scholarly journals Dementia, Alzheimer’s Disease, and Mortality after Hemodialysis Initiation

2018 ◽  
Vol 13 (9) ◽  
pp. 1339-1347 ◽  
Author(s):  
Mara A. McAdams-DeMarco ◽  
Matthew Daubresse ◽  
Sunjae Bae ◽  
Alden L. Gross ◽  
Michelle C. Carlson ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Confidence Interval ◽  
Competing Risks ◽  
Older Patients ◽  
Disease Diagnosis ◽  
Hazard Ratio ◽  
Old Patients ◽  
Diagnosis Of Dementia

Background and objectivesOlder patients with ESKD experience rapid declines in executive function after initiating hemodialysis; these impairments might lead to high rates of dementia and Alzheimer’s disease in this population. We estimated incidence, risk factors, and sequelae of diagnosis with dementia and Alzheimer’s disease among older patients with ESKD initiating hemodialysis.Design, setting, participants, & measurementsWe studied 356,668 older (age ≥66 years old) patients on hemodialysis (January 1, 2001 to December 31, 2013) from national registry data (US Renal Data System) linked to Medicare. We estimated the risk (cumulative incidence) of diagnosis of dementia and Alzheimer’s disease and studied factors associated with these disorders using competing risks models to account for death, change in dialysis modality, and kidney transplant. We estimated the risk of subsequent mortality using Cox proportional hazards models.ResultsThe 1- and 5-year risks of diagnosed dementia accounting for competing risks were 4.6% and 16% for women, respectively, and 3.7% and 13% for men, respectively. The corresponding Alzheimer’s disease diagnosis risks were 0.6% and 2.6% for women, respectively, and 0.4% and 2.0% for men, respectively. The strongest independent risk factors for diagnosis of dementia and Alzheimer’s disease were age ≥86 years old (dementia: hazard ratio, 2.11; 95% confidence interval, 2.04 to 2.18; Alzheimer’s disease: hazard ratio, 2.11; 95% confidence interval, 1.97 to 2.25), black race (dementia: hazard ratio, 1.70; 95% confidence interval, 1.67 to 1.73; Alzheimer’s disease: hazard ratio, 1.78; 95% confidence interval, 1.71 to 1.85), women (dementia: hazard ratio, 1.10; 95% confidence interval, 1.08 to 1.12; Alzheimer’s disease: hazard ratio, 1.12; 95% confidence interval, 1.08 to 1.16), and institutionalization (dementia: hazard ratio, 1.36; 95% confidence interval, 1.33 to 1.39; Alzheimer’s disease: hazard ratio, 1.10; 95% confidence interval, 1.05 to 1.15). Older patients on hemodialysis with a diagnosis of dementia were at 2.14-fold (95% confidence interval, 2.07 to 2.22) higher risk of subsequent mortality; those with a diagnosis of Alzheimer’s disease were at 2.01-fold (95% confidence interval, 1.89 to 2.15) higher mortality risk.ConclusionsOlder patients on hemodialysis are at substantial risk of diagnosis with dementia and Alzheimer’s disease, and carrying these diagnoses is associated with a twofold higher mortality.

scholarly journals The Use of Auditory Event-Related Potentials in Alzheimer's Disease Diagnosis

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Fabrizio Vecchio ◽  
Sara Määttä
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Event Related Potentials ◽  
Disease Diagnosis ◽  
Strategic Role ◽  
Diagnosis Of Dementia ◽  
Related Potentials ◽  
Dementing Illness ◽  
Early Alzheimer’S Disease ◽  
Auditory Event Related Potentials

Event-related potentials (ERPs) are important clinical and research instruments in neuropsychiatry, particularly due to their strategic role for the investigation of brain function. These techniques are often underutilized in the evaluation of neurological and psychiatric disorders, but ERPs are noninvasive instruments that directly reflect cortical neuronal activity. Previous studies using the P300, P3a, and MMN components of the ERP to study dementing illness are reviewed. The results suggest that particularly the P300 brain potential is sensitive to Alzheimer's disease processes during its early stages, and that easily performed stimulus discrimination tasks are the clinically most useful. Finally, these data suggest that the P300 ERP can aid in the diagnosis of dementia and may help in the assessment of early Alzheimer's disease.

