The Consortium to Establish a Registry for Alzheimer's Disease (CERAD)

Morris, John C.; Edland, Steve; Clark, Christine; Galasko, Doug; Koss, Elisabeth; Mohs, Richard C.; Belle, Gerald van; Fillenbaum, Gerda G.; Heyman, Albert

doi:10.1212/wnl.43.12.2457

Cited by 536 publications

(447 citation statements)

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“…back-calculated by using the information on the estimated FAST stage durations). There were no significant correlations with these factors, which is consistent with previous reports [2,13,[31][32][33][34][35][36].…”

Section: Resultssupporting

confidence: 92%

Alzheimer's disease: rapid and slow progression

Thalhauser

Komarova

2011

J. R. Soc. Interface.

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The variability in the progression of Alzheimer's disease (AD) across patients has made identification of disease-delaying treatments difficult. Quantitative analysis of this variability has important implications in understanding the pathophysiology of AD and identifying disease-delaying treatments. The functional assessment staging (FAST) procedure characterizes seven stages in the course of AD from normal ageing to severe dementia. The present study applied statistical methods to analyse FAST stage durations from a dataset of 648 AD patients. These methods uncovered two distinct types of disease progression, characterized by different mean progression rates. We identified two separate distributions of FAST stage progression times differing by up to 2 years in mean duration within each stage. These results further indicate that if a patient progresses rapidly through a given FAST stage, then their further progression is also likely to be rapid. These findings support the hypothesis that progression of AD can occur via two different pathophysiological mechanisms that lead to distinct average rates of decline.

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Section: Resultssupporting

confidence: 92%

Alzheimer's disease: rapid and slow progression

Thalhauser

Komarova

2011

J. R. Soc. Interface.

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“…39 Decline in performance was also identified longitudinally, the rate of decline depending on initial level of performance. 40 …”

Section: Neuropsychological Assessmentmentioning

confidence: 99%

Consortium to Establish a Registry for Alzheimer's Disease (CERAD): The first twenty years

Fillenbaum

Belle

Morris

et al. 2008

Alzheimer's & Dementia

373

274

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The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) was funded by the National Institute on Aging in 1986 to develop standardized, validated measures for the assessment of Alzheimer's disease (AD). The present report describes the measures that CERAD developed during its first decade, and their continued use in their original and translated forms. These measures include clinical, neuropsychological, neuropathological and behavioral assessments of AD, and also assessment of family history and parkinsonism in AD. An approach to evaluating neuroimages did not meet the standards desired. Further evaluations which could not be completed because of lack of funding (but where some materials are available), include evaluation of very severe AD, and of service use and need by patient and caregiver. The information that was developed in the U.S. and abroad permits standardized assessment of AD in clinical practice, facilitates epidemiological studies, and provides information valuable for individual and public health planning. CERAD materials and data remain available for those wishing to use them. KeywordsConsortium to Establish a Registry for Alzheimer's Disease; CERAD; Alzheimer's disease; clinical assessment; neuropsychological assessment; neuropathological assessment; norms; prevalence; incidence BackgroundDementing disorders have long been recognized, 1 with the identification of Alzheimer's disease (AD) typically dated back to Alzheimer's century-old paper. 2 Although considerable attention has been paid to Alzheimer's disease and substantial progress has been made in identifying its characteristics, nevertheless much remains unclear. As diagnostic procedures improve, the complexities of this disease become more apparent, and the threat it imposes becomes increasingly evident. In the population 65 years of age and older, both the incidence and prevalence of this disorder double every succeeding five years, 3 with estimated prevalence as high as 40% among those over the age of 85. AD, not recognized as a leading cause of death in 1980, was recognized as the fifth leading cause of death in 2003 among persons 65 years of age and older. 4 There is presently no cure and inadequate amelioration for this condition. It can not only strip personality and capability, but is demanding on family members, seriously disrupting their lives and their work. It is expensive for the long term care system, where about half of the residents may suffer from dementia, a substantial proportion of whom can no longer afford their own care. Although people are now reaching their older years in better health, 5,6 it remains to be seen whether there will be a decrease in the incidence of AD. Currently the fastest growing element of the population is among those 85 years of age and older, the age group where the incidence of AD is greatest.A major step in the management of a disease lies in accurate diagnosis. Relevant to current work, clinical diagnostic criteria for dementia and AD were specified about 25 years ago, and the...

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“…All patients underwent a neuropsychological examination, including the German Version of the CERAD test battery [23][24][25][26][27], which is composed of the MMSE, a 15-item short version of the Boston Naming Test, semantic word fluency test for animals (one minute),word list learning (10 words, three trials), word list recall after distraction, word list recognition (10 target and 10 distractor words), figure copying and delayed figure recall. For additionally testing, we used the first-letter fluency test from the Leistungsprüfsystem 50+ test [28], which is a German version of the FAS test (generation of words starting with these letters for 1 minute), the Mehrfachwahl-Wortschatz-Intelligenztest [29], which was used as a measure for extent of and access to the vocabulary, the Zahlenverbindungstest of the Nürnburger Alters Inventar [30], which is similar to the Trail Making Test A, and the digit span forwards and backwards from the German version of the Wechsler Memory Scale [31], to investigate verbal working memory performance.…”

Section: Neuropsychological Investigationmentioning

confidence: 99%

Correlation between Cognitive Impairment and CSF Biomarkers in Amnesic MCI, non-Amnesic MCI, and Alzheimer's Disease

Haldenwanger

Eling

Kastrup

et al. 2010

JAD

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Abstract. Decreased delayed recall, decreased amyloid-β peptides (Aβ1−42), and increased tau protein concentration in cerebrospinal fluid (CSF) are generally regarded to be valid neuropsychological and biological markers for Alzheimer's disease (AD). Previous studies failed to demonstrate clear-cut correlations between neuropsychological impairment and CSF markers. In this study we test recent models of disease progression, that propose that changes in CSF biomarkers already reach a plateau in a preclinical phase, before cognitive decline begins, that is, even before MCI can be diagnosed. We recruited 73 patients with probable AD (n = 36) and mild cognitive impairment (MCI) (amnesic MCI = 25; non-amnesic MCI = 12). We used the CERAD-NP, a widely used neuropsychological battery with norms for different age and education groups, and additional neuropsychological tests for assessing the cognitive profile of these patient groups. We found a significant correlation between Aβ1−42 in the CSF and memory performance for amnesic MCI patients, but not for non-amnesic MCI and AD patients. All other correlations between cognitive tasks and Aβ1−42 were not significant. Tau protein concentration in the CSF was not correlated with any neuropsychological marker in any of the patients groups. We conclude that the decrease of Aβ1−42 in the CSF mirrors disease progression during the early stages up into AD and therefore is not restricted to the preclinical phase. The decrease of Aβ1−42 reaches a plateau only in the full blown demented syndrome and further functional disease progression is then related to neurodegeneration without further reduction of Aβ1−42 in the CSF.

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The Consortium to Establish a Registry for Alzheimer's Disease (CERAD)

Cited by 536 publications

References 0 publications

Alzheimer's disease: rapid and slow progression

Alzheimer's disease: rapid and slow progression

Consortium to Establish a Registry for Alzheimer's Disease (CERAD): The first twenty years

Correlation between Cognitive Impairment and CSF Biomarkers in Amnesic MCI, non-Amnesic MCI, and Alzheimer's Disease

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