Article

Comparison of International Working Group criteria and National Institute on Aging–Alzheimer’s Association criteria for Alzheimer’s disease

Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands
Alzheimer's & dementia: the journal of the Alzheimer's Association (Impact Factor: 17.47). 11/2012; 8(6):560-3. DOI: 10.1016/j.jalz.2011.10.008
Source: PubMed

ABSTRACT Two sets of research criteria for Alzheimer's disease are now available: those published by an International Working Group in 2007, and the recommendations published by the National Institute on Aging and the Alzheimer's Association (NIA-AA) in 2011. They both provide guidelines for the diagnosis of asymptomatic and symptomatic Alzheimer's disease. The coexistence of two sets of criteria for the same disorder raises the question of which set of criteria should be preferred. A comparison of the criteria revealed differences in approach, terminology, and use of cognitive markers and biomarkers. Most persons who meet the International Working Group criteria will also meet the NIA-AA criteria and vice versa. However, the NIA-AA criteria allow for a subclassification of persons based on biomarker results within each diagnostic category. Further research is needed to validate the criteria. Modifications are likely to be made before the criteria can be used in daily practice.

0 Followers
 · 
212 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background We investigated the pattern of disease progression in the asymptomatic, mild cognitive impairment (MCI), and dementia stage of Alzheimer's disease (AD). Methods We selected 284 subjects with AD pathology, defined as abnormal levels of amyloid beta 1–42 (Aβ1–42) in cerebrospinal fluid (CSF). Disease outcome measures included six biomarkers and five cognitive markers. We compared differences in baseline measures and decline over 4 years between the AD stages and tested whether these changes differed from subjects, without AD pathology (N = 132). Results CSF Aβ1–42 reached the maximum abnormality level in the asymptomatic stage and tau in the MCI stage. The imaging and cognitive markers started to decline in the asymptomatic stage, and decline accelerated with advancing clinical stage. Conclusion This study provides further evidence for a temporal evolution of AD biomarkers. Our findings may be helpful to determine stage specific outcome measures for clinical trials.
    Alzheimer's and Dementia 08/2014; 11(5). DOI:10.1016/j.jalz.2014.05.1754 · 17.47 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Alzheimer's disease (AD) is the most common form of dementia. Its most important pathological hallmarks are profound neuronal loss, presence of intracellular neurofibrillary tangles, and extracellular deposition of beta-amyloid protein (Aβ) as beta-amyloid plaques. These latter aggregations result in neuronal degeneration in brain regions important not only for memory, but also for other cognitive functions. One of the most important risk factors for AD is age and with the increase of life-expectancy AD has thus become the most common form of dementia. It is now formally recognized by several new diagnostic criteria that AD is not a homogeneous disease. The current "Holy Grail" is to be able to diagnose variants of AD before they manifest clinically and before irreparable brain damage is done. To achieve this goal, robust and reliable biomarkers that reflect the pathogenesis of AD have to be implemented. This is of paramount importance because such biomarkers may provide clues to pathways that can be targeted for interventions aimed at disease prevention or improvement. Although much attention has focused on Aβ as a major component of AD, Aβ may be a less attractive target since an increasing amount of data has raised concerns about its causative role in AD. This review will be in two parts, this first part will deal with the current clinical knowledge and the questions raised by the Aβ cascade hypothesis in the pathogenesis of AD and the second part will aim to synthesize our current knowledge and to discuss new data that suggest how immune alterations may contribute to the development of AD and may therefore provide beneficial targets in novel approaches for the treatment of AD.
    Discovery medicine 01/2013; 15(80):23-32. · 3.50 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Alzheimer's disease (AD) is the most common form of dementia. Its most important pathological hallmarks are profound neuronal loss, presence of intracellular neurofibrillary tangles, and extracellular deposition of beta-amyloid protein (Aβ) as beta-amyloid plaques. One of the most important risk factors for AD is age and with the increase of life-expectancy AD has become the most common form of dementia. The current "Holy Grail" is to be able to diagnose variants of AD before they manifest clinically and before irreparable brain damage is done. To be able to do so, we need robust and reliable biomarkers which reflect the pathogenesis of AD. This is essential because such biomarkers might indicate pathways that could be targeted for interventions aiming at disease prevention or amelioration. Although much attention has been focused on Aβ in this respect, it may not be as attractive a target as thought if current doubts concerning its causative role are substantiated. This review will be in two parts, the first part dealt with the current clinical knowledge and the questions raised by the Aβ cascade hypothesis in the pathogenesis of AD and this second part aims to synthesize our current knowledge and new data suggesting how immunity may contribute to the development of AD and may itself be targeted in future treatments.
    Discovery medicine 01/2013; 15(80):33-42. · 3.50 Impact Factor