Evidence map›Paper›PMID 29673549›Full record

ReviewBiomedical journal2018

Tau and neuroinflammation: What impact for Alzheimer's Disease and Tauopathies?

Cyril Laurent, Luc Buée, David Blum

Open access · goldAbstract readReview
In one paragraph

Review in Biomedical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 1 pooled it
23.6field-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

188 citing papers in PubMed, 1 synthesis or guideline pooled it, 339 citations in OpenAlex.

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  5. From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
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128 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

3 authors at 1 institution in 1 country.

Cyril LaurentUniversity of Lille, Lille, France; Inserm UMR-S 1172, "Alzheiumer & Tauopathies", Lille, France; Labex DISTALZ, Lille, France.
Luc BuéeUniversity of Lille, Lille, France; Inserm UMR-S 1172, "Alzheiumer & Tauopathies", Lille, France; Labex DISTALZ, Lille, France.
David BlumUniversity of Lille, Lille, France; Inserm UMR-S 1172, "Alzheiumer & Tauopathies", Lille, France; Labex DISTALZ, Lille, France. Electronic address: david.blum@inserm.fr.
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is a chronic neurodegenerative disorder and the most common type of dementia (60-80% of cases). In 2016, nearly 44 million people were affected by AD or related dementia. AD is characterized by progressive neuronal damages leading to subtle and latter obvious decline in cognitive functions including symptoms such as memory loss or confusion, which ultimately require full-time medical care. Its neuropathology is defined by the extracellular accumulation of amyloid-β (Aβ) peptide into amyloid plaques, and intraneuronal neurofibrillary tangles (NFT) consisting of aggregated hyper- and abnormal phosphorylation of tau protein. The latter, identified also as Tau pathology, is observed in a broad spectrum of neurological diseases commonly referred to as "Tauopathies". Besides these lesions, sustained neuroinflammatory processes occur, involving notably micro- and astro-glial activation, which contribute to disease progression. Recent findings from genome wide association studies further support an instrumental role of neuroinflammation. While the interconnections existing between this innate immune response and the amyloid pathogenesis are widely characterized and described as complex, elaborated and evolving, only few studies focused on Tau pathology. An adaptive immune response takes place conjointly during the disease course, as indicated by the presence of vascular and parenchymal T-cell in AD patients' brain. The underlying mechanisms of this infiltration and its consequences with regards to Tau pathology remain understudied so far. In the present review, we highlight the interplays existing between Tau pathology and the innate/adaptive immune responses.

Indexed as

Adaptive ImmunityAlzheimer DiseaseBlood-Brain BarrierHumansImmunity, InnateInflammationNeurogliaPhosphorylationTauopathiestau Proteinstau ProteinsAlzheimer's diseaseAstrocytesGliaInflammationMicrogliaTau

Identifiers

PMID29673549
PMCPMC6138617
OpenAlexW2802395419

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.