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"In 2003, Lorna Drew and Leo Ferrari made a shocking discovery: Leo wasn't just an absent-minded professor; he had Alzheimer Disease. In Different Minds, Lorna describes her fluctuating emotional journey and outlines her coping strategies, while Leo vividly - and humorously - expresses what AD feels like from the inside."--Jacket

OBJECTIVE: To examine whether the presence of motor signs has predictive value for important outcomes in Alzheimer disease (AD). METHODS: A total of 533 patients with AD at early stages (mean Folstein Mini-Mental State Examination [MMSE] 21/30 at entry) were recruited and followed semiannually for up to 13.1 years (mean 3) in five University-based AD centers in the United States and European Union. Four outcomes, assessed every 6 months, were used in Cox models: cognitive endpoint (Columbia Mini-Mental State Examination or = 10), institutionalization equivalent index, and death. Using a standardized portion of the Unified PD Rating Scale (administered every 6 months for a total of 3,149 visit-assessments, average 5.9 per patient), the presence of motor signs, as well as of individual motor sign domains, was examined as time-dependent predictor. The models controlled for cohort, recruitment center, sex, age, education, a comorbidity index, and baseline cognitive and functional performance. RESULTS: A total of 39% of the patients reached the cognitive, 41% the functional, 54% the institutionalization, and 47% the mortality endpoint. Motor signs were noted for 14% of patients at baseline and for 45% at any evaluation. Their presence was associated with increased risk for cognitive decline (RR, 1.72; 95% CI, 1.24 to 2.38), functional decline (1.80 [1.33 to 2.45]), institutionalization (1.68 [1.26 to 2.25]), and death (1.38 [1.05 to 1.82]). Tremor was associated with increased risk for reaching the cognitive and bradykinesia for reaching the functional endpoints. Postural-gait abnormalities carried increased risk for institutionalization and mortality. Faster rates of motor sign accumulation were associated with increased risk for all outcomes. CONCLUSIONS: Motor signs predict cognitive and functional decline, institutionalization, and mortality in Alzheimer disease. Different motor sign domains predict different outcomes.

Objective: To examine whether the presence of motor signs has predictive value for important outcomes in Alzheimer disease (AD). Methods: A total of 533 patients with AD at early stages (mean Folstein Mini-Mental State Examination [MMSE] 21/30 at entry) were recruited and followed semiannually for up to 13.1 years (mean 3) in five University-based AD centers in the United States and European Union. Four outcomes, assessed every 6 months, were used in Cox models: cognitive endpoint (Columbia Mini-Mental State Examination Յ 20/57 [فMMSE Յ 10/30]), functional endpoint (Blessed Dementia Rating Scale Ն 10), institutionalization equivalent index, and death. Using a standardized portion of the Unified PD Rating Scale (administered every 6 months for a total of 3,149 visit-assessments, average 5.9 per patient), the presence of motor signs, as well as of individual motor sign domains, was examined as time-dependent predictor. The models controlled for cohort, recruitment center, sex, age, education, a comorbidity index, and baseline cognitive and functional performance. Results: A total of 39% of the patients reached the cognitive, 41% the functional, 54% the institutionalization, and 47% the mortality endpoint. Motor signs were noted for 14% of patients at baseline and for 45% at any evaluation. Their presence was associated with increased risk for cognitive decline (RR, 1.72; 95% CI, 1.24 to 2.38), functional decline (1.80 [1.33 to 2.45]), institutionalization (1.68 [1.26 to 2.25]), and death (1.38 [1.05 to 1.82]). Tremor was associated with increased risk for reaching the cognitive and bradykinesia for reaching the functional endpoints. Postural-gait abnormalities carried increased risk for institutionalization and mortality. Faster rates of motor sign accumulation were associated with increased risk for all outcomes. Conclusions: Motor signs predict cognitive and functional decline, institutionalization, and mortality in Alzheimer disease. Different motor sign domains predict different outcomes.

