共查询到20条相似文献，搜索用时 17 毫秒
1.
Jianping Jia Serge Gauthier Sarah Pallotta Yong Ji Wenshi Wei Shifu Xiao Dantao Peng Qihao Guo Liyong Wu Shengdi Chen Weihong Kuang Junjian Zhang Cuibai Wei Yi Tang 《Alzheimer's & dementia》2017,13(5):592-597
Introduction
Rapid cognitive decline (RCD) occurs in dementia due to Alzheimer's disease (AD).Methods
Literature review, consensus meetings, and a retrospective chart review of patients with probable AD were conducted.Results
Literature review showed that RCD definitions varied. Mini-Mental State Examination scores <20 at treatment onset, vascular risk factors, age <70 years at symptom onset, higher education levels, and early appearance of hallucinations, psychosis, or extrapyramidal symptoms are recognized RCD risk factors. Chart review showed that RCD (Mini-Mental State Examination score decline ≥3 points/year) is more common in moderate (43.2%) than in mild patients (20.1%; P < .001). Rapid and slow decliners had similar age, gender, and education levels at baseline.Discussion
RCD is sufficiently common to interfere with randomized clinical trials. We propose a 6-month prerandomization determination of the decline rate or use of an RCD risk score to ensure balanced allocation among treatment groups. 相似文献2.
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3.
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4.
Suzanne E. Schindler Yan Li Kaitlin W. Todd Elizabeth M. Herries Rachel L. Henson Julia D. Gray Guoqiao Wang Danielle L. Graham Leslie M. Shaw John Q. Trojanowski Jason J. Hassenstab Tammie L.S. Benzinger Carlos Cruchaga Mathias Jucker Johannes Levin Jasmeer P. Chhatwal James M. Noble John M. Ringman Anne M. Fagan 《Alzheimer's & dementia》2019,15(5):655-665
IntroductionFour less well-studied but promising “emerging” cerebrospinal fluid (CSF) biomarkers are elevated in late-onset Alzheimer disease (AD): neurogranin, synaptosomal-associated protein-25 (SNAP-25), visinin-like protein 1 (VILIP-1), and chitinase-3-like protein 1 (YKL-40).MethodsCSF neurogranin, SNAP-25, VILIP-1, and YKL-40 were measured in families carrying autosomal-dominant AD mutations.ResultsThe four emerging CSF biomarkers were significantly elevated in the mutation carriers (n = 235) versus noncarriers (n = 145). CSF SNAP-25, VILIP-1, and YKL-40 were altered very early in the AD time course, approximately 15–19 years before estimated symptom onset. All CSF biomarkers predicted important AD-related outcomes including performance on a cognitive composite, brain amyloid burden as measured by amyloid positron emission tomography, and the estimated years from symptom onset.DiscussionEarly abnormalities in CSF tTau, pTau, SNAP-25, VILIP-1, and YKL-40 suggest that synaptic damage, neuronal injury, and neuroinflammation begin shortly after the commencement of brain amyloid accumulation. 相似文献
5.
Juho Tynkkynen Vincent Chouraki Sven J. van der Lee Jussi Hernesniemi Qiong Yang Shuo Li Alexa Beiser Martin G. Larson Katri Sääksjärvi Martin J. Shipley Archana Singh-Manoux Robert E. Gerszten Thomas J. Wang Aki S. Havulinna Peter Würtz Krista Fischer Ayse Demirkan M. Arfan Ikram Veikko Salomaa 《Alzheimer's & dementia》2018,14(6):723-733
Introduction
Metabolite, lipid, and lipoprotein lipid profiling can provide novel insights into mechanisms underlying incident dementia and Alzheimer's disease.Methods
We studied eight prospective cohorts with 22,623 participants profiled by nuclear magnetic resonance or mass spectrometry metabolomics. Four cohorts were used for discovery with replication undertaken in the other four to avoid false positives. For metabolites that survived replication, combined association results are presented.Results
Over 246,698 person-years, 995 and 745 cases of incident dementia and Alzheimer's disease were detected, respectively. Three branched-chain amino acids (isoleucine, leucine, and valine), creatinine and two very low density lipoprotein (VLDL)-specific lipoprotein lipid subclasses were associated with lower dementia risk. One high density lipoprotein (HDL; the concentration of cholesterol esters relative to total lipids in large HDL) and one VLDL (total cholesterol to total lipids ratio in very large VLDL) lipoprotein lipid subclass was associated with increased dementia risk. Branched-chain amino acids were also associated with decreased Alzheimer's disease risk and the concentration of cholesterol esters relative to total lipids in large HDL with increased Alzheimer's disease risk.Discussion
Further studies can clarify whether these molecules play a causal role in dementia pathogenesis or are merely markers of early pathology. 相似文献6.
