Cited by 84Alzheimer's disease research and treatmentsParkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration Mechanisms

α-Synuclein Oligomers Induce a Unique Toxic Tau Strain

Open access
Castillo-Carranza, Diana L., Guerrero-Muñoz, Marcos J., Sengupta, Urmi, Gerson, Julia E., Kayed, Rakez·2018·Biological Psychiatry

Abstract

BACKGROUND: The coexistence of α-synuclein and tau aggregates in several neurodegenerative disorders, including Parkinson's disease and Alzheimer's disease, raises the possibility that a seeding mechanism is involved in disease progression. METHODS: To further investigate the role of α-synuclein in the tau aggregation pathway, we performed a set of experiments using both recombinant and brain-derived tau and α-synuclein oligomers to seed monomeric tau aggregation in vitro and in vivo. Brain-derived tau oligomers were isolated from well-characterized cases of progressive supranuclear palsy (n = 4) and complexes of brain-derived α-synuclein/tau oligomers isolated from patients with Parkinson's disease (n = 4). The isolated structures were purified and characterized by standard biochemical methods, then injected into Htau mice (n = 24) to assess their toxicity and role in tau aggregation. RESULTS: We found that α-synuclein induced a distinct toxic tau oligomeric strain that avoids fibril formation. In vivo, Parkinson's disease brain-derived α-synuclein/tau oligomers administered into Htau mouse brains accelerated endogenous tau oligomer formation concurrent with increasing cell loss. CONCLUSIONS: Our findings provide evidence, for the first time, that α-synuclein enhances the harmful effects of tau, thus contributing to disease progression.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.biopsych.2017.12.018

Cites

48 of 48 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Castillo-Carranza, D. L., Guerrero-Muñoz, M. J., Sengupta, U., Gerson, J. E., & Kayed, R.
Affiliations
The University of Texas Medical Branch at Galveston (US)
Corresponding author
Kayed, Rakez
Venue
Biological Psychiatry
Publisher
Elsevier BV
Published
2018-10
Volume
84
Issue
7
Pages
499-508
ISSN
0006-3223 (ISSN-L)
OpenAlex
W2782823547
Cited by
84
References
48
Citations by year
2026: 5 · 2025: 7 · 2024: 7 · 2023: 7 · 2022: 13 · 2021: 6 · 2020: 24 · 2019: 10 · 2018: 5
FWCI
7.71
Type
journal article
Language
en
Open access
Locations
  • Biological Psychiatry (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion, other-oa)
  • PubMed Central (acceptedVersion, cc-by-nc-nd)
Funders
  • Michael J. Fox Foundation for Parkinson's Research
  • National Institutes of Health
  • Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch
  • National Institute on Aging (RF1AG055771, R01AG054025)
  • National Institute of Neurological Disorders and Stroke (R01NS094557)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
alpha-synuclein, tau oligomers, tau aggregation, Parkinson's disease, progressive supranuclear palsy, neurodegeneration, fibril formation, cell loss
MeSH terms
Animals, Brain, Humans, Parkinson Disease, Recombinant Proteins, Supranuclear Palsy, Progressive, tau Proteins, Disease Progression, Mice, alpha-Synuclein

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review