Cover -- Contents -- Foreword -- Preface -- Acknowledgments -- List of Contributors -- Introduction: Historical Overview of a Current Global Challenge -- Part I: The Health Care Challenge of Alzheimer Disease: Basic Societal, Pathological, and Clinical Issues -- ONE: Darkness Cometh: Personal, Social, and Economic Burdens of Alzheimer Disease -- TWO: Neuropathology and Symptomatology in Alzheimer Disease: Implications for Caregiving and Competence -- THREE: The Clinical Challenge of Uncertain Diagnosis and Prognosis in Patients with Dementia -- Part II: European Voices on U.S. and European Models of Palliative Care -- FOUR: Expanding the Scope of Palliative Care -- FIVE: Hospital-based Palliative Care and Dementia, or What Do We Treat Patients For and How Do We Do It? -- SIX: Elderly Persons with Advanced Dementia: An Opportunity for a Palliative Culture in Medicine -- Part III: Philosophical and Theological Explorations -- SEVEN: Autonomy and the Lived Body in Cases of Severe Dementia -- EIGHT: The Moral Self as Patient -- NINE: The Practice of Palliative Care and the Theory of Medical Ethics: Alzheimer Disease as an Example -- Part IV: Clinical Ethics Issues: Focus on Patients and Caregivers -- TEN: The Tendency of Contemporary Decision-making Strategies to Deny the Condition of Alzheimer Disease -- ELEVEN: Advance Directives and End-of-Life Decision Making in Alzheimer Disease: Practical Challenges -- TWELVE: Saying No to Patients with Alzheimer Disease: Rethinking Relations among Personhood, Autonomy, and World -- THIRTEEN: The Ethical Challenge of Treating Pain in Alzheimer Disease: A Dental Case -- FOURTEEN: Alzheimer Disease and Euthanasia -- Part V: Organizational Ethics Issues: Educational Initiatives, Laws, and Allocation Decisions -- FIFTEEN: The Role of Nurses and Nursing Education in the Palliative Care of Patients and Their Families

[EN] Background Understanding the functional status of people with Alzheimer Disease (AD), both in a single (ST) and cognitive dual task (DT) activities is essential for identifying signs of early-stage neurodegeneration. This study aims to compare the performance quality of several tasks using sensors embedded in an Android device, among people at different stages of Alzheimer and people without dementia. The secondary aim is to analyze the effect of cognitive task performance on mobility tasks. Methods This is a cross-sectional study including 22 participants in the control group (CG), 18 in the group with mild AD and 22 in the group with moderate AD. They performed two mobility tests, under ST and DT conditions, which were registered using an Android device. Postural control was measured by medial-lateral and anterior-posterior displacements of the COM (MLDisp and APDisp, respectively) and gait, with the vertical and medial-lateral range of the COM (Vrange and MLrange). Further, the sit-to-stand (PStand) and turning and sit power (PTurnSit), the total time required to complete the test and the reaction time were measured. Results There were no differences between the two AD stages either for ST or DT in any of the variables (p > 0.05). Nevertheless, people at both stages showed significantly lower values of PStand and PTurnSit and larger Total time and Reaction time compared to CG (p 0.05). Further, Vrange is also lower in CDR1G than in CG (p 0.05). The DT had a significant deleterious effect on MLDisp in all groups (p 0.05) and on APDisp only in moderate AD for DT. Conclusions Our findings indicate that AD patients present impairments in some key functional abilities, such as gait, turning and sitting, sit to stand, and reaction time, both in mild and moderate AD. Nevertheless, an exclusively cognitive task only influences the postural control in people with AD. ; This work was funded by the Spanish Government, Secretaria de Estado de Investigacion, Desarrollo e Innovacion, and co-financed by EU FEDER ...

Objective: To comprehend the knowledge and practices of caregivers of elderly people with Alzheimer disease (AD). Method: A descriptive and qualitative conducted with relatives and/or caregivers of AD patients enrolled in the Unimed of North of Minas Gerais. Data were obtained by interview and recorded. Results: The results showed the following categories: "Knowledge about Alzheimer disease", "Care provided to patients with the disease", "Feelings when caring for the elderly with Alzheimer Disease". It is observed that the knowledge of caregivers about AD is confused. Due to this daily care performed by these caregivers, many impacts can be seen in the lives of respondents, such as changes in daily life, financial difficulties and impacts on their health. Conclusion: The need of a multidisciplinary team of caregivers for guidance on issues related to the disease in order to they can learn to deal with the elderly suffering from Alzheimer disease.

