Evidence map›Paper›PMID 39651679›Full record

ArticleHuman brain mapping2024

Connectivity, Pathology, and ApoE4 Interactions Predict Longitudinal Tau Spatial Progression and Memory.

Jacob Ziontz, Theresa M Harrison, Corrina Fonseca, Joseph Giorgio, Feng Han, JiaQie Lee, William J Jagust, Alzheimer's Disease Neuroimaging Initiative

Abstract read
In one paragraph

Article in Human brain mapping, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
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

8 authors.

Jacob ZiontzDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.ORCID https://orcid.org/0000-0002-1995-3827
Theresa M HarrisonDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.
Corrina FonsecaDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.
Joseph GiorgioDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.
Feng HanDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.
JiaQie LeeDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.
William J JagustDepartment of Neuroscience, UC Berkeley, Berkeley, California, USA.
Alzheimer's Disease Neuroimaging Initiative

Funding

Project 1U19AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI Laurel A Beckett · 2016 to 2026
$226.7M
Neural and Biochemical Mechanisms of Cognitive AgingR01AG034570 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI William J. Jagust · 2009 to 2026
$12.0M
Neuroscience Training Program at UC BerkeleyT32NS095939 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BATEUP, HELEN S. · 2016 to 2025
$6.3M
Linking basal forebrain and entorhinal cortex vulnerability to preclinical Alzheimer's diseaseK01AG078443 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI Theresa M. Harrison · 2022 to 2026
$656k
Functional networks underlying cognitive decline in aging and Alzheimer's diseaseF31AG079595 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI ZIONTZ, JACOB · 2022 to 2023
$86k
Alzheimer's Association 23AARF-1026883BrightFocus Foundation A2021004FNIA NIH HHS U19 AG024904NIH HHS F31 AG079595NIH HHS K01 AG078443NIH HHS R01 AG034570NIH HHS U19 AG024904NINDS NIH HHS T32 NS095939
6 · The paper itself

Abstract

Tau pathology spread into neocortex indicates a transition from healthy aging to Alzheimer's disease (AD). Connectivity between tau epicenters and later accumulating regions of cortex has been proposed as a mechanism of tau spread, but how this relationship changes with greater AD pathology burden or genotype is not understood. We investigated tau accumulation in two key regions, precuneus and inferior temporal cortex, using resting state functional connectivity (rsFC) and longitudinal PET imaging from a multicohort sample of cognitively unimpaired older adults. We examined how baseline tau PET, Aβ PET, and ApoE4 genotype status interact with rsFC between hippocampus and these downstream regions to predict rate of tau accumulation in neocortex. We found that the 3-way interaction between connectivity, baseline tau, and baseline Aβ or ApoE4 status was associated with neocortical tau accumulation in precuneus and inferior temporal cortex. In addition, baseline tau, Aβ, and ApoE4 status also moderated the association between connectivity and rate of memory decline. Together, these results suggest that the extent and distribution of future tau accumulation may be predicted by the interaction of baseline connectivity, AD pathology, and genetic risk.

Indexed as

Apolipoprotein E4Disease ProgressionMagnetic Resonance ImagingPositron-Emission Tomographytau ProteinsAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesFemaleHumansLongitudinal StudiesMaleMemory DisordersMiddle AgedNeural PathwaysAmyloid beta-PeptidesApolipoprotein E4MAPT protein, humantau ProteinsagingAlzheimer'sfunctional connectivitylongitudinaltau pathology

Identifiers

PMID39651679
PMCPMC11626484

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.