Martin Prince | Renata Bryce | Emiliano Albanese | Anders Wimo | Wagner Ribeiro | Cleusa P. Ferri
Background: The evidence base on the prevalence of dementia is expanding rapidly, particularly in countries with low and middle incomes. A reappraisal of global prevalence and numbers is due, given the significant implications for social and public policy and planning. Methods: In this study we provide a systematic review of the global literature on the prevalence of dementia (1980-2009) and metaanalysis to estimate the prevalence and numbers of those affected, aged ≥60 years in 21 Global Burden of Disease regions. Results: Age-standardized prevalence for those aged ≥60 years varied in a narrow band, 5%-7% in most world regions, with a higher prevalence in Latin America (8.5%), and a distinctively lower prevalence in the four sub-Saharan African regions (2%-4%). It was estimated that 35.6 million people lived with dementia worldwide in 2010, with numbers expected to almost double every 20 years, to 65.7 million in 2030 and 115.4 million in 2050. In 2010, 58% of all people with dementia lived in countries with low or middle incomes, with this proportion anticipated to rise to 63% in 2030 and 71% in 2050. Conclusion: The detailed estimates in this study constitute the best current basis for policymaking, planning, and allocation of health and welfare resources in dementia care. The age-specific prevalence of dementia varies little between world regions, and may converge further. Future projections of numbers of people with dementia may be modified substantially by preventive interventions (lowering incidence), improvements in treatment and care (prolonging survival), and disease-modifying interventions (preventing or slowing progression). All countries need to commission nationally representative surveys that are repeated regularly to monitor trends. © 2013 The Alzheimer's Association. All rights reserved.
This report provides information to increase understanding of the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality rates, health expenditures and costs of care, and effect on caregivers and society in general. It also explores the roles and unique challenges of long-distance caregivers, as well as interventions that target those challenges. An estimated 5.2 million Americans have AD. Approximately 200,000 people younger than 65 years with AD comprise the younger onset AD population; 5 million comprise the older onset AD population. Throughout the coming decades, the baby boom generation is projected to add about 10 million to the total number of people in the United States with AD. Today, someone in America develops AD every 68 seconds. By 2050, one new case of AD is expected to develop every 33 seconds, or nearly a million new cases per year, and the total estimated prevalence is expected to be 13.8 million. AD is the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age 65 years or older. Between 2000 and 2010, the proportion of deaths resulting from heart disease, stroke, and prostate cancer decreased 16%, 23%, and 8%, respectively, whereas the proportion resulting from AD increased 68%. The number of deaths from AD as determined by official death certificates (83,494 in 2010) likely underrepresents the number of AD-related deaths in the United States. A projected 450,000 older Americans with AD will die in 2013, and a large proportion will die as a result of complications of AD. In 2012, more than 15 million family members and other unpaid caregivers provided an estimated 17.5 billion hours of care to people with AD and other dementias, a contribution valued at more than $216 billion. Medicare payments for services to beneficiaries age 65 years and older with AD and other dementias are three times as great as payments for beneficiaries without these conditions, and Medicaid payments are 19 times as great. Total payments in 2013 for health care, long-term care, and hospice services for people age 65 years and older with dementia are expected to be $203 billion (not including the contributions of unpaid caregivers). An estimated 2.3 million caregivers of people with AD and other dementias live at least 1 hour away from the care recipient. These "long-distance caregivers" face unique challenges, including difficulty in assessing the care recipient's true health condition and needs, high rates of family disagreement regarding caregiving decisions, and high out-of-pocket expenses for costs related to caregiving. Out-of-pocket costs for long-distance caregivers are almost twice as high as for local caregivers. © 2013 The Alzheimer's Association. All rights reserved.
