Evidence map›Paper›PMID 36277399›Full record

ArticleFrontiers in bioengineering and biotechnology2022

SMaRT modulation of tau isoforms rescues cognitive and motor impairments in a preclinical model of tauopathy.

Javier Andrés Muñiz, Carolina Lucía Facal, Leandro Urrutia, Ramiro Clerici-Delville, Ana Damianich, Juan E Ferrario, Germán Falasco, María Elena Avale

Open access · goldAbstract read
In one paragraph

Article in Frontiers in bioengineering and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  7. Tau reduction with artificial microRNAs modulates neuronal physiology and improves tauopathy phenotypes in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
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

8 authors at 3 institutions in 1 country.

Javier Andrés MuñizConsejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr Héctor N Torres", Buenos Aires, Argentina.
Carolina Lucía FacalConsejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr Héctor N Torres", Buenos Aires, Argentina.
Leandro UrrutiaLaboratorio De Imágenes Preclínicas, Centro de Imágenes Moleculares, FLENI, Buenos Aires, Argentina.
Ramiro Clerici-DelvilleConsejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr Héctor N Torres", Buenos Aires, Argentina.
Ana DamianichConsejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr Héctor N Torres", Buenos Aires, Argentina.
Juan E FerrarioUniversidad de Buenos Aires, Facultad de Ciencias Exactas y Naturales, Instituto de Biociencias, Biotecnología y Biología traslacional (iB3), Buenos Aires, Argentina.
Germán FalascoLaboratorio De Imágenes Preclínicas, Centro de Imágenes Moleculares, FLENI, Buenos Aires, Argentina.
María Elena AvaleConsejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr Héctor N Torres", Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARFundación para la Lucha contra las Enfermedades Neurológicas de la Infancia · ARFundación Ciencias Exactas y Naturales · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau is a microtubule-associated protein predominantly expressed in neurons, which participates in microtubule polymerization and axonal transport. Abnormal tau metabolism leads to neurodegenerative diseases named tauopathies, such as Alzheimer's disease and frontotemporal dementia. The alternative splicing of exon 10 (E10) in the primary transcript produces tau protein isoforms with three (3R) or four (4R) microtubule binding repeats, which are found in equal amounts in the normal adult human brain. Several tauopathies are associated with abnormal E10 alternative splicing, leading to an imbalance between 3R and 4R isoforms, which underlies disease. Correction of such imbalance represents a potential disease-modifying therapy for those tauopathies. We have previously optimized a

Indexed as

DementiaFDG-microPETMAPTRNA therapyTrans-Splicing

Identifiers

PMID36277399
PMCPMC9581281
OpenAlexW4301585140

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.