Evidence map›Paper›PMID 33343276›Full record

ArticleFrontiers in neuroscience2020

Prodromal Alzheimer's Disease: Constitutive Upregulation of Neuroglobin Prevents the Initiation of Alzheimer's Pathology.

Silvia de Vidania, Irene Palomares-Perez, Ana Frank-García, Takashi Saito, Takaomi C Saido, Jonathan Draffin, María Szaruga, Lucía Chávez-Gutierrez, Miguel Calero, Miguel Medina and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Enhanced mGluRCell death & disease · 2024
    Article
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  6. Review
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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

12 authors at 7 institutions in 3 countries.

Silvia de VidaniaMolecular Neuropathology, Physiological and Pathological Processes, Centro de Biología Molecular Severo Ochoa, CSIC/UAM, Madrid, Spain.
Irene Palomares-PerezMolecular Neuropathology, Physiological and Pathological Processes, Centro de Biología Molecular Severo Ochoa, CSIC/UAM, Madrid, Spain.
Ana Frank-GarcíaDepartment of Neurology, Instituto de Salud Carlos III (ISCIII), Division Neurodegenerative Disease, University Hospital La Paz, Madrid, Spain.
Takashi SaitoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako-shi, Japan.
Takaomi C SaidoDepartment of Neurocognitive Science, Nagoya City University Graduate School of Medical Science, Nagoya, Japan.
Jonathan DraffinMolecular Neuropathology, Physiological and Pathological Processes, Centro de Biología Molecular Severo Ochoa, CSIC/UAM, Madrid, Spain.
María SzarugaKU Leuven Department for Neurosciences, VIB-KU Leuven Center for Brain and Disease Research, Leuven, Belgium.
Lucía Chávez-GutierrezKU Leuven Department for Neurosciences, VIB-KU Leuven Center for Brain and Disease Research, Leuven, Belgium.
Miguel CaleroCIBERNED, Queen Sofia Foundation Alzheimer Center, CIEN Foundation, Instituto de Salud Carlos III, Madrid, Spain.
Miguel MedinaCIBERNED, Queen Sofia Foundation Alzheimer Center, CIEN Foundation, Instituto de Salud Carlos III, Madrid, Spain.
Francesc X GuixMolecular Neuropathology, Physiological and Pathological Processes, Centro de Biología Molecular Severo Ochoa, CSIC/UAM, Madrid, Spain.
Carlos G DottiMolecular Neuropathology, Physiological and Pathological Processes, Centro de Biología Molecular Severo Ochoa, CSIC/UAM, Madrid, Spain.
Universidad Autónoma de Madrid · ESCentro de Biología Molecular Severo Ochoa · ESInstituto de Salud Carlos III · ESVIB-KU Leuven Center for Brain & Disease Research · BEFundacion Centro De Investigacion De Enfermedades Neurologicas · ESNagoya City University · JPRIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In humans, a considerable number of the autopsy samples of cognitively normal individuals aged between 57 and 102 years have revealed the presence of amyloid plaques, one of the typical signs of AD, indicating that many of us use mechanisms that defend ourselves from the toxic consequences of Aß. The human APP NL/F (hAPP NL/F) knockin mouse appears as the ideal mouse model to identify these mechanisms, since they have high Aß42 levels at an early age and moderate signs of disease when old. Here we show that in these mice, the brain levels of the hemoprotein Neuroglobin (Ngb) increase with age, in parallel with the increase in Aß42.

Indexed as

Alzheimer’s diseaseAmyloid-beta peptidedendritic complexityneuroglobinresilience

Identifiers

PMID33343276
PMCPMC7744294
OpenAlexW3107170460

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.