© 2015 The Authors. This report discusses the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality rates, costs of care and the overall effect on caregivers and society. It also examines the challenges encountered by health care providers when disclosing an AD diagnosis to patients and caregivers. An estimated 5.3 million Americans have AD; 5.1 million are age 65 years, and approximately 200,000 are age < 65 years and have younger onset AD. By mid-century, the number of people living with AD in the United States is projected to grow by nearly 10 million, fueled in large part by the aging baby boom generation. Today, someone in the country develops AD every 67 seconds. By 2050, one new case of AD is expected to develop every 33 seconds, resulting in nearly 1 million new cases per year, and the estimated prevalence is expected to range from 11 million to 16 million. In 2013, official death certificates recorded 84,767 deaths from AD, making AD the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age 65 years. Between 2000 and 2013, deaths resulting from heart disease, stroke and prostate cancer decreased 14%, 23% and 11%, respectively, whereas deaths from AD increased 71%. The actual number of deaths to which AD contributes (or deaths with AD) is likely much larger than the number of deaths from AD recorded on death certificates. In 2015, an estimated 700,000 Americans age 65 years will die with AD, and many of them will die from complications caused by AD. In 2014, more than 15 million family members and other unpaid caregivers provided an estimated 17.9 billion hours of care to people with AD and other dementias, a contribution valued at more than $217 billion. Average per-person Medicare payments for services to beneficiaries age 65 years with AD and other dementias are more than two and a half times as great as payments for all beneficiaries without these conditions, and Medicaid payments are 19 times as great. Total payments in 2015 for health care, long-term care and hospice services for people age 65 years with dementia are expected to be $226 billion. Among people with a diagnosis of AD or another dementia, fewer than half report having been told of the diagnosis by their health care provider. Though the benefits of a prompt, clear and accurate disclosure of an AD diagnosis are recognized by the medical profession, improvements to the disclosure process are needed. These improvements may require stronger support systems for health care providers and their patients.
Anders Wimo | Linus Jönsson | John Bond | Martin Prince | Bengt Winblad
Objective: To acquire an understanding of the societal costs of dementia and how they affect families, health and social care services, and governments to improve the lives of people with dementia and their caregivers. Methods: The basic design of this study was a societal, prevalence-based, gross cost-of-illness study in which costs were aggregated to World Health Organization regions and World Bank income groupings. Results: The total estimated worldwide costs of dementia were US$604 billion in 2010. About 70% of the costs occurred in western Europe and North America. In such high-income regions, costs of informal care and the direct costs of social care contribute similar proportions of total costs, whereas the direct medical costs were much lower. In low- and middle-income countries, informal care accounts for the majority of total costs; direct social care costs are negligible. Conclusions: Worldwide costs of dementia are enormous and distributed inequitably. There is considerable potential for cost increases in coming years as the diagnosis and treatment gap is reduced. There is also likely to be a trend in low- and middle-income countries for social care costs to shift from the informal to the formal sector, with important implications for future aggregated costs and the financing of long-term care. Only by investing now in research and the development of cost-effective approaches to early diagnosis and care can future societal costs be anticipated and managed. © 2013 The Alzheimer's Association. All rights reserved.
Joseph Gaugler | Bryan James | Tricia Johnson | Ken Scholz | Jennifer Weuve
© 2016 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved. This report describes the public health impact of Alzheimer's disease, including incidence and prevalence, mortality rates, costs of care, and the overall impact on caregivers and society. It also examines in detail the financial impact of Alzheimer's on families, including annual costs to families and the difficult decisions families must often make to pay those costs. An estimated 5.4 million Americans have Alzheimer's disease. By mid-century, the number of people living with Alzheimer's disease in the United States is projected to grow to 13.8 million, fueled in large part by the aging baby boom generation. Today, someone in the country develops Alzheimer's disease every 66 seconds. By 2050, one new case of Alzheimer's is expected to develop every 33 seconds, resulting in nearly 1 million new cases per year. In 2013, official death certificates recorded 84,767 deaths from Alzheimer's disease, making it the sixth leading cause of death in the United States and the fifth leading cause of death in Americans age ≥65 years. Between 2000 and 2013, deaths resulting from stroke, heart disease, and prostate cancer decreased 23%, 14%, and 11%, respectively, whereas deaths from Alzheimer's disease increased 71%. The actual number of deaths to which Alzheimer's disease contributes is likely much larger than the number of deaths from Alzheimer's disease recorded on death certificates. In 2016, an estimated 700,000 Americans age ≥65 years will die with Alzheimer's disease, and many of them will die because of the complications caused by Alzheimer's disease. In 2015, more than 15 million family members and other unpaid caregivers provided an estimated 18.1 billion hours of care to people with Alzheimer's and other dementias, a contribution valued at more than $221 billion. Average per-person Medicare payments for services to beneficiaries age ≥65 years with Alzheimer's disease and other dementias are more than two and a half times as great as payments for all beneficiaries without these conditions, and Medicaid payments are 19 times as great. Total payments in 2016 for health care, long-term care and hospice services for people age ≥65 years with dementia are estimated to be $236 billion. The costs of Alzheimer's care may place a substantial financial burden on families, who often have to take money out of their retirement savings, cut back on buying food, and reduce their own trips to the doctor. In addition, many family members incorrectly believe that Medicare pays for nursing home care and other types of long-term care. Such findings highlight the need for solutions to prevent dementia-related costs from jeopardizing the health and financial security of the families of people with Alzheimer's and other dementias.
