Evidence map›Paper›PMID 29137322›Full record

ArticleOncotarget2017

The c-jun N-terminal kinase plays a key role in ocular degenerative changes in a mouse model of Alzheimer disease suggesting a correlation between ocular and brain pathologies.

Lucia Buccarello, Alessandra Sclip, Matteo Sacchi, Anna Maria Castaldo, Ilaria Bertani, Andrea ReCecconi, Silvia Maestroni, Gianpaolo Zerbini, Paolo Nucci, Tiziana Borsello

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Age-Related Retinal Layer Thickness Changes Measured by OCT inInternational journal of molecular sciences · 2024
    Article
  3. Alzheimer's disease pathophysiology in the Retina.Progress in retinal and eye research · 2024
    Review
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  6. Acrolein Induces Retinal Abnormalities of Alzheimer's Disease in Mice.International journal of molecular sciences · 2023
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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

10 authors at 4 institutions in 1 country.

Lucia BuccarelloIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Alessandra SclipIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Matteo SacchiUniversity Eye Clinic, San Giuseppe Hospital, University of Milan, Milan, Italy.
Anna Maria CastaldoIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Ilaria BertaniIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Andrea ReCecconiIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Silvia MaestroniUnità Complicanze del Diabete, Istituto Scientifico San Raffaele, Milan, Italy.
Gianpaolo ZerbiniUnità Complicanze del Diabete, Istituto Scientifico San Raffaele, Milan, Italy.
Paolo NucciUniversity Eye Clinic, San Giuseppe Hospital, University of Milan, Milan, Italy.
Tiziana BorselloIRCCS-Istituto di Ricerche Farmacologiche "Mario Negri", Milan, Italy.
Istituti di Ricovero e Cura a Carattere Scientifico · ITMario Negri Institute for Pharmacological Research · ITOspedale San Giuseppe · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently a range of ocular manifestations such as retinal and lens amyloid-beta accumulation and retinal nerve fiber layer loss have been proposed as potential biomarkers in Alzheimer disease (AD). The TgCRND8 mouse model of AD exhibits age-dependent amyloid β (Aβ) oligomers accumulation and cognitive defects, amyloid plaques and hyperphosphorylated Tau deposition and inflammation. We proved the correlation between ocular pathologies and AD, observing increased levels of p-APP and p-Tau, accumulation of Aβ oligomers in the retina, eye, and optic nerve. The accumulation of amyloid markers was significantly stronger in the retinal ganglion cell (RGC) layer, suggesting that RGC might be more susceptible to degeneration. We detected a thinning of the RGC layer as well as RGC death in the retina of TgCRND8 mice, by using a combination of Optical Coherence Tomography (OCT), immunofluorescence, immunohistochemistry and Western blotting techniques. We proved for the first time the key role of C-Jun N-terminal Kinase (JNK) in the ocular degeneration. In support of this, the administration of the JNK inhibitor, D-JNKI1, was able to counteract the Aβ and p-Tau accumulation in the retina of TgCRND8 mice, and consequently reduce RGCs loss. These results confirm that degenerative changes in the retina/eye of AD mouse model mirrors the events observed in the brain parenchyma. Ocular changes can be detected by non-invasive imaging techniques, such as OCT, to study and test different therapeutic strategies against degenerative events associated to AD.

Indexed as

Alzheimer’s diseaseJNKoptical coherence tomographyretinal ganglion cell layerstress signaling pathway

Identifiers

PMID29137322
PMCPMC5669948
OpenAlexW2742842977

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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.