scholarly journals SPIKES-D: a proposal to adapt the SPIKES protocol to deliver the diagnosis of dementia

2020 ◽  
Vol 14 (4) ◽  
pp. 333-339
Author(s):  
Vanessa Giffoni de Medeiros Nunes Pinheiro Peixoto ◽  
Rosiane Viana Zuza Diniz ◽  
Clécio de Oliveira Godeiro Junior
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Communication Skills ◽  
Disease Diagnosis ◽  
Bad News ◽  
Diagnosis Disclosure ◽  
Specific Protocol ◽  
Diagnosis Of Dementia ◽  
Life Threatening ◽  
Effective Diagnosis

ABSTRACT. Dementia is a life-threatening and stigmatizing condition, with devastating impacts on the patient's personal identity and caregivers. There are many barriers to an effective diagnosis disclosure of dementia, including fear of causing distress, uncertainty of diagnosis, caregivers’ objection and lack of training in communication skills in undergraduate medical schools. Although some studies have been published on how to help physicians deliver an Alzheimer's disease diagnosis, no specific protocol has been published yet. The SPIKES protocol is a didactic approach designed to deliver bad news related to cancer, but it has been used globally and in a variety of clinical settings, including the teaching of communication skills to medical students and residents. It is known, however, that the cognitive impairment of Alzheimer's disease and other dementias may limit the understanding of the diagnosis’ complexity; hence, a few adaptations of this model were made after reviewing the current literature on dementia diagnosis disclosure. The suggested SPIKES-D protocol seems to encompass current guidelines about the communication of the diagnosis of dementia, keeping its didactic approach on breaking bad news and helping fulfill the gaps in this topic.

scholarly journals Predictors of the Progression of Dementia Severity in Brazilian Patients with Alzheimer's Disease and Vascular Dementia

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Márcia L. Chaves ◽  
Ana L. Camozzato ◽  
Cristiano Köhler ◽  
Jeffrey Kaye
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Vascular Dementia ◽  
Cox Regression ◽  
Strong Predictor ◽  
Disease Diagnosis ◽  
Vascular Risk Factors ◽  
Vascular Risk

Introduction. This study evaluates the progression of dementia and identifies prognostic risk factors for dementia.Methods. A group of 80 Brazilian community residents with dementia (34 with Alzheimer's disease and 46 with vascular dementia) was assessed over the course of 2 years. Data were analyzed with Cox regression survival analysis.Results. The data showed that education predicted cognitive decline (HR=1.2;P<.05) when analyzed without controlling for vascular risk factors. After the inclusion of vascular risk factors, education (HR=1.32;P<.05) and hypertension were predictive for cognitive decline (HR=38;P<.05), and Alzheimer's disease diagnosis was borderline predictive (P=.055).Conclusion.Vascular risk factors interacted with the diagnosis of vascular dementia. Education was a strong predictor of decline.

scholarly journals Short leukocyte telomeres predict 25-year Alzheimer’s disease incidence in non-APOE ε4-carriers

2021 ◽  
Author(s):  
Fernanda Schäfer Hackenhaar ◽  
Maria Josefsson ◽  
Annelie Nordin Adolfsson ◽  
Mattias Landfors ◽  
Karolina Kauppi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Competing Risks ◽  
Hazard Ratio ◽  
Competing Risk ◽  
Time To Event ◽  
Apoe Ε4 ◽  
Specific Risk ◽  
Event Models