Anna E. Leeuwis Marije R. Benedictus Joost P.A. Kuijer Maja A.A. Binnewijzend Astrid M. Hooghiemstra Sander C.J. Verfaillie Teddy Koene Philip Scheltens Frederik Barkhof Niels D. Prins Wiesje M. van der Flier 《Alzheimer's & dementia》2017,13(5):531-540
Introduction
We examined the association between decreased cerebral blood flow (CBF) and cognitive impairment in Alzheimer's disease (AD), mild cognitive impairment (MCI), and subjective cognitive decline (SCD).Methods
We included 161 AD, 95 MCI, and 143 SCD patients from the Amsterdam Dementia Cohort. We used 3-T pseudo-continuous arterial spin labeling to estimate whole-brain and regional partial volume–corrected CBF. Neuropsychological tests covered global cognition and five cognitive domains. Associations were investigated using linear regression analyses.Results
In the whole sample, reduced overall and regional CBF was associated with impairment in all cognitive domains. We found significant interactions between diagnosis and CBF for language and between diagnosis and parietal CBF for global cognition and executive functioning. Stratification showed that decreased CBF was associated with worse performance in AD patients but not in MCI or SCD.Discussion
Our results suggest that CBF may have potential as a functional marker of disease severity. 相似文献7.
Pamela L. Lutsey Jeffrey R. Misialek Thomas H. Mosley Rebecca F. Gottesman Naresh M. Punjabi Eyal Shahar Richard MacLehose Rachel P. Ogilvie David Knopman Alvaro Alonso 《Alzheimer's & dementia》2018,14(2):157-166
Introduction
This study tested the hypotheses that late-midlife obstructive sleep apnea (OSA) and short and long sleep duration are associated with dementia over 15 years of follow-up.Methods
A total of 1667 Atherosclerosis Risk in Communities Study participants underwent in-home polysomnography (1996–1998) and were followed for dementia. Dementia was defined by (1) hospitalization diagnosis codes (1996–2012) and (2) a comprehensive neurocognitive examination (2011–2013) with adjudication.Results
OSA and sleep duration were not associated with risk of incident dementia. When using adjudicated outcomes, severe OSA (≥30 vs. <5 apnea-hypopnea events/hour) was associated with higher risk of all-cause dementia (risk ratio [95% confidence interval], 2.35 [1.06–5.18]) and Alzheimer's disease dementia (1.66 [1.03–2.68]); associations were attenuated with cardiovascular risk factor adjustment. Sleeping <7 versus 8 to ≤9 hours was associated with higher risk of all-cause dementia (2.00 [1.03–3.86]).Discussion
When adjudicated outcome definitions were used, late-midlife OSA and short sleep duration were associated with all-cause and Alzheimer's disease dementia in later life. 相似文献8.
Karen Ritchie Michael Ropacki Bruce Albala John Harrison Jeffrey Kaye Joel Kramer Christopher Randolph Craig W. Ritchie 《Alzheimer's & dementia》2017,13(2):186-195
The Horizon 2020/IMI European Prevention of Alzheimer's Dementia (EPAD) project will undertake large-scale proof-of-concept trials in predementia Alzheimer's disease (AD). Within EPAD, the monitoring of cognitive trajectories in the preclinical period will constitute a central outcome measure; however, there are currently no clear guidelines as to how this should be achieved as most measures have been developed for the period around dementia diagnosis. The EPAD Scientific Advisory Group for Clinical and Cognitive Outcomes identified appropriate cognitive measures based on a literature search covering both cognitive correlates of preclinical brain changes from imaging studies and cognitive changes observed over time in nondementia population cohorts developing incident dementia. These measures were evaluated according to the following criteria: validity, coherence with biomarker changes, psychometric properties, cross-cultural suitability, availability of alternative forms, and normative data limited practice effects. The resulting consensus statement provides recommendations for both future drug trials and research into preclinical Alzheimer's disease. 相似文献
9.