<p><strong>Objective: </strong>To investigate the association between statin use, incident dementia, and Alzheimer disease (AD) in a prospective elderly African American cohort.</p><p><strong>Design: </strong>Two stage design with a screening interview followed by a comprehensive in-home assessment conducted over an eight-year period. Diagnoses of incident AD and dementia were made by consensus. Statin use was collected at each evaluation. Measurements of low-density lipoprotein cholesterol (LDL), C-reactive protein (CRP) and APOE genotype were obtained from baseline blood samples. Logistic regression models were used to test the association of statin use on incident dementia and AD and its possible association with lipid and CRP levels.</p><p><strong>Setting: </strong>Indianapolis, Indiana</p><p><strong>Participants: </strong>From an original cohort of 2629 participants, a subsample of 974 Afri­can Americans aged &gt;70 years with normal cognition, at least one follow up evaluation, complete statin information, and biomarker availability were included.</p><p><strong>Main Outcome Measures: </strong>Incident de­mentia and incident AD.</p><p><strong>Results: </strong>After controlling for age at diag­nosis, sex, education level, presence of the APOE ε4 allele and history of stroke for the incident dementia model, baseline use of statins was associated with a significantly de­creased risk of incident dementia (OR=.44, <em>P</em>=.029) and incident AD (OR=.40, <em>P</em>=.029). The significant effect of statin use on reduced AD risk and trend for dementia risk was found only for those participants who reported consistent use over the observational period (incident AD: <em>P</em>=.034; incident dementia: <em>P</em>=.061). Additional models found no significant interaction between baseline statin use, baseline LDL, or CRP level and incident dementia/AD.</p><p><strong>Conclusions: </strong>Consistent use of statin medications during eight years of follow-up resulted in significantly reduced risk for incident AD and a trend toward reduced risk for incident dementia. <em>Ethn Dis.</em>2015;25(3):345-354.</p>

