Evidence map›Paper›PMID 22798965›Full record

ArticleNeurodegenerative disease management2012

Appraisal of cognition in preclinical Alzheimer's disease: a conceptual review.

David S Knopman, Richard J Caselli

Open access · greenAbstract read
In one paragraph

Article in Neurodegenerative disease management, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Primary age-related tauopathy.Acta neuropathologica · 2025
    Review
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  7. Article
  8. Article
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  10. Article
  11. "New Old Pathologies": AD, PART, and Cerebral Age-Related TDP-43 With Sclerosis (CARTS).Journal of neuropathology and experimental neurology · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

David S KnopmanDepartment of Neurology, College of Medicine, Mayo Clinic Rochester & Mayo Clinic Alzheimer's Disease Research Center, 200 First Street SW, Rochester, MN 55905, USA.
Richard J Caselli
Mayo Clinic in Florida · US

Funding

SUPPLEMENT TO ALZHEIMERS DISEASE PATIENT REGISTRYU01AG006786 · NIA · MAYO CLINIC ROCHESTER · PI GRAFF-RADFORD, JONATHAN, JACK, CLIFFORD R. · 1986 to 2023
$49.6M
THE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI BU, GUOJUN · 1999 to 2018
$36.9M
Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI GONZALEZ HERNANDEZ, GRACIELA · 2001 to 2020
$32.5M
PET, APOE & the Preclinical Course of Alzheimer's DiseaseR01AG031581 · NIA · BANNER ALZHEIMER'S INSTITUTE · PI CASELLI, RICHARD J., REIMAN, ERIC MICHAEL · 2008 to 2018
$16.6M
PREDICTING ALZHEIMERS DISEASE WITH MAGNETIC RESONANCER01AG011378 · NIA · MAYO CLINIC ROCHESTER · PI JACK, CLIFFORD R. · 1993 to 2017
$12.1M
NIA NIH HHS P30 AG019610NIA NIH HHS P50 AG016574NIA NIH HHS R01 AG011378NIA NIH HHS R01 AG031581NIA NIH HHS U01 AG006786
6 · The paper itself

Abstract

Biomarker evidence and clinical observations support the hypothesis that there is a diagnosable condition termed preclinical Alzheimer's disease (AD). Recently, a workgroup convened under the auspices of the National Institute on Aging and the Alzheimer's Association proposed a framework for defining preclinical AD. The definition was based on the presence of biomarkers that are indicative of the AD pathophysiological process. In the context of abnormal AD biomarkers, the workgroup postulated that 'subtle cognitive changes' occurred as well. Based on studies of genetically at-risk individuals and those destined to become demented, who were observed while still cognitively normal, low performance on learning and memory functions may be the earliest cognitive manifestations of preclinical AD, at the group level at least. It is not clear whether subtle cognitive decline can be detected reliably on an individual basis. Preclinical AD cognitive changes could be diagnosed by traditional neuropsychological testing, computerized testing, assessments of subjective memory loss, assessments of levels of participation in cognitively stimulating activities and direct measurement of activity using recently developed monitoring technology. Confounding effects of normal aging, test-retest variability, variations in educational attainment, as well as the presence of other brain diseases make diagnosing cognitive decline due to preclinical AD challenging.

Identifiers

PMID22798965
PMCPMC3395065
OpenAlexW2125334134

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.