Cecilia S. Lee Eric B. Larson Laura E. Gibbons Aaron Y. Lee Susan M. McCurry James D. Bowen Wayne C. McCormick Paul K. Crane 《Alzheimer's & dementia》2019,15(1):34-41
Introduction
Identifying ophthalmic diseases associated with increased risk of Alzheimer's disease (AD) may enable better screening and understanding of those at risk of AD.Methods
Diagnoses of glaucoma, age-related macular degeneration (AMD), and diabetic retinopathy (DR) were based on International Classification of Diseases, 9th revision, codes for 3877 participants from the Adult Changes in Thought study. The adjusted hazard ratio for developing probable or possible AD for recent (within 5 years) and established (>5 years) diagnoses were assessed.Results
Over 31,142 person-years of follow-up, 792 AD cases occurred. The recent and established hazard ratio were 1.46 (P = .01) and 0.87 (P = .19) for glaucoma, 1.20 (P = .12) and 1.50 (P < .001) for AMD, and 1.50 (P = .045) and 1.50 (P = .03) for DR.Discussion
Increased AD risk was found for recent glaucoma diagnoses, established AMD diagnoses, and both recent and established DR. People with certain ophthalmic conditions may have increased AD risk. 相似文献10.
Matthew P. Pase Jayandra J. Himali Paul F. Jacques Charles DeCarli Claudia L. Satizabal Hugo Aparicio Ramachandran S. Vasan Alexa S. Beiser Sudha Seshadri 《Alzheimer's & dementia》2017,13(9):955-964
Introduction
Excess sugar consumption has been linked with Alzheimer's disease (AD) pathology in animal models.Methods
We examined the cross-sectional association of sugary beverage consumption with neuropsychological (N = 4276) and magnetic resonance imaging (N = 3846) markers of preclinical Alzheimer's disease and vascular brain injury (VBI) in the community-based Framingham Heart Study. Intake of sugary beverages was estimated using a food frequency questionnaire.Results
Relative to consuming less than one sugary beverage per day, higher intake of sugary beverages was associated with lower total brain volume (1–2/day, β ± standard error [SE] = ?0.55 ± 0.14 mean percent difference, P = .0002; >2/day, β ± SE = ?0.68 ± 0.18, P < .0001), and poorer performance on tests of episodic memory (all P < .01). Daily fruit juice intake was associated with lower total brain volume, hippocampal volume, and poorer episodic memory (all P < .05). Sugary beverage intake was not associated with VBI in a consistent manner across outcomes.Discussion
Higher intake of sugary beverages was associated cross-sectionally with markers of preclinical AD. 相似文献11.
Lidia Sarro Nirubol Tosakulwong Christopher G. Schwarz Jonathan Graff-Radford Scott A. Przybelski Timothy G. Lesnick Samantha M. Zuk Robert I. Reid Mekala R. Raman Bradley F. Boeve Tanis J. Ferman David S. Knopman Giancarlo Comi Massimo Filippi Melissa E. Murray Joseph E. Parisi Dennis W. Dickson Ronald C. Petersen Kejal Kantarci 《Alzheimer's & dementia》2017,13(3):257-266
Introduction
Cerebrovascular lesions on MRI are common in Alzheimer's disease (AD) dementia, but less is known about their frequency and impact on dementia with Lewy bodies (DLB).Methods
White-matter hyperintensities (WMHs) and infarcts on MRI were assessed in consecutive DLB (n = 81) and AD dementia (n = 240) patients and compared to age-matched and sex-matched cognitively normal subjects (CN) from a population-based cohort.Results
DLB had higher WMH volume compared to CN, and WMH volume was higher in the occipital and posterior periventricular regions in DLB compared to AD. Higher WMH volume was associated with history of cardiovascular disease and diabetes but not with clinical disease severity in DLB. Frequency of infarcts in DLB was not different from CN and AD dementia.Discussion
In DLB, WMH volume is higher than AD and CN and appears to be primarily associated with history of vascular disease. 相似文献12.
Vincent Chouraki Sarah R. Preis Qiong Yang Alexa Beiser Shuo Li Martin G. Larson Galit Weinstein Thomas J. Wang Robert E. Gerszten Ramachandran S. Vasan Sudha Seshadri 《Alzheimer's & dementia》2017,13(12):1327-1336
Introduction
The identification of novel biomarkers associated with Alzheimer's disease (AD) could provide key biological insights and permit targeted preclinical prevention. We investigated circulating metabolites associated with incident dementia and AD using metabolomics.Methods
Plasma levels of 217 metabolites were assessed in 2067 dementia-free Framingham Offspring Cohort participants (mean age = 55.9 ± 9.7 years; 52.4% women). We studied their associations with future dementia and AD risk in multivariate Cox models.Results
Ninety-three participants developed incident dementia (mean follow-up = 15.6 ± 5.2 years). Higher plasma anthranilic acid levels were associated with greater risk of dementia (hazard ratio [HR] = 1.40; 95% confidence interval [CI] = [1.15–1.70]; P = 8.08 × 10?4). Glutamic acid (HR = 1.38; 95% CI = [1.11–1.72]), taurine (HR = 0.74; 95% CI = [0.60–0.92]), and hypoxanthine (HR = 0.74; 95% CI = [0.60–0.92]) levels also showed suggestive associations with dementia risk.Discussion
We identified four biologically plausible, candidate plasma biomarkers for dementia. Association of anthranilic acid implicates the kynurenine pathway, which modulates glutamate excitotoxicity. The associations with hypoxanthine and taurine strengthen evidence that uric acid and taurine may be neuroprotective. 相似文献13.
