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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Mild cognitive impairment

Topic: Amyloid, tau and blood-test diagnosis

Objectives The current model of Alzheimer disease (AD) stipulates that brain amyloidosis biomarkers turn abnormal earliest, followed by cortical hypometabolism, and finally brain atrophy ones. The aim of this study is to provide clinical evidence of the model in patients with mild cognitive impairment (MCI). Methods A total of 73 patients with MCI from 3 European memory clinics were included. Brain amyloidosis was assessed by CSF Aβ42 concentration, cortical metabolism by an index of temporoparietal hypometabolism on FDG-PET, and brain atrophy by automated hippocampal volume. Patients were divided into groups based on biomarker positivity: 1) Aβ42- FDG-PET- Hippo-, 2) Aβ42+ FDG-PET- Hippo-, 3) Aβ42 + FDG-PET + Hippo-, 4) Aβ42 + FDG-PET+ Hippo+, and 5) any other combination not in line with the model. Measures of validity were prevalence of group 5, increasing incidence of progression to dementia with increasing biological severity, and decreasing conversion time. Results When patients with MCI underwent clinical follow-up, 29 progressed to dementia, while 44 remained stable. A total of 26% of patients were in group 5. Incident dementia was increasing with greater biological severity in groups 1 to 5 from 4% to 27%, 64%, and 100% (p for trend Conclusions The core biomarker pattern is in line with the current pathophysiologic model of AD. Fully normal and fully abnormal pattern is associated with exceptional and universal development of dementia. Cases not in line might be due to atypical neurobiology or inaccurate thresholds for biomarker (ab)normality.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Prestia, A., Caroli, A., van der Flier, W. M., Ossenkoppele, R., Van Berckel, B., Barkhof, F., et al. (2013). Prediction of dementia in MCI patients based on core diagnostic markers for Alzheimer disease. Neurology. https://doi.org/10.1212/wnl.0b013e3182872830

Vancouver

Prestia A, Caroli A, van der Flier WM, Ossenkoppele R, Van Berckel B, Barkhof F, et al. Prediction of dementia in MCI patients based on core diagnostic markers for Alzheimer disease. Neurology. 2013. doi:10.1212/wnl.0b013e3182872830. PMID: 23390179.

BibTeX

@article{prestia2013-23390179,
  author  = {Prestia, A. and Caroli, A. and van der Flier, W. M. and Ossenkoppele, R. and Van Berckel, B. and Barkhof, F. and Teunissen, C. E. and Wall, A. E. and others},
  title   = {{Prediction of dementia in MCI patients based on core diagnostic markers for Alzheimer disease}},
  journal = {Neurology},
  year    = {2013},
  doi     = {10.1212/wnl.0b013e3182872830},
  pmid    = {23390179},
  url     = {https://doi.org/10.1212/wnl.0b013e3182872830}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Why it matters

In 73 patients with mild cognitive impairment followed clinically, incident dementia increased with greater biological severity based on amyloid, metabolism and atrophy biomarkers. The authors conclude the core biomarker pattern is in line with the current pathophysiologic model of Alzheimer's disease.

Study details

How this study scored 55/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 4 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 1 of 4; Effect reported 0 of 3; Studied in people 3 of 3; Randomized / blinded 0 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 4 of 6; Cited by studies here 3 of 6; Still being cited 2 of 4; Senior author's track record 4 of 4; Institution's track record 1 of 3; Multicenter collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 55 of 100.55 of 100 points earned45 not earned

Published in a leading specialty journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (Neurology)
Journal's citation record 4 / 4 Neurology: journal h-index 525 (OpenAlex, 2026-10-29)
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence 1 / 5 Rated “low” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 1 / 5 2013 — within 20 year(s) of the newest study here
Sample size 1 / 4 73 participants
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 3 / 3 Studied in people (participant count stated)
Randomized / blinded 0 / 2 No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 5 / 7 Cited 185 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 12.3 citations a year over 15 year(s) since 2013
Impact for its field and year 4 / 6 Cited 15.8× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 26 other studies in this library
Still being cited 2 / 4 Cited 20 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Giovanni Battista Frisoni: h-index 120 (OpenAlex, whole career)
Institution's track record 1 / 3 Karolinska Institutet: institution h-index 1,477 (OpenAlex)
Multicenter collaboration 2 / 3 OpenAlex lists 7 institution(s) in 3 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 23390179)
Free to read 0 / 2 Behind a paywall — scores zero
Total 55 / 100 —

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