Evidence map›Paper›PMID 32778792›Full record

ReviewNature neuroscience2020

Synergy between amyloid-β and tau in Alzheimer's disease.

Marc Aurel Busche, Bradley T Hyman

Open access · greenAbstract readReview
In one paragraph

Review in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 701 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
701citing papers in PubMed, 1 pooled it
71.4field-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

701 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,152 citations in OpenAlex.

  1. Pooled it
  2. A randomized phase 1b/2 trial of ABBV-916 in adults with early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Effects ofFoods (Basel, Switzerland) · 2026
    Article
  15. Article
  16. Progressive behavioral and cognitive decline inbioRxiv : the preprint server for biology · 2026
    Article
  17. Article
  18. Article
  19. Cross-disease protein aggregate interactions in neurodegeneration: from molecular mechanisms to therapeutic strategies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  20. Article

641 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 2 institutions in 2 countries.

Marc Aurel BuscheUK Dementia Research Institute at UCL, University College London, London, UK. m.busche@ucl.ac.uk.ORCID http://orcid.org/0000-0002-4416-7553
Bradley T HymanMassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Boston, USA.ORCID http://orcid.org/0000-0002-7959-9401
Harvard University · USUK Dementia Research Institute · GB

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
Are multiple tau species toxic in Alzheimer's Disease?RF1AG059789 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2018 to 2018
$2.7M
Synergy between amyloid and tau in Alzheimer's DiseaseRF1AG058674 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2018 to 2018
$2.6M
Complexity and Heterogeneity of Alzheimer diseaseR56AG061196 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2019 to 2019
$654k
Medical Research Council MR/S017003/1NIA NIH HHS P30 AG062421NIA NIH HHS R56 AG061196NIA NIH HHS RF1 AG058674NIA NIH HHS RF1 AG059789
6 · The paper itself

Abstract

Patients with Alzheimer's disease (AD) present with both extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles in the brain. For many years, the prevailing view of AD pathogenesis has been that changes in Aβ precipitate the disease process and initiate a deleterious cascade involving tau pathology and neurodegeneration. Beyond this 'triggering' function, it has been typically presumed that Aβ and tau act independently and in the absence of specific interaction. However, accumulating evidence now suggests otherwise and contends that both pathologies have synergistic effects. This could not only help explain negative results from anti-Aβ clinical trials but also suggest that trials directed solely at tau may need to be reconsidered. Here, drawing from extensive human and disease model data, we highlight the latest evidence base pertaining to the complex Aβ-tau interaction and underscore its crucial importance to elucidating disease pathogenesis and the design of next-generation AD therapeutic trials.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalHumansNeuronsPlaque, Amyloidtau ProteinsAmyloid beta-PeptidesMAPT protein, humantau Proteins

Identifiers

PMID32778792
PMCPMC11831977
OpenAlexW3048109944

What OpenQuestion holds

Textmetadata
LicenceTDM
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.