Camille Amadieu Sophie Lefèvre-Arbogast Cécile Delcourt Jean-François Dartigues Catherine Helmer Catherine Féart Cécilia Samieri 《Alzheimer's & dementia》2017,13(10):1125-1132
Introduction
Several nutrients may predict dementia risk. We characterized nutrient biomarker patterns, which integrate the complexity of nutrient exposure and biodisponibility associated with long-term risk of dementia in a large cohort of older persons, the Three-City study.Methods
We included 666 nondemented participants with plasma measurements of 22 fat-soluble nutrients at baseline, who were followed up for 12 years for dementia.Results
A “deleterious” pattern combining lower blood status in vitamin D, carotenoids, and polyunsaturated fats and higher saturated fats was strongly associated with a higher risk of dementia. Compared with individuals in the first quintile of the pattern score, participants in the highest quintile of score had an approximately fourfold increased risk of dementia (hazard ratio = 4.53 [95% confidence interval 1.99, 10.32], P for trend <.001) in multivariate models.Discussion
A blood pattern reflecting lower status in several nutrients among nondemented individuals appeared strongly associated with the long-term risk of dementia in this cohort. 相似文献14.
Clifford R. Jack David A. Bennett Kaj Blennow Maria C. Carrillo Billy Dunn Samantha Budd Haeberlein David M. Holtzman William Jagust Frank Jessen Jason Karlawish Enchi Liu Jose Luis Molinuevo Thomas Montine Creighton Phelps Katherine P. Rankin Christopher C. Rowe Philip Scheltens Eric Siemers Nina Silverberg 《Alzheimer's & dementia》2018,14(4):535-562
In 2011, the National Institute on Aging and Alzheimer's Association created separate diagnostic recommendations for the preclinical, mild cognitive impairment, and dementia stages of Alzheimer's disease. Scientific progress in the interim led to an initiative by the National Institute on Aging and Alzheimer's Association to update and unify the 2011 guidelines. This unifying update is labeled a “research framework” because its intended use is for observational and interventional research, not routine clinical care. In the National Institute on Aging and Alzheimer's Association Research Framework, Alzheimer's disease (AD) is defined by its underlying pathologic processes that can be documented by postmortem examination or in vivo by biomarkers. The diagnosis is not based on the clinical consequences of the disease (i.e., symptoms/signs) in this research framework, which shifts the definition of AD in living people from a syndromal to a biological construct. The research framework focuses on the diagnosis of AD with biomarkers in living persons. Biomarkers are grouped into those of β amyloid deposition, pathologic tau, and neurodegeneration [AT(N)]. This ATN classification system groups different biomarkers (imaging and biofluids) by the pathologic process each measures. The AT(N) system is flexible in that new biomarkers can be added to the three existing AT(N) groups, and new biomarker groups beyond AT(N) can be added when they become available. We focus on AD as a continuum, and cognitive staging may be accomplished using continuous measures. However, we also outline two different categorical cognitive schemes for staging the severity of cognitive impairment: a scheme using three traditional syndromal categories and a six-stage numeric scheme. It is important to stress that this framework seeks to create a common language with which investigators can generate and test hypotheses about the interactions among different pathologic processes (denoted by biomarkers) and cognitive symptoms. We appreciate the concern that this biomarker-based research framework has the potential to be misused. Therefore, we emphasize, first, it is premature and inappropriate to use this research framework in general medical practice. Second, this research framework should not be used to restrict alternative approaches to hypothesis testing that do not use biomarkers. There will be situations where biomarkers are not available or requiring them would be counterproductive to the specific research goals (discussed in more detail later in the document). Thus, biomarker-based research should not be considered a template for all research into age-related cognitive impairment and dementia; rather, it should be applied when it is fit for the purpose of the specific research goals of a study. Importantly, this framework should be examined in diverse populations. Although it is possible that β-amyloid plaques and neurofibrillary tau deposits are not causal in AD pathogenesis, it is these abnormal protein deposits that define AD as a unique neurodegenerative disease among different disorders that can lead to dementia. We envision that defining AD as a biological construct will enable a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment that is associated with AD, as well as the multifactorial etiology of dementia. This approach also will enable a more precise approach to interventional trials where specific pathways can be targeted in the disease process and in the appropriate people. 相似文献
15.