Frank Jessen | Rebecca E. Amariglio | Martin Van Boxtel | Monique Breteler | Mathieu Ceccaldi | Gaël Chételat | Bruno Dubois | Carole Dufouil | Kathryn A. Ellis | Wiesje M. Van Der Flier | Lidia Glodzik | Argonde C. Van Harten | Mony J. De Leon | Pauline McHugh | Michelle M. Mielke | Jose Luis Molinuevo | Lisa Mosconi | Ricardo S. Osorio | Audrey Perrotin | Ronald C. Petersen | Laura A. Rabin | Lorena Rami | Barry Reisberg | Dorene M. Rentz | Perminder S. Sachdev | Vincent De La Sayette | Andrew J. Saykin | Philip Scheltens | Melanie B. Shulman | Melissa J. Slavin | Reisa A. Sperling | Robert Stewart | Olga Uspenskaya | Bruno Vellas | Pieter Jelle Visser | Michael Wagner
© 2014 The Alzheimer's Association. All rights reserved. There is increasing evidence that subjective cognitive decline (SCD) in individuals with unimpaired performance on cognitive tests may represent the first symptomatic manifestation of Alzheimer's disease (AD). The research on SCD in early AD, however, is limited by the absence of common standards. The working group of the Subjective Cognitive Decline Initiative (SCD-I) addressed this deficiency by reaching consensus on terminology and on a conceptual framework for research on SCD in AD. In this publication, research criteria for SCD in pre-mild cognitive impairment (MCI) are presented. In addition, a list of core features proposed for reporting in SCD studies is provided, which will enable comparability of research across different settings. Finally, a set of features is presented, which in accordance with current knowledge, increases the likelihood of the presence of preclinical AD in individuals with SCD. This list is referred to as SCD plus.
Chun Fang Xia | Janna Arteaga | Gang Chen | Umesh Gangadharmath | Luis F. Gomez | Dhanalakshmi Kasi | Chung Lam | Qianwa Liang | Changhui Liu | Vani P. Mocharla | Fanrong Mu | Anjana Sinha | Helen Su | A. Katrin Szardenings | Joseph C. Walsh | Eric Wang | Chul Yu | Wei Zhang | Tieming Zhao | Hartmuth C. Kolb
Objective: We wished to develop a highly selective positron emission tomography (PET) imaging agent targeting PHF-tau in human Alzheimer's disease (AD) brains. Methods: To screen potential tau binders, human AD brain sections were used as a source of native paired helical filament (PHF)-tau and Aβ rather than synthetic tau aggregates or Aβ fibrils generated in vitro to measure the affinity and selectivity of [ 18 F]T807 to tau and Aβ. Brain uptake and biodistribution of [ 18 F]T807 in mice were also tested. Results: In vitro autoradiography results show that [ 18 F]T807 exhibits strong binding to PHF-tau-positive human brain sections. A dissociation constant (K d ) of [ 18 F]T807 (14.6 nM) was measured using brain sections from the frontal lobe of AD patients. A comparison of autoradiography and double immunohistochemical staining of PHF-tau and Aβ on adjacent sections demonstrated that [ 18 F]T807 binding colocalized with immunoreactive PHF-tau pathology, but did not highlight Aβ plaques. In vivo studies in mice demonstrated that [ 18 F]T807 was able to cross the blood-brain barrier and washed out quickly. Conclusions: [ 18 F]T807 demonstrates high affinity and selectivity to PHF-tau as well as favorable in vivo properties, making this a promising candidate as an imaging agent for AD. © 2013 The Alzheimer's Association. All rights reserved.
