Evidence map›Paper›PMID 35447369›Full record

ArticleNeurobiology of aging2022

Rates of β-amyloid deposition indicate widespread simultaneous accumulation throughout the brain.

Molly R LaPoint, Suzanne L Baker, Susan M Landau, Theresa M Harrison, William J Jagust

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Gene-Modulated Network Diffusion for Improved Modeling of Amyloid-bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. Quantification of Alzheimer disease neuropathology using tissue microarrays.Journal of neuropathology and experimental neurology · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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

5 authors at 3 institutions in 1 country.

Molly R LaPointHelen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720, USA. Electronic address: mlapoint17@berkeley.edu.
Suzanne L BakerMolecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, CA 94720, USA.
Susan M LandauHelen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720, USA; Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, CA 94720, USA.
Theresa M HarrisonHelen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720, USA.
William J JagustHelen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720, USA; Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, CA 94720, USA.
Lawrence Berkeley National Laboratory · USBerkeley College · USUniversity of California, Berkeley · US

Funding

Neural and Biochemical Mechanisms of Cognitive AgingR01AG034570 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI William J. Jagust · 2009 to 2026
$12.0M
Mechanisms of Alzheimer's Disease Progression in the Aging BrainR01AG062542 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI JAGUST, WILLIAM J. · 2019 to 2023
$4.2M
NIA NIH HHS R01 AG034570NIA NIH HHS R01 AG062542
6 · The paper itself

Abstract

Amyloid plaque aggregation is a pathologic hallmark of Alzheimer's disease (AD) that occurs early in the disease. However, little is known about its progression throughout the brain. Using Pittsburgh Compound B (PIB)-PET imaging, we investigated the progression of regional amyloid accumulation in cognitively normal older adults. We found that all examined regions reached their peak accumulation rates 24-28 years after an estimated initiation corresponding to the mean baseline PIB-PET signal in amyloid-negative older adults. We also investigated the effect of increased genetic risk conferred by the apolipoprotein-E ɛ4 allele on rates of amyloid accumulation, as well as the relationship between regional amyloid accumulation and regional tau pathology, another hallmark of AD, measured with Flortaucipir-PET. Carriers of the ɛ4 allele had faster amyloid accumulation in all brain regions. Furthermore, in all regions excluding the temporal lobe, faster amyloid accumulation was associated with greater tau burden. These results indicate that amyloid accumulates near-simultaneously throughout the brain and is associated with higher AD pathology, and that genetic risk of AD is associated with faster amyloid accumulation.

Indexed as

Alzheimer Diseasetau ProteinsAgedAmyloidAmyloid beta-PeptidesBrainHumansMagnetic Resonance ImagingPositron-Emission TomographyAmyloidAmyloid beta-Peptidestau ProteinsAgingAlzheimer's DiseaseAmyloidAPOELongitudinalTau

Identifiers

PMID35447369
PMCPMC9986974
OpenAlexW4221063338

What OpenQuestion holds

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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.