Evidence map›Paper›PMID 31293377›Full record

ReviewFrontiers in neuroscience2019

Alzheimer Disease Pathogenesis: Insights From Molecular and Cellular Biology Studies of Oligomeric Aβ and Tau Species.

Xu-Qiao Chen, William C Mobley

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 5 pooled it
20.6field-weighted citation impact, top 1% 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

153 citing papers in PubMed, 5 syntheses or guidelines pooled it, 281 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Article
  8. TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026
    Review
  9. Article
  10. Review
  11. Native PLGA nanoparticles attenuate disease pathology via multiple pathways in 5xFAD Alzheimer's model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  13. Article
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  15. Review
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93 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Xu-Qiao ChenDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
William C MobleyDepartment of Neurosciences, University of California, San Diego, San Diego, CA, United States.
University of California, San Diego · US

Funding

Project 3: TRiC modulation of CNS pathogenesis in HD mouse modelsP01NS092525 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI THOMPSON, LESLIE MICHELS · 2016 to 2020
$6.3M
Treating with Gamma-Secretase Modulators to Prevent Neurodegeneration in Mouse Models of Down Syndrome and Alzheimer DiseaseR01AG055523 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MOBLEY, WILLIAM C · 2018 to 2022
$3.2M
NIA NIH HHS R01 AG055523NINDS NIH HHS P01 NS092525
6 · The paper itself

Abstract

Alzheimer disease (AD) represents an oncoming epidemic that without an effective treatment promises to exact extraordinary human and financial burdens. Studies of pathogenesis are essential for defining targets for discovering disease-modifying treatments. Past studies of AD neuropathology provided valuable, albeit limited, insights. Nevertheless, building on these findings, recent studies have provided an increasingly rich harvest of genetic, molecular and cellular data that are creating unprecedented opportunities to both understand and treat AD. Among the most significant are those documenting the presence within the AD brain of toxic oligomeric species of Aβ and tau. Existing data support the view that such species can propagate and spread within neural circuits. To place these findings in context we first review the genetics and neuropathology of AD, including AD in Down syndrome (AD-DS). We detail studies that support the existence of toxic oligomeric species while noting the significant unanswered questions concerning their precise structures, the means by which they spread and undergo amplification and how they induce neuronal dysfunction and degeneration. We conclude by offering a speculative synthesis for how oligomers of Aβ and tau initiate and drive pathogenesis. While 100 years after Alzheimer's first report there is much still to learn about pathogenesis and the discovery of disease-modifying treatments, the application of new concepts and sophisticated new tools are poised to deliver important advances for combatting AD.

Indexed as

Alzheimer diseaseamyloid plaquesAβDown syndromeneurofibrillary tanglesoligomerPETtau

Identifiers

PMID31293377
PMCPMC6598402
OpenAlexW2951060040

What OpenQuestion 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 OpenQuestion graph.