Evidence map›Paper›PMID 35969330›Full record

ArticleMolecular neurobiology2022

Adult-Onset Deficiency of Mitochondrial Complex III in a Mouse Model of Alzheimer's Disease Decreases Amyloid Beta Plaque Formation.

Milena Pinto, Francisca Diaz, Nadee Nissanka, Chelsey S Guastucci, Placido Illiano, Roberta Brambilla, Carlos T Moraes

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

7 authors at 1 institution in 1 country.

Milena PintoDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA. mpinto@med.miami.edu.ORCID http://orcid.org/0000-0001-9202-1527
Francisca DiazDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID http://orcid.org/0000-0002-1252-0594
Nadee NissankaDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID http://orcid.org/0000-0002-4639-7192
Chelsey S GuastucciThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID http://orcid.org/0000-0001-5575-8714
Placido IllianoThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID http://orcid.org/0000-0002-8755-5986
Roberta BrambillaThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID http://orcid.org/0000-0001-5792-7497
Carlos T MoraesDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA. cmoraes@med.miami.edu.ORCID http://orcid.org/0000-0002-8077-7092
University of Miami · US

Funding

SETTING THE STAGE FOR REPLACEMENT OF MITOCHONDRIAL GENESR01EY010804 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 1995 to 2025
$9.4M
Cellular and Molecular Consequences of Respiratory Chain Defects in NeuronsR01NS079965 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2012 to 2023
$3.9M
Mitochondrial Dysfunction in Neurodegeneration and Compensatory ApproachesR01AG036871 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2010 to 2020
$3.3M
Imaging mitochondrial signaling in B-cells ectopically implanted in the eyeR33ES025673 · NIEHS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CAICEDO, ALEJANDRO, MORAES, CARLOS TORRES · 2018 to 2019
$761k
Use of NMNAT chaperone activity against Alzheimer related proteinpathy.K01AG057815 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PINTO, MILENA · 2019 to 2023
$617k
florida biomedical foundation 5AZ06NEI NIH HHS R01 EY010804NIA NIH HHS 1R01NS079965NIA NIH HHS K01 AG057815NIA NIH HHS K01AG057815NIA NIH HHS R01 AG036871NIEHS NIH HHS R33 ES025673NINDS NIH HHS R01 NS079965
6 · The paper itself

Abstract

For decades, mitochondrial dysfunctions and the generation of reactive oxygen species have been proposed to promote the development and progression of the amyloid pathology in Alzheimer's disease, but this association is still debated. It is unclear whether different mitochondrial dysfunctions, such as oxidative phosphorylation deficiency and oxidative stress, are triggers or rather consequences of the formation of amyloid aggregates. Likewise, the role of the different mitochondrial oxidative phosphorylation complexes in Alzheimer's patients' brain remains poorly understood. Previous studies showed that genetic ablation of oxidative phosphorylation enzymes from early age decreased amyloid pathology, which were unexpected results. To better model oxidative phosphorylation defects in aging, we induced the ablation of mitochondrial Complex III (CIII

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalElectron Transport Complex IIIMiceMice, KnockoutOxidative StressPlaque, AmyloidAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorElectron Transport Complex IIIAlzheimer’s diseaseMitochondria dysfunctionsMouse modelOxidative phosphorylation deficiencyOxidative stress

Identifiers

PMID35969330
PMCPMC9464722
OpenAlexW4291777671

What OpenQuestion holds

Textmetadata
LicenceTDM
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.