Abstract Background: Leukocyte telomere length (LTL) has been shown to predict Alzheimer's disease (AD), albeit inconsistently. Failing to account for the competing risks between AD, other dementia types, and mortality, can be an explanation for the inconsistent findings in previous time-to-event analyses. Furthermore, previous studies indicate that the association between LTL and AD is non-linear and may differ depending on apolipoprotein E ( APOE ) ε4 allele carriage, the strongest genetic AD predictor. Methods: We analysed whether baseline LTL in interaction with APOE ε4 predicts AD, by following 1306 initially non-demented subjects for 25 years. Gender- and age-residualized LTL (rLTL) was categorized into tertiles of short, medium, and long rLTLs. Two complementary time-to-event models that account for competing risks were used; the Fine-Gray model to estimate the association between the rLTL tertiles and the cumulative incidence of AD, and the cause-specific hazard model to assess the cause-specific risk of AD between rLTL groups. Vascular dementia and death were considered competing risk events. Models were adjusted for baseline lifestyle-related risk factors, gender, age, and non-proportional hazards. Results: After follow-up, 149 were diagnosed with AD, 96 were diagnosed with vascular dementia, 465 died without dementia, and 596 remained healthy. Baseline rLTL and other covariates were assessed on average 8 years before AD onset (range 1-24). APOE ε4-carriers had significantly increased incidence of AD, as well as increased cause-specific AD risk. A significant rLTL- APOE interaction indicated that short rLTL at baseline was significantly associated with an increased incidence of AD among non- APOE ε4-carriers (subdistribution hazard ratio = 3.24, CI 1.404–7.462, P = 0.005), as well as borderline associated with increased cause-specific risk of AD (cause-specific hazard ratio = 1.67, CI 0.947–2.964, P = 0.07). Among APOE ε4-carriers, short or long rLTLs were not significantly associated with AD incidence, nor with the cause-specific risk of AD. Conclusions: Our findings from two complementary competing risk time-to-event models indicate that short rLTL may be a valuable predictor of the AD incidence in non- APOE ε4-carriers, on average 8 years before AD onset. More generally, the findings highlight the importance of accounting for competing risks, as well as the APOE status of participants in AD biomarker research.

scholarly journals Short leukocyte telomeres predict 25-year Alzheimer's disease incidence in non-APOE ε4-carriers

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Fernanda Schäfer Hackenhaar ◽  
Maria Josefsson ◽  
Annelie Nordin Adolfsson ◽  
Mattias Landfors ◽  
Karolina Kauppi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Competing Risks ◽  
Disease Incidence ◽  
Hazard Ratio ◽  
Competing Risk ◽  
Time To Event ◽  
Specific Risk ◽  
Event Models

Abstract Background Leukocyte telomere length (LTL) has been shown to predict Alzheimer’s disease (AD), albeit inconsistently. Failing to account for the competing risks between AD, other dementia types, and mortality, can be an explanation for the inconsistent findings in previous time-to-event analyses. Furthermore, previous studies indicate that the association between LTL and AD is non-linear and may differ depending on apolipoprotein E (APOE) ε4 allele carriage, the strongest genetic AD predictor. Methods We analyzed whether baseline LTL in interaction with APOE ε4 predicts AD, by following 1306 initially non-demented subjects for 25 years. Gender- and age-residualized LTL (rLTL) was categorized into tertiles of short, medium, and long rLTLs. Two complementary time-to-event models that account for competing risks were used; the Fine-Gray model to estimate the association between the rLTL tertiles and the cumulative incidence of AD, and the cause-specific hazard model to assess whether the cause-specific risk of AD differed between the rLTL groups. Vascular dementia and death were considered competing risk events. Models were adjusted for baseline lifestyle-related risk factors, gender, age, and non-proportional hazards. Results After follow-up, 149 were diagnosed with AD, 96 were diagnosed with vascular dementia, 465 died without dementia, and 596 remained healthy. Baseline rLTL and other covariates were assessed on average 8 years before AD onset (range 1–24). APOE ε4-carriers had significantly increased incidence of AD, as well as increased cause-specific AD risk. A significant rLTL-APOE interaction indicated that short rLTL at baseline was significantly associated with an increased incidence of AD among non-APOE ε4-carriers (subdistribution hazard ratio = 3.24, CI 1.404–7.462, P = 0.005), as well as borderline associated with increased cause-specific risk of AD (cause-specific hazard ratio = 1.67, CI 0.947–2.964, P = 0.07). Among APOE ε4-carriers, short or long rLTLs were not significantly associated with AD incidence, nor with the cause-specific risk of AD. Conclusions Our findings from two complementary competing risk time-to-event models indicate that short rLTL may be a valuable predictor of the AD incidence in non-APOE ε4-carriers, on average 8 years before AD onset. More generally, the findings highlight the importance of accounting for competing risks, as well as the APOE status of participants in AD biomarker research.