Eero Pekkonen Iiro P Jääskeläinen Marja Hietanen Minna Huotilainen Risto Näätänen Risto J Ilmoniemi Timo Erkinjuntti 《Clinical neurophysiology》1999,110(11):1942-1947
Objective: To study whether preconscious auditory processing is deteriorated in patients with Alzheimer's disease (AD) having mild to moderate cognitive symptoms. To investigate whether auditory processing correlates with the impairment of the higher cortical functions.Methods: P50m and N100m responses elicited by a sequence of repetitive tones were recorded with a whole-head magnetometer from 22 patients with probable AD and from 18 healthy age-matched controls. In addition, an extensive neuropsychological test battery assessing main cognitive domains was administered to all subjects.Results: The patients with AD had significantly delayed N100m responses in the left hemisphere that correlated with the impairment of the language functions.Conclusions: N100m auditory responses measured with magnetoencephalography may be useful in evaluating the severity and progression of the cortical dysfunction in dementia. 相似文献
16.
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17.
Introduction
Lifetime risks are the probabilities of progressing to Alzheimer's disease (AD) dementia during one's lifespan. Here, we report the first estimates of the lifetime and ten-year risks of AD dementia based on age, gender, and biomarker tests for preclinical disease.Methods
We used a multistate model for the disease process together with US death rates.Results
Lifetime risks of AD dementia vary considerably by age, gender, and the preclinical or clinical disease state of the individual. For example, the lifetime risks for a female with only amyloidosis are 8.4% for a 90-year old and 29.3% for a 65-year old. Persons younger than 85 years with mild cognitive impairment, amyloidosis, and neurodegeneration have lifetime risks of AD dementia greater than 50%.Discussion
Most persons with preclinical AD will not develop AD dementia during their lifetimes. Lifetime risks help interpret the clinical significance of biomarker screening tests for AD. 相似文献18.
The TOMM40 poly-T is a polymorphism in intron 6 of the TOMM40 gene, which is adjacent to and in linkage disequilibrium with APOE. Roses et al. identified the association between the length of TOMM40 poly-T with the risk and age of onset of late-onset Alzheimer's disease (LOAD). Following the original discovery, additional studies found associations between the TOMM40 poly-T and LOAD-related phenotypes independent of APOE genotypes, while others did not replicate these associations. Furthermore, the identity of the TOMM40 poly-T risk allele has been controversial between different LOAD-related phenotypes. Here, we propose a framework to address the conflicting findings with respect to the TOMM40 poly-T allele associations with LOAD phenotypes and their functional effects. The framework is used to interpret previous studies as means to gain insights regarding the nature of the risk allele, very long versus short. We suggest that the identity of the TOMM40 poly-T risk allele depends on the phenotype being evaluated, the ages of the study subjects at the time of assessment, and the context of the APOE genotypes. In concluding remarks, we outline future studies that will inform the mechanistic interpretation of the genetic data. 相似文献
19.
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20.
《Sleep medicine》2021
IntroductionParkinson's disease (PD) and Dementia with Lewy Bodies (DLB) prognosis depends on cognitive function evolution. Sleep disorders, as objectivated by polysomnography (PSG), are intimately connected with PD and DLB pathophysiology, but have seldomly been used to predict cognitive decline.Methods20 DLB and 49 PD patients underwent one-night in-lab video-PSG. Sleep variables were defined, including REM sleep motor events, Tonic and phasic REM sleep muscular tone and RBD diagnosis. Cognitive state (assessed with the Global Deterioration Scale (GDS) was collected from case files for 6 months intervals, for a maximum period of 3.5 years or until death/drop-out.). The relation between PSG data at baseline and variation of GDS scores over time was tested with mixed linear regression analysis.ResultsGDS scores were higher in DLB, than in PD. We confirmed significant cognitive decline in both disorders, but no significant differences in progression between them. There were no significant interactions between PSG data and GDS variation for the entire group and DLB separately. In PD patients, there was a significant interaction between RBD diagnosis and tonic excessive muscular tone and GDS increase.ConclusionOur data suggests that PSG data can be useful in predicting cognitive decline in PD but not in DLB patients. In PD patients, an RBD diagnosis is predictive of cognitive deterioration, confirming the notion that this non-motor symptom relates to a malignant sub-type. Tonic excessive muscular activity, but not other RBD features, had predictive value in this group, pointing to a specific relation with the disease pathophysiology. 相似文献