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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 50 out of 100. Brain scans and imaging

Topic: Amyloid, tau and blood-test diagnosis

Objective To investigate whether baseline CSF biomarkers are associated with hippocampal atrophy rate as a measure of disease progression in patients with Alzheimer disease (AD), patients with mild cognitive impairment (MCI), and controls, controlling for baseline neuropsychological and MRI findings. Methods We assessed data from 31 patients with AD, 25 patients with MCI, and 19 controls (mean age 68 +/- 8 years; 39 [52%] female) who visited our memory clinic and had received serial MRI scanning (scan interval 1.7 +/- 0.7 years). At baseline, CSF biomarkers (amyloid beta 1-42, tau, and tau phosphorylated at threonine 181 [p-tau]) were obtained, as well as neuropsychological data. Baseline MRI scans were assessed using visual rating scales for medial temporal lobe atrophy (MTA), global cortical atrophy, and white matter hyperintensities. Hippocampal atrophy rates were estimated using regional nonlinear "fluid" registration of follow-up scan to baseline scan. Results Stepwise multiple linear regression, adjusted for age and sex, showed that increased CSF p-tau levels (beta [standard error]: -0.79 [0.35]) at baseline was independently associated with higher subsequent hippocampal atrophy rates (p Conclusions Baseline CSF levels of tau phosphorylated at threonine 181 are independently associated with subsequent disease progression, as reflected by hippocampal atrophy rate. This effect is independent of baseline neuropsychological and MRI predictors. Our results imply that predicting disease progression can best be achieved by combining information from different modalities.

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

APA 7th

Henneman, W. J., Vrenken, H., Barnes, J., Sluimer, I. C., Verwey, N. A., Blankenstein, M. A., et al. (2009). Baseline CSF p-tau levels independently predict progression of hippocampal atrophy in Alzheimer disease. Neurology. https://doi.org/10.1212/wnl.0b013e3181b879ac

Vancouver

Henneman WJ, Vrenken H, Barnes J, Sluimer IC, Verwey NA, Blankenstein MA, et al. Baseline CSF p-tau levels independently predict progression of hippocampal atrophy in Alzheimer disease. Neurology. 2009. doi:10.1212/wnl.0b013e3181b879ac. PMID: 19770469.

BibTeX

@article{henneman2009-19770469,
  author  = {Henneman, W. J. and Vrenken, H. and Barnes, J. and Sluimer, I. C. and Verwey, N. A. and Blankenstein, M. A. and Klein, M. and Fox, N. C. and others},
  title   = {{Baseline CSF p-tau levels independently predict progression of hippocampal atrophy in Alzheimer disease}},
  journal = {Neurology},
  year    = {2009},
  doi     = {10.1212/wnl.0b013e3181b879ac},
  pmid    = {19770469},
  url     = {https://doi.org/10.1212/wnl.0b013e3181b879ac}
}

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 this small study of 75 people, higher baseline CSF p-tau levels independently predicted faster hippocampal atrophy over time. This is a marker of disease progression, not a treatment, cure or prevention for Alzheimer's disease.

Study details

How this study scored 50/100
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; Randomised / blinded 0 of 2; Times cited 4 of 7; Citations per year 2 of 5; Impact for its field and year 3 of 6; Cited by studies here 2 of 6; Still being cited 1 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 50 of 100.50 of 100 points earned50 not earned

Published in a leading specialty journal. Scored zero for study design, effect reported and randomised / 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 2009 — within 20 year(s) of the newest study here
Sample size 1 / 4 31 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)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 4 / 7 Cited 76 times (OpenAlex, 2026-10-10)
Citations per year 2 / 5 4.0 citations a year over 19 year(s) since 2009
Impact for its field and year 3 / 6 Cited 3.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 2 / 6 Cited by 8 other studies in this library
Still being cited 1 / 4 Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Wiesje M. van der Flier: h-index 132 (OpenAlex, whole career)
Institution's track record 2 / 3 University College London: institution h-index 2,029 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 19770469)
Free to read 0 / 2 Behind a paywall — scores zero
Total 50 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

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