Elucidating the risk factors for progression from amyloid-negative amnestic mild cognitive impairment to dementia

2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amnestic Mild Cognitive Impairment ◽  
Amyloid Pet ◽  
Clinical Progression ◽  
Amnestic Mci

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.

Identification of a Pathogenic PSEN1 Ala285Val Mutation Associated with Early-Onset Alzheimer’s Disease

2020 ◽  
Vol 17 (5) ◽  
pp. 438-445
Author(s):  
Van Giau Vo ◽  
Jung-Min Pyun ◽  
Eva Bagyinszky ◽  
Seong S.A. An ◽  
Sang Y. Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Temporal Lobe ◽  
Early Onset ◽  
Parietal Lobe ◽  
Disease Diagnosis ◽  
Random Coil ◽  
Magnetic Resonance Imaging Scan ◽  
Preclinical Ad ◽  
Early Onset Alzheimer’S Disease

Background: Presenilin 1 (PSEN1) was suggested as the most common causative gene of early onset Alzheimer’s Disease (AD). Methods: Patient who presented progressive memory decline in her 40s 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 whole exome sequencing. The pathogenic nature of missense mutation and its 3D protein structure prediction were performed by in silico prediction programs. Results: A pathogenic mutation in PSEN1 (NM_000021.3: c.1027T>C p.Ala285Val), which was found in a Korean EOAD patient. Magnetic resonance imaging scan showed mild left temporal lobe atrophy. Hypometabolism appeared through 18F-fludeoxyglucose Positron Emission Tomography (FDG-PET) scanning in bilateral temporal and parietal lobe, and 18F-Florbetaben-PET (FBB-PET) showed increased amyloid deposition in bilateral frontal, parietal, temporal lobe and hence presumed preclinical AD. Protein modeling showed that the p.Ala285Val is located in the random coil region and could result in extra stress in this region, resulting in the replacement of an alanine residue with a valine. This prediction was confirmed previous in vitro studies that the p.Trp165Cys resulted in an elevated Aβ42/Aβ40 ratio in both COS-1 and HEK293 cell lines compared that of wild-type control. Conclusion: Together, the clinical characteristics and the effect of the mutation would facilitate our understanding of PSEN1 in AD pathogenesis for the disease diagnosis and treatment. Future in vivo study is needed to evaluate the role of PSEN1 p.Ala285Val mutation in AD progression.

Association Between the APOE ɛ2/ɛ4 Genotype and Alzheimer’s Disease and Mild Cognitive Impairment Among African Americans

2021 ◽  
pp. 1-6
Author(s):  
Dianxu Ren ◽  
Oscar L. Lopez ◽  
Jennifer H. Lingler ◽  
Yvette Conley
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
African Americans ◽  
Hazard Ratio ◽  
Adjusted Hazard Ratio ◽  
Increased Risk ◽  
Similar Risk

We examined the association between APOE ɛ2/ɛ4 with incident Alzheimer’s disease (AD) and mild cognitive impairment (MCI) among African Americans using the national dataset from the National Alzheimer’s Coordinating Center (NACC) from 2005 to September 2019. Compared to ɛ3/ɛ3 carriers, ɛ2/ɛ4 carriers exhibited a similar risk of incident AD (adjusted hazard ratio [aHR] = 0.85, 95% CI [0.39, 1.84]) among the AD cohort and similar risk of incident MCI (aHR = 0.88, 95% CI [0.51, 1.50]) among the MCI cohort. Our findings suggest that, unlike the increased risk of AD and MCI in non-Latino whites, APOE ɛ2/ɛ4 genotype is not associated with the incidence of AD and MCI among African Americans.

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