Michael W. Weiner | Dallas P. Veitch | Paul S. Aisen | Laurel A. Beckett | Nigel J. Cairns | Robert C. Green | Danielle Harvey | Clifford R. Jack | William Jagust | Enchi Liu | John C. Morris | Ronald C. Petersen | Andrew J. Saykin | Mark E. Schmidt | Leslie Shaw | Li Shen | Judith A. Siuciak | Holly Soares | Arthur W. Toga | John Q. Trojanowski
The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). The study aimed to enroll 400 subjects with early mild cognitive impairment (MCI), 200 subjects with early AD, and 200 normal control subjects; $67 million funding was provided by both the public and private sectors, including the National Institute on Aging, 13 pharmaceutical companies, and 2 foundations that provided support through the Foundation for the National Institutes of Health. This article reviews all papers published since the inception of the initiative and summarizes the results as of February 2011. The major accomplishments of ADNI have been as follows: (1) the development of standardized methods for clinical tests, magnetic resonance imaging (MRI), positron emission tomography (PET), and cerebrospinal fluid (CSF) biomarkers in a multicenter setting; (2) elucidation of the patterns and rates of change of imaging and CSF biomarker measurements in control subjects, MCI patients, and AD patients. CSF biomarkers are consistent with disease trajectories predicted by β-amyloid cascade (Hardy, J Alzheimers Dis 2006;9(Suppl 3):151-3) and tau-mediated neurodegeneration hypotheses for AD, whereas brain atrophy and hypometabolism levels show predicted patterns but exhibit differing rates of change depending on region and disease severity; (3) the assessment of alternative methods of diagnostic categorization. Currently, the best classifiers combine optimum features from multiple modalities, including MRI, [ 18 F]-fluorodeoxyglucose-PET, CSF biomarkers, and clinical tests; (4) the development of methods for the early detection of AD. CSF biomarkers, β-amyloid 42 and tau, as well as amyloid PET may reflect the earliest steps in AD pathology in mildly symptomatic or even nonsymptomatic subjects, and are leading candidates for the detection of AD in its preclinical stages; (5) the improvement of clinical trial efficiency through the identification of subjects most likely to undergo imminent future clinical decline and the use of more sensitive outcome measures to reduce sample sizes. Baseline cognitive and/or MRI measures generally predicted future decline better than other modalities, whereas MRI measures of change were shown to be the most efficient outcome measures; (6) the confirmation of the AD risk loci CLU, CR1, and PICALM and the identification of novel candidate risk loci; (7) worldwide impact through the establishment of ADNI-like programs in Europe, Asia, and Australia; (8) understanding the biology and pathobiology of normal aging, MCI, and AD through integration of ADNI biomarker data with clinical data from ADNI to stimulate research that will resolve controversies about competing hypotheses on the etiopathogenesis of AD, thereby advancing efforts to find disease-modifying drugs for AD; and (9) the establishment of infrastructure to allow sharing of all raw and processed data without embargo to interested scientific investigators throughout the world. The ADNI study was extended by a 2-year Grand Opportunities grant in 2009 and a renewal of ADNI (ADNI-2) in October 2010 through to 2016, with enrollment of an additional 550 participants. © 2013 The Alzheimer¢s Association. All rights reserved.
Niklas Mattsson | Ulf Andreasson | Staffan Persson | Maria C. Carrillo | Steven Collins | Sonia Chalbot | Neal Cutler | Diane Dufour-Rainfray | Anne M. Fagan | Niels H.H. Heegaard | Ging Yuek Robin Hsiung | Bradley Hyman | Khalid Iqbal | D. Richard Lachno | Alberto Lleó | Piotr Lewczuk | José L. Molinuevo | Piero Parchi | Axel Regeniter | Robert Rissman | Hanna Rosenmann | Giuseppe Sancesario | Johannes Schröder | Leslie M. Shaw | Charlotte E. Teunissen | John Q. Trojanowski | Hugo Vanderstichele | Manu Vandijck | Marcel M. Verbeek | Henrik Zetterberg | Kaj Blennow | Stephan A. Käser
Background: The cerebrospinal fluid (CSF) biomarkers amyloid beta 1-42, total tau, and phosphorylated tau are used increasingly for Alzheimer's disease (AD) research and patient management. However, there are large variations in biomarker measurements among and within laboratories. Methods: Data from the first nine rounds of the Alzheimer's Association quality control program was used to define the extent and sources of analytical variability. In each round, three CSF samples prepared at the Clinical Neurochemistry Laboratory (Mölndal, Sweden) were analyzed by single-analyte enzyme-linked immunosorbent assay (ELISA), a multiplexing xMAP assay, or an immunoassay with electrochemoluminescence detection. Results: A total of 84 laboratories participated. Coefficients of variation (CVs) between laboratories were around 20% to 30%; within-run CVs, less than 5% to 10%; and longitudinal within-laboratory CVs, 5% to 19%. Interestingly, longitudinal within-laboratory CV differed between biomarkers at individual laboratories, suggesting that a component of it was assay dependent. Variability between kit lots and between laboratories both had a major influence on amyloid beta 1-42 measurements, but for total tau and phosphorylated tau, between-kit lot effects were much less than between-laboratory effects. Despite the measurement variability, the between-laboratory consistency in classification of samples (using prehoc-derived cutoffs for AD) was high ( > 90% in 15 of 18 samples for ELISA and in 12 of 18 samples for xMAP). Conclusions: The overall variability remains too high to allow assignment of universal biomarker cutoff values for a specific intended use. Each laboratory must ensure longitudinal stability in its measurements and use internally qualified cutoff levels. Further standardization of laboratory procedures and improvement of kit performance will likely increase the usefulness of CSF AD biomarkers for researchers and clinicians. © 2013 The Alzheimer's Association. All rights reserved.
