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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 59 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer's disease (AD) is a major cause of dementia and cognitive decline. Here, we assessed how episodic memory (EM) network dysfunction, a hallmark of AD, is related to the longitudinal progression of AD biomarkers, neurodegeneration and cognition using data from the DZNE DELCODE study. This data set includes over 1000 longitudinal functional magnetic resonance imaging measurements of EM network function. We related activation and deactivation of EM to individual disease progression scores from a disease progression model. Voxel-wise analyses revealed widespread loss of deactivation and activation with disease progression. Trajectories for the loss of deactivation were nonlinear, associated with amyloid- and tau-positivity and visually preceded trajectories of cognitive decline. The relationship between deactivation and cognitive decline was partly independent of neurodegeneration. Our results provide evidence that synaptic dysfunction and neurodegeneration are independent drivers of cognitive decline, providing a rationale for targeting synaptic dysfunction along the AD cascade.

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

APA 7th

Lattmann, R., Vockert, N., Bernal, J., Wesenberg, J., Suksangkharn, Y., Yakupov, R., et al. (2026). Dysfunction of the episodic memory network in the Alzheimer’s disease cascade. Nature Communications. https://doi.org/10.1038/s41467-026-71831-z

Vancouver

Lattmann R, Vockert N, Bernal J, Wesenberg J, Suksangkharn Y, Yakupov R, et al. Dysfunction of the episodic memory network in the Alzheimer’s disease cascade. Nature Communications. 2026. doi:10.1038/s41467-026-71831-z. PMID: 41997924.

BibTeX

@article{lattmann2026-41997924,
  author  = {Lattmann, René and Vockert, Niklas and Bernal, Jose and Wesenberg, Judith and Suksangkharn, Yanin and Yakupov, Renat and Schütze, Hartmut and Glanz, Wenzel and others},
  title   = {{Dysfunction of the episodic memory network in the Alzheimer’s disease cascade}},
  journal = {Nature Communications},
  year    = {2026},
  doi     = {10.1038/s41467-026-71831-z},
  pmid    = {41997924},
  url     = {https://doi.org/10.1038/s41467-026-71831-z}
}

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

Using longitudinal imaging from over 1000 measurements in the DELCODE study, loss of episodic memory network deactivation was linked to amyloid and tau positivity and appeared before cognitive decline. The authors conclude that synaptic dysfunction and neurodegeneration are independent drivers of cognitive decline, providing a rationale for targeting synaptic dysfunction, but no treatment is tested.

Study details

How this study scored 59/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 4 of 4; Study design 7 of 12; Strength of evidence 3 of 5; Peer-review validation 10 of 10; How recent 5 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 2 of 7; Citations per year 2 of 5; Impact for its field and year 4 of 6; Cited by studies here 0 of 6; Still being cited 1 of 4; Senior author's track record 3 of 4; Institution's track record 2 of 3; Multi-centre collaboration 3 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 59 of 100.59 of 100 points earned41 not earned

Published in a leading specialty journal, and it is a longitudinal study following the same people over time. Scored zero for sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (Nature Communications)
Journal's citation record 4 / 4 Nature Communications: journal h-index 747 (OpenAlex, 2026-10-29)
Study design 7 / 12 A longitudinal study following the same people over time
Strength of evidence 3 / 5 Rated “moderate” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 5 / 5 2026 — within 1 year(s) of the newest study here
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 2 / 7 Cited 8 times (OpenAlex, 2026-10-10)
Citations per year 2 / 5 4.0 citations a year over 2 year(s) since 2026
Impact for its field and year 4 / 6 Cited 18.9× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 1 / 4 Cited 8 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author Emrah Düzel: h-index 90 (OpenAlex, whole career)
Institution's track record 2 / 3 University College London: institution h-index 2,029 (OpenAlex)
Multi-centre collaboration 3 / 3 OpenAlex lists 22 institution(s) in 3 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 41997924)
Free to read 2 / 2 Free to read
Total 59 / 100 —

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

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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