Evidence map›Paper›PMID 30497516›Full record

ArticleActa neuropathologica communications2018

Different tau species lead to heterogeneous tau pathology propagation and misfolding.

Simon Dujardin, Séverine Bégard, Raphaëlle Caillierez, Cédrick Lachaud, Sébastien Carrier, Sarah Lieger, Jose A Gonzalez, Vincent Deramecourt, Nicole Déglon, Claude-Alain Maurage and 4 more

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
–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

69 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Olfactory decline tracks central-to-peripheral spread of tau pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  17. In situ seeding assay: A novel technique for direct tissue localization of bioactive tau.Journal of neuropathology and experimental neurology · 2024
    Article
  18. Article
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  20. Rapidly reversible persistent long-term potentiation inhibition by patient-derived brain tau and amyloid ß proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article

9 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

14 authors.

Simon DujardinUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Séverine BégardUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Raphaëlle CaillierezUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Cédrick LachaudUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Sébastien CarrierUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Sarah LiegerUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Jose A GonzalezDepartment of Neurology, Massachusetts General Hospital, MassGeneral Institute of Neurodegenerative Diseases (MIND), Charlestown, MA, USA.
Vincent DeramecourtUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Nicole DéglonLausanne University Hospital (CHUV), Neuroscience Research Center (CRN), Laboratory of Neurotherapies and Neuromodulation (LNTM), CH-1011, Lausanne, Switzerland.
Claude-Alain MaurageUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France.
Matthew P FroschDepartment of Neurology, Massachusetts General Hospital, MassGeneral Institute of Neurodegenerative Diseases (MIND), Charlestown, MA, USA.
Bradley T HymanDepartment of Neurology, Massachusetts General Hospital, MassGeneral Institute of Neurodegenerative Diseases (MIND), Charlestown, MA, USA.
Morvane ColinUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France. morvane.colin@inserm.fr.
Luc BuéeUniv. Lille, Inserm, CHU-Lille, UMR-S 1172, Alzheimer & Tauopathies, School of Medicine, 1 rue Polonovski, 59045, Lille, France. luc.buee@inserm.fr.ORCID 0000-0002-6261-4230

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
NIA NIH HHS P50 AG005134
6 · The paper itself

Abstract

Tauopathies are a heterogeneous group of pathologies characterized by tau aggregation inside neurons. Most of them are sporadic but certain tauopathies rely on tau gene (MAPT) mutations. They particularly differ from one to another by their different neuropathological signatures e.g. lesion shapes, regions affected and molecular composition of aggregates. Six isoforms of tau exist, but they do not all co-aggregate in each tauopathy but rather have a unique signature for each one. In some tauopathies such as Alzheimer's disease (AD), tau protein aggregation follows stereotypical anatomical stages. Recent data suggest that this progression is due to an active process of tau protein propagation from neuron-to-neuron. We wondered how tau isoforms or mutations could influence the process of tau aggregation and tau propagation. In human neuropathological material, we found that MAPT mutations induce a faster misfolding compared to tau found in sporadic AD patients. In the rat brain, we observed cell-to-cell transfer of non-pathological tau species irrespective of the tested isoform or presence of a mutation. By contrast, we found that the species of tau impact the propagation of tau pathology markers such as hyperphosphorylation and misfolding. Indeed, misfolding and hyperphosphorylated tau proteins do not spread at the same rate when tau is mutated, or the isoform composition is modified. These results clearly argue for the existence of specific folding properties of tau depending on isoforms or mutations impacting the behavior of pathological tau species.

Indexed as

TauopathiesAdultAgedAged, 80 and overAnimalsBrainDisease Models, AnimalDisease ProgressionFemaleHumansInjections, IntraventricularMaleMiddle AgedMutationPhosphorylationProtein IsoformsProtein Isoformstau ProteinsAlzheimer’s diseaseHeterogeneityIsoformsMisfoldingPropagationTau

Identifiers

PMID30497516
PMCPMC6263555

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Registered trials

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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.