This report discusses the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality rates, costs of care, and overall effect on caregivers and society. It also examines the impact of AD on women compared with men. An estimated 5.2 million Americans have AD. Approximately 200,000 people younger than 65 years with AD comprise the younger onset AD population; 5 million are age 65 years or older. By mid-century, fueled in large part by the baby boom generation, the number of people living with AD in the United States is projected to grow by about 9 million. Today, someone in the country develops AD every 67 seconds. By 2050, one new case of AD is expected to develop every 33 seconds, or nearly a million new cases per year, and the total estimated prevalence is expected to be 13.8 million. In 2010, official death certificates recorded 83,494 deaths from AD, making AD the sixth leading cause of death in the United States and the fifth leading cause of death in Americans aged 65 years or older. Between 2000 and 2010, the proportion of deaths resulting from heart disease, stroke, and prostate cancer decreased 16%, 23%, and 8%, respectively, whereas the proportion resulting from AD increased 68%. The actual number of deaths to which AD contributes (or deaths with AD) is likely much larger than the number of deaths from AD recorded on death certificates. In 2014, an estimated 700,000 older Americans will die with AD, and many of them will die from complications caused by AD. In 2013, more than 15 million family members and other unpaid caregivers provided an estimated 17.7 billion hours of care to people with AD and other dementias, a contribution valued at more than $220 billion. Average per-person Medicare payments for services to beneficiaries aged 65 years and older with AD and other dementias are more than two and a half times as great as payments for all beneficiaries without these conditions, and Medicaid payments are 19 times as great. Total payments in 2014 for health care, long-term care, and hospice services for people aged 65 years and older with dementia are expected to be $214 billion. AD takes a stronger toll on women than men. More women than men develop the disease, and women are more likely than men to be informal caregivers for someone with AD or another dementia. As caregiving responsibilities become more time consuming and burdensome or extend for prolonged durations, women assume an even greater share of the caregiving burden. For every man who spends 21 to more than 60 hours per week as a caregiver, there are 2.1 women. For every man who lives with the care recipient and provides around-the-clock care, there are 2.5 women. In addition, for every man who has provided caregiving assistance for more than 5 years, there are 2.3 women. © 2014 The Alzheimers Association. All rights reserved.
Cyndy B. Cordell | Soo Borson | Malaz Boustani | Joshua Chodosh | David Reuben | Joe Verghese | William Thies | Leslie B. Fried
The Patient Protection and Affordable Care Act added a new Medicare benefit, the Annual Wellness Visit (AWV), effective January 1, 2011. The AWV requires an assessment to detect cognitive impairment. The Centers for Medicare and Medicaid Services (CMS) elected not to recommend a specific assessment tool because there is no single, universally accepted screen that satisfies all needs in the detection of cognitive impairment. To provide primary care physicians with guidance on cognitive assessment during the AWV, and when referral or further testing is needed, the Alzheimer's Association convened a group of experts to develop recommendations. The resulting Alzheimer's Association Medicare Annual Wellness Visit Algorithm for Assessment of Cognition includes review of patient Health Risk Assessment (HRA) information, patient observation, unstructured queries during the AWV, and use of structured cognitive assessment tools for both patients and informants. Widespread implementation of this algorithm could be the first step in reducing the prevalence of missed or delayed dementia diagnosis, thus allowing for better healthcare management and more favorable outcomes for affected patients and their families and caregivers. © 2013 The Alzheimer's Association. All rights reserved.