Alzheimer's Disease Neuroimaging Initiative. ; [Importance] Plasma phosphorylated tau at threonine 181 (p-tau181) has been proposed as an easily accessible biomarker for the detection of Alzheimer disease (AD) pathology, but its ability to monitor disease progression in AD remains unclear. ; [Objective] To study the potential of longitudinal plasma p-tau181 measures for assessing neurodegeneration progression and cognitive decline in AD in comparison to plasma neurofilament light chain (NfL), a disease-nonspecific marker of neuronal injury. ; [Design, Setting, and Participants] This longitudinal cohort study included data from the Alzheimer's Disease Neuroimaging Initiative from February 1, 2007, to June 6, 2016. Follow-up blood sampling was performed for up to 8 years. Plasma p-tau181 measurements were performed in 2020. This was a multicentric observational study of 1113 participants, including cognitively unimpaired participants as well as patients with cognitive impairment (mild cognitive impairment and AD dementia). Participants were eligible for inclusion if they had available plasma p-tau181 and NfL measurements and at least 1 fluorine-18–labeled fluorodeoxyglucose (FDG) positron emission tomography (PET) or structural magnetic resonance imaging scan performed at the same study visit. Exclusion criteria included any significant neurologic disorder other than suspected AD; presence of infection, infarction, or multiple lacunes as detected by magnetic resonance imaging; and any significant systemic condition that could lead to difficulty complying with the protocol. ; [Exposures] Plasma p-tau181 and NfL measured with single-molecule array technology. ; [Main Outcomes and Measures] Longitudinal imaging markers of neurodegeneration (FDG PET and structural magnetic resonance imaging) and cognitive test scores (Preclinical Alzheimer Cognitive Composite and Alzheimer Disease Assessment Scale–Cognitive Subscale with 13 tasks). Data were analyzed from June 20 to August 15, 2020. ; [Results] Of the 1113 participants (mean [SD] age, 74.0 [7.6] years; 600 men [53.9%]; 992 non-Hispanic White participants [89.1%]), a total of 378 individuals (34.0%) were cognitively unimpaired (CU) and 735 participants (66.0%) were cognitively impaired (CImp). Of the CImp group, 537 (73.1%) had mild cognitive impairment, and 198 (26.9%) had AD dementia. Longitudinal changes of plasma p-tau181 were associated with cognitive decline (CU: r = –0.24, P < .001; CImp: r = 0.34, P < .001) and a prospective decrease in glucose metabolism (CU: r = –0.05, P = .48; CImp: r = –0.27, P < .001) and gray matter volume (CU: r = –0.19, P < .001; CImp: r = –0.31, P < .001) in highly AD-characteristic brain regions. These associations were restricted to amyloid-β–positive individuals. Both plasma p-tau181 and NfL were independently associated with cognition and neurodegeneration in brain regions typically affected in AD. However, NfL was also associated with neurodegeneration in brain regions exceeding this AD-typical spatial pattern in amyloid-β–negative participants. Mediation analyses found that approximately 25% to 45% of plasma p-tau181 outcomes on cognition measures were mediated by the neuroimaging-derived markers of neurodegeneration, suggesting links between plasma p-tau181 and cognition independent of these measures. ; [Conclusions and Relevance] Study findings suggest that plasma p-tau181 was an accessible and scalable marker for predicting and monitoring neurodegeneration and cognitive decline and was, unlike plasma NfL, AD specific. The study findings suggest implications for the use of plasma biomarkers as measures to monitor AD progression in clinical practice and treatment trials. ; This work was supported by the "Miguel Servet" program grant CP19/00031 of the Spanish Instituto de Salud Carlos III (Dr Grothe); research fellowship A202f0812F from the Brightfocus Foundation, grant AF-930627 from the Swedish Alzheimer Foundation, grant FO2020-0240 from the Swedish Brain Foundation, grant 2020-00124 from the Agneta Prytz-Folkes & Gösta Folkes Foundation, and support from the Swedish Dementia Foundation, the Aina (Ann) Wallströms and Mary-Ann Sjöbloms Foundation, the Anna Lisa and Brother Björnsson's Foundation, Gamla Tjänarinnor, and the Gun and Bertil Stohnes Foundation (Dr Karikari); the Paulo Foundation and the Orion Research Foundation (Dr Snellman); grant 752310 from the European Union's Horizon 2020 Research and Innovation Program under the Marie Skłodowska-Curie action grant agreement, grant PI19/00155 from the Instituto de Salud Carlos III, and grant IJC2018-037478-I from the Spanish Ministry of Science, Innovation and Universities (Juan de la Cierva Programme) (Dr Suárez-Calvet); grant 2018-02532 from the Swedish Research Council, 681712 from the European Research Council, ALFGBG-720931 from the Swedish State Support for Clinical Research, 201809-2016862 from the Alzheimer Drug Discovery Foundation USA, and the UK Dementia Research Institute at University College London (Dr Zetterberg); grant 2017-00915 from the Swedish Research Council, RDAPB-201809-2016615 from the Alzheimer Drug Discovery Foundation USA, AF-742881 from the Swedish Alzheimer Foundation, FO2017-0243 from Hjärnfonden, Sweden, the Swedish state under the agreement between the Swedish government and the County Councils, ALFGBG-715986 from the ALF-agreement, and JPND2019-466-236 from the European Union Joint Program for Neurodegenerative Disorders (Dr Blennow); KAW 2014.0363 from the Knut and Alice Wallenberg Foundation (Wallenberg Centre for Molecular and Translational Medicine, 2017-02869 from the Swedish Research Council, ALFGBG-813971 from the Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement, and AF-740191 from the Swedish Alzheimer Foundation (Dr. Schöll). Data collection and sharing for this project was funded by the Alzheimer's Disease Neuroimaging Initiative (ADNI) (grant AG024904) and Department of Defense ADNI (grant W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc; Cogstate; Eisai Inc; Elan Pharmaceuticals, Inc; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc; Fujirebio; GE Healthcare; IXICO Ltd; Janssen Alzheimer Immunotherapy Research & Development, LLC; Johnson & Johnson Pharmaceutical Research & Development LLC; Lumosity; Lundbeck; Merck & Co, Inc; Meso Scale Diagnostics, LLC; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ; Peer reviewed

