & dementia》2017,13(11):1207-1216
Introduction
Hypovitaminosis D has been associated with several chronic conditions; yet, its association with cognitive decline and the risk of dementia and Alzheimer's disease (AD) has been inconsistent.Methods
The study population consisted of 916 participants from the Three-City Bordeaux cohort aged 65+, nondemented at baseline, with assessment of vitamin D status and who were followed for up to 12 years.Results
In multivariate analysis, compared with individuals with 25(OH)D sufficiency (n = 151), participants with 25(OH)D deficiency (n = 218) exhibited a faster cognitive decline. A total of 177 dementia cases (124 AD) occurred: 25(OH)D deficiency was associated with a nearly three-fold increased risk of AD (hazard ratio = 2.85, 95% confidence interval 1.37–5.97).Discussion
This large prospective study of French older adults suggests that maintaining adequate vitamin D status in older age could contribute to slow down cognitive decline and to delay or prevent the onset of dementia, especially of AD etiology. 相似文献17.
Sirwan K.L. Darweesh Frank J. Wolters M. Arfan Ikram Frank de Wolf Daniel Bos Albert Hofman 《Alzheimer's & dementia》2018,14(11):1450-1459
Introduction
Inflammatory markers are often elevated in patients with dementia, including Alzheimer's disease (AD). However, it remains unclear whether inflammatory markers are associated with the risk of developing dementia.Methods
We searched PubMed, Embase, and Cochrane library for prospective population-based studies reporting associations between inflammatory markers and all-cause dementia or AD. We used random effects meta-analyses to obtain pooled hazard ratios (HRs) and 95% confidence intervals of inflammatory markers (highest vs. lowest quantile) for all-cause dementia and AD.Results
Fifteen articles from 13 studies in six countries reported data that could be meta-analyzed. C-reactive protein (HR = 1.37 [1.05; 1.78]), interleukin-6 (HR = 1.40 [1.13; 1.73]), α1-antichymotrypsin (HR = 1.54 [1.14; 2.80]), lipoprotein-associated phospholipase A2 activity (HR = 1.40 [1.03; 1.90]), and fibrinogen were each associated with all-cause dementia, but neither was significantly associated with AD.Discussion
Several inflammatory markers are associated with an increased risk of all-cause dementia; however, these markers are not specific for AD. Whether inflammatory markers closely involved in AD pathology are associated with the risk of AD remains to be elucidated. 相似文献18.
Kristin Aaser Lunde Janete Chung Ingvild Dalen Kenn Freddy Pedersen Jan Linder Magdalena E. Domellöf Eva Elgh Angus D. Macleod Charalampos Tzoulis Jan Petter Larsen Ole-Bjørn Tysnes Lars Forsgren Carl E. Counsell Guido Alves Jodi Maple-Grødem 《Alzheimer's & dementia》2018,14(10):1293-1301
Introduction
Both polymorphisms and mutations in glucocerebrosidase (GBA) may influence the development of dementia in patients with Parkinson's disease.Methods
Four hundred forty-two patients and 419 controls were followed for 7 years. Dementia was diagnosed using established criteria. Participants were analyzed for GBA genetic variants, including E326K, T369M, and L444P. Associations between GBA carrier status and dementia were assessed with Cox survival analysis.Results
A total of 12.0% of patients with Parkinson's disease carried a GBA variant, and nearly half (22/53) of them progressed to dementia during follow-up. Carriers of deleterious GBA mutations (adjusted hazard ratio 3.81, 95% confidence interval 1.35 to 10.72; P = .011) or polymorphisms (adjusted hazard ratio 1.79; 95% confidence interval 1.07 to 3.00; P = .028) progressed to dementia more rapidly than noncarriers.Discussion
GBA variants are of great clinical relevance for the development of dementia in Parkinson's disease, especially due to the relatively higher frequency of these alleles compared with other risk alleles. 相似文献19.
May A. Beydoun Hind A. Beydoun Martine Elbejjani Gregory A. Dore Alan B. Zonderman 《Alzheimer's & dementia》2018,14(9):1148-1158
Introduction
Infectious agents were recently implicated in Alzheimer's disease (AD) and etiology of other dementias, notably Helicobacter pylori.Methods
We tested associations of H. pylori seropositivity with incident all-cause and AD dementia and with AD-related mortality among US adults in a retrospective cohort study. Data from the National Health and Nutrition Surveys III, phase 1 (1988–1991) and 1999–2000 linked with Medicare and National Death Index registries, were used (baseline age ≥45 y, follow-up to 2013, Npooled = 5927).Results
A positive association between H. pylori seropositivity and AD mortality was found in men (hazard ratioadj, pooled = 4.33, 95% confidence interval: 1.51–12.41, P = .006), which was replicated for incident AD and all-cause dementia, with hazard ratioadj, pooled = 1.45 (95% confidence interval: 1.03–2.04, P = .035) and hazard ratioadj, III = 1.44 (95% confidence interval: 1.05–1.98, P = .022), respectively. These associations were also positive among higher socioeconomic status groups.Discussion
In sum, H. pylori seropositivity's direct association with AD mortality, all-cause dementia, and AD dementia was restricted to men and to higher socioeconomic status groups. 相似文献20.
Sven J. van der Lee Charlotte E. Teunissen René Pool Martin J. Shipley Alexander Teumer Vincent Chouraki Debora Melo van Lent Juho Tynkkynen Krista Fischer Jussi Hernesniemi Toomas Haller Archana Singh-Manoux Aswin Verhoeven Gonneke Willemsen Francisca A. de Leeuw Holger Wagner Jenny van Dongen Johannes Hertel Cornelia M. van Duijn 《Alzheimer's & dementia》2018,14(6):707-722