Bruno Dubois | Harald Hampel | Howard H. Feldman | Philip Scheltens | Paul Aisen | Sandrine Andrieu | Hovagim Bakardjian | Habib Benali | Lars Bertram | Kaj Blennow | Karl Broich | Enrica Cavedo | Sebastian Crutch | Jean François Dartigues | Charles Duyckaerts | Stéphane Epelbaum | Giovanni B. Frisoni | Serge Gauthier | Remy Genthon | Alida A. Gouw | Marie Odile Habert | David M. Holtzman | Miia Kivipelto | Simone Lista | José Luis Molinuevo | Sid E. O'Bryant | Gil D. Rabinovici | Christopher Rowe | Stephen Salloway | Lon S. Schneider | Reisa Sperling | Marc Teichmann | Maria C. Carrillo | Jeffrey Cummings | Cliff R. Jack
© 2016 The Alzheimer's Association. During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum. Thanks to evolving biomarker research and substantial discoveries, it is now possible to identify the disease even at the preclinical stage before the occurrence of the first clinical symptoms. This preclinical stage of AD has become a major research focus as the field postulates that early intervention may offer the best chance of therapeutic success. To date, very little evidence is established on this "silent" stage of the disease. A clarification is needed about the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage. This article is aimed at addressing all the different issues by providing for each of them an updated review of the literature and evidence, with practical recommendations.
Matthew Baumgart | Heather M. Snyder | Maria C. Carrillo | Sam Fazio | Hye Kim | Harry Johns
© 2015 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association. An estimated 47 million people worldwide are living with dementia in 2015, and this number is projected to triple by 2050. In the absence of a disease-modifying treatment or cure, reducing the risk of developing dementia takes on added importance. In 2014, the World Dementia Council (WDC) requested the Alzheimer's Association evaluate and report on the state of the evidence on modifiable risk factors for cognitive decline and dementia. This report is a summary of the Association's evaluation, which was presented at the October 2014 WDC meeting. The Association believes there is sufficient evidence to support the link between several modifiable risk factors and a reduced risk for cognitive decline, and sufficient evidence to suggest that some modifiable risk factors may be associated with reduced risk of dementia. Specifically, the Association believes there is sufficiently strong evidence, from a population-based perspective, to conclude that regular physical activity and management of cardiovascular risk factors (diabetes, obesity, smoking, and hypertension) reduce the risk of cognitive decline and may reduce the risk of dementia. The Association also believes there is sufficiently strong evidence to conclude that a healthy diet and lifelong learning/cognitive training may also reduce the risk of cognitive decline.
Flora H. Duits | Charlotte E. Teunissen | Femke H. Bouwman | Pieter Jelle Visser | Niklas Mattsson | Henrik Zetterberg | Kaj Blennow | Oskar Hansson | Lennart Minthon | Niels Andreasen | Jan Marcusson | Anders Wallin | Marcel Olde Rikkert | Magda Tsolaki | Lucilla Parnetti | Sanna Kaisa Herukka | Harald Hampel | Mony J. De Leon | Johannes Schröder | Dag Aarsland | Marinus A. Blankenstein | Philip Scheltens | Wiesje M. Van Der Flier
© 2014 The Alzheimer's Association. All rights reserved. Background We aimed to identify the most useful definition of the "cerebrospinal fluid Alzheimer profile," based on amyloid-ß < inf > 1-42 < /inf > (Aβ < inf > 42 < /inf > ), total tau, and phosphorylated tau (p-tau), for diagnosis and prognosis of Alzheimer's disease (AD). Methods We constructed eight Alzheimer profiles with previously published combinations, including regression formulas and simple ratios. We compared their diagnostic accuracy and ability to predict dementia due to AD in 1385 patients from the Amsterdam Dementia Cohort. Results were validated in an independent cohort (n = 1442). Results Combinations outperformed individual biomarkers. Based on the sensitivity of the best performing regression formulas, cutoffs were chosen at 0.52 for the tau/Aβ < inf > 42 < /inf > ratio and 0.08 for the p-tau/Aβ < inf > 42 < /inf > ratio. Ratios performed similar to formulas (sensitivity, 91%-93%; specificity, 81%-84%). The same combinations best predicted cognitive decline in mild cognitive impairment patients. Validation confirmed these results, especially regarding the tau/Aβ < inf > 42 < /inf > ratio. Conclusions A tau/Aβ < inf > 42 < /inf > ratio of > 0.52 constitutes a robust cerebrospinal fluid Alzheimer profile. We recommend using this ratio to combine biomarkers.
Heather M. Snyder | Roderick A. Corriveau | Suzanne Craft | James E. Faber | Steven M. Greenberg | David Knopman | Bruce T. Lamb | Thomas J. Montine | Maiken Nedergaard | Chris B. Schaffer | Julie A. Schneider | Cheryl Wellington | Donna M. Wilcock | Gregory J. Zipfel | Berislav Zlokovic | Lisa J. Bain | Francesca Bosetti | Zorina S. Galis | Walter Koroshetz | Maria C. Carrillo
© 2015 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved. Scientific evidence continues to demonstrate the linkage of vascular contributions to cognitive impairment and dementia such as Alzheimer's disease. In December, 2013, the Alzheimer's Association, with scientific input from the National Institute of Neurological Disorders and Stroke and the National Heart, Lung and Blood Institute from the National Institutes of Health, convened scientific experts to discuss the research gaps in our understanding of how vascular factors contribute to Alzheimer's disease and related dementia. This manuscript summarizes the meeting and the resultant discussion, including an outline of next steps needed to move this area of research forward.
Frank Jessen | Steffen Wolfsgruber | Birgitt Wiese | Horst Bickel | Edelgard Mösch | Hanna Kaduszkiewicz | Michael Pentzek | Steffi G. Riedel-Heller | Tobias Luck | Angela Fuchs | Siegfried Weyerer | Jochen Werle | Hendrik Van Den Bussche | Martin Scherer | Wolfgang Maier | Michael Wagner
Objective: To compare the risk of developing Alzheimer's disease (AD) dementia in late mild cognitive impairment (LMCI), early MCI (EMCI), and subjective memory impairment (SMI) with normal test performance. Methods: The baseline sample (n = 2892) of the prospective cohort study in nondemented individuals (German Study on Aging, Cognition and Dementia in Primary Care Patients) was divided into LMCI, EMCI, SMI, and control subjects by delayed recall performance. These groups were subdivided by the presence of self-reported concerns associated with experienced memory impairment. AD dementia risk was assessed over 6 years. Results: Across all groups, risk of AD dementia was greatest in LMCI. In those with self-reported concerns regarding their memory impairment, SMI and EMCI were associated with a similarly increased risk of AD dementia. In those subgroups without concerns, SMI was not associated with increased risk of AD dementia, but EMCI remained an at-risk condition. Conclusions: SMI and EMCI with self-reported concerns were associated with the same risk of AD dementia, suggesting that pre-LMCI risk conditions should be extended to SMI with concerns. © 2014 The Alzheimer's Association. All rights reserved.
“Alzheimer’s disease is a progressive disease of the human brain that is characterized by impairment of memory and a disturbance in at least one other thinking function” (Bronstein & Pulst, 2003). When we hear about Alzheimer’s disease we automatically think of older people. This is because this disease most often occurs in adults after the age of 65. Statistics show that one in eight individuals will have Alzheimer’s after they reach age 65 (Cavanaugh & Blanchard-Fields, 2002). Alzheimer’s disease is a form of dementia, which is any medical condition that affects the brain (Cavanaugh & Blanchard-Fields, 2002).
A diagnosis of Alzheimer’s is said to be a “diagnosis by exclusion” (Bronstein & Pulst, 2003). This means that there is no certain test just for Alzheimer’s, but many tests that rule out other diseases. The early stages deal with short-term memory loss. Examples of this include forgetting to turn off the stove, forgetting what medications were taken in a particular day, or forgetting which medications need to be taken. As the disease progresses there is more visibility in the declines in abstract thinking and intellectual function development (Bronstein & Pulst, 2003). As the disease enters the final stages, individuals become very confused and disorientated. At this point the individual’s health status has become severely deteriorated and this can cause them to develop pneumonia or other illnesses that may lead to death. Consequently, most people do not die from Alzheimer’s, but other health related problems. Alzheimer’s disease can last anywhere from six to eight years, however it can be present without obvious symptoms for two to twenty years. The on-set of Alzheimer’s disease is very slow (Bronstein & Pulst, 2003).
There are many factors that play a role in the cause of Alzheimer’s disease. This disease is also genetic—a person that has family members with the disease possesses an increased chance of being diagnosed with Alzheimer’s also. This disease supposedly caused by many effects on the brain. A mutation of a single gene is one condition that is found in the brain of Alzheimer’s patients (Bronstein & Pulst, 2003). There are also proteins in the brain that are linked to Alzheimer’s. They are the amyloid precursor and two presenilins, (Bronstein & Pulst, 2003) which are responsible in the early on-set of the disease (Brzyska & Elbaum, 2003). The number one indicator of Alzheimer’s is a gene called apolipoproteinE (apoE). There are three forms of this gene. ApoE 4 is the one that is most closely related to Alzheimer’s sufferers. This gene is inherited and when a child receives two of them, one from each parent. As a result, the child’s chances of developing the disease are largely increased. ApoE2 is another form of the gene but this one takes on the opposite route – this gene decreases one’s chances of getting Alzheimer’s disease.
There are not many prevention methods for Alzheimer’s; it’s a genetic disease, and it also depends on how your genes react to our environment. It has been thought that drinking out of aluminum cans can cause Alzheimer’s, but this has been proven to now be false. Many scientists believe that Alzheimer’s disease occurs from an increase in the production of a specific protein, beta amyloid, which leads to nerve cell death (Bronstein & Pulst, 2003).
Although there is no cure for Alzheimer’s disease, there are treatments that prolong the individual’s awareness and memory. Their medications can be taken in the early stages to minimize memory loss that the patient is experiencing. One drug that has a positive effect is tacrine, a drug that is used to increase acetylcholine, which helps to improve memory (Cavanaugh & Blanchard-Fields, 2002). Patients are also given anti-depressants and anti-anxiety medicines to address their mood (Cavanaugh & Blanchard-Fields, 2002). These drugs are called chiolinesterase inhibitors (ChEIs); the FDA has approved them for the treatment of Alzheimer’s disease. Along with tacrine, aricept is another drug that is commonly used and found to be very successful in delaying the effects of Alzheimer’s. These drugs have been found to help patients in most cases, but genetics dictate that each case is different; signs and symptoms for Alzheimer’s vary for each patient. These drugs are most effective when used in the earliest stages of the disease. When a patient is taking these drugs, doctors should not prescribe more than one because there are too many side effects when in taken in combination. Alzheimer sufferers do not have to take these medicines for their whole life, but when they are experiencing withdrawals from them they have to be monitored.
There are four principle disturbances in Alzheimer’s disease. They are agitation, depression, psychosis, and anxiety. Agitation occurs in about 70% of patients and is more common as the disease gets worse (Bronstein & Pulst, 2003). To calm a patient’s agitation doctors often prescribe them antipsychotic drugs. Psychosis is common among Alzheimer’s patients also, but not as often, occurring in about 50 % of cases. In another 50 % of the cases we find them suffering from depression–usually a mild depression that is treated with antidepressants. Anxiety is the last principle disturbance that is found in Alzheimer’s and it occurs in about 40-50 % of cases. Most patients do not require medication to treat their anxiety (Bronstein & Pulst, 2003). Finally, one last effect that may occur from time to time in the course of Alzheimer’s disease is difficulty sleeping.
There is not yet a cure for this disease but with all the continued research, hopefully in the future, researchers will find one. Having the knowledge about the brain and its abnormalities that occur with this disease will provide physicians with more treatment and maybe a cure. According to Bronstein and Pulst animal testing such as immunization of beta-amyloid antibodies have been showing very promising results in the next step for a cure.
The reason I choose to research this disease is because my grandmother is currently ailing from it. She is eighty-seven years old and along with some other health problems, Alzheimer’s disease has become a major concern. She is well into the latent stages of the disease, but the disease has not completely overtaken her. However, there are many things that the disease has done to her normal capabilities. When my family first noticed that she was becoming more and more forgetful, we did not think much about it. As the disease progressed, we became more concerned for her safety. My grandmother takes medications for her other illnesses, and like most other Alzheimer patients she was starting to forget to take them. My grandmother also drove up until her later years, which was not a safe idea for her or other drivers on the road. She once got lost and we had to go out searching for her. A major tragedy was averted after we had to call the police and she was discovered after she backed her car into the side of her home. When confronting her on with these situations, she was able to make up excuses or she just easily denied that she did that. She is not yet in the stage where she forgets who we are, but she does need to be reminded from time to time. The one good thing about my grandmother’s condition is that she is now aware that there is a problem.
A conversation with my grandma consists of a lot of repeating. Some times she will catch herself asking the same questions and her famous quote is, “my thinker is a stinker”. One thing that I do notice in my grandmother that coincides with my research is that a majority of her forgetfulness is short-term memory loss. When asking my grandmother about her childhood, or how she met my grandfather, she remembers it like it was yesterday. Not only does my grandmother have other health-related problems, she also lived alone for a while and has fallen causing great injury to her body. The worst occurrence of this happening is when she once fell in her kitchen and broke her hip. At this point in her life, she was more disorientated than ever. We now have a nurse that stays with her to make sure that she is safe, but this is another issue for her because she feels that there is a stranger in her house.
Alzheimer’s is an intimidating and threatening disease. Possessing the knowledge that I now have is an advantage in being a preventable measure for me. Being that this disease is genetic, my chances of having it are increased. Knowing all of this information about it will help me in the future to be able to detect it early so I can take the proper course of action that will delay the progression of this disease for me. If tragedy ever should strike, by then, hopefully, more curable treatments will exist.
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