Abstract

Background
It is unknown whether older adults with preclinical Alzheimer disease (AD) experience changes in postural sway compared with those without preclinical AD. The purpose of this study was to understand the effect of dual tasking on standing balance, or postural sway, for people with and without preclinical AD.


Methods
A cross-sectional analysis of baseline data from a longitudinal cohort study. Participants were cognitively normal older adults with and without preclinical AD. Postural sway (path length) was tested using a force plate under standard and dual task balance conditions. Dual task cost (DTC) was calculated to examine performance change in balance conditions. Logistic regression models were used to predict preclinical AD status as a function of DTC.


Results
203 participants (65 preclinical AD+) were included. DTC for path length was significantly greater for participants with preclinical AD (DTC path length mean difference 19.8, 95% CI 2.6–37.0, t(201) = 2.29, p = .024). Greater DTC was significantly associated with increased odds of having preclinical AD (adjusted odds ratio for a 20-unit increase in DTC 1.16, 95% CI 1.02–1.32).


Conclusions
Older adults with preclinical AD are more likely to demonstrate significantly greater DTC in postural sway than those without preclinical AD. Dual tasking should be integrated into balance and fall risk assessments and may inform early detection of preclinical AD.

Hargrave et al, (2002) y Brueckner & Moritz, (2009) postulan que los déficits en la capacidad de asociar el nombre de una emoción con su expresión facial apropiada en la Demencia tipo Alzheimer (DTA) son independientes a los déficits no emocionales. Interpretan sus resultados como evidencia de un deterioro específico en el proceso emocional. Sin embargo Cadieux & Greve (1997) y Burnham & Hogervorst (2004) hallaron déficits significativos en pruebas de reconocimiento facial de emociones en pacientes con DTA, sugiriendo que los mismos fueron el resultado secundario de déficits en el procesamiento visual-perceptivo de características faciales no emocionales. El objetivo es estudiar el reconocimiento facial de emociones básicas en pacientes con DTA. Se evaluaron 16 pacientes con diagnóstico de DTA y se compararon con un Grupo Control. Se administraron 3 pruebas de reconocimiento facial de emociones con 60 fotografías del POFA (Ekman & Friesen, 1976). Se obtuvieron diferencias significativas en las 3 pruebas entre el grupo control y los pacientes DTA. Nuestros resultados concuerdan con la evidencia de los autores que plantean que en la DTA existe un deterioro específico en el procesamiento emocional. ; Hargrave et al, (2002) and Brueckner & Moritz, (2009) postulate that deficits in recognition of emotional facial expression in Dementia Alzheimer's Type (DAT) are independent non-emotional deficits. They interpret their results as evidence of a specific impairment in the emotional process. However Cadieux &Greve (1997) and Burnham & Hogervorst (2004) found significant deficits on tests of facial emotion recognition in patients with DAT, suggesting that they were the secondary outcome deficits in visual-perceptual processing of nonemotional facial features. The goal is study the basic emotional face recognition in patients with DAT. We evaluated 16 patients with a diagnosis of DAT and were compared with a control group. Three tests were administered facial recognition of emotion with 60 photographs of POFA (Ekman and Friesen, 1976). There were significant differences in the three tests between the control group and DAT patients. Our results are consistent with the evidence of the authors suggest that the DAT specific impairment in emotional processing. ; Fil: Cossini, Florencia Carla. Universidad de Buenos Aires. Facultad de Psicología; Argentina ; Fil: Rubinstein, Wanda Yanina. Universidad de Buenos Aires. Facultad de Psicología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina ; Fil: Politis, Daniel Gustavo. Universidad de Buenos Aires. Facultad de Psicología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina