Evidence map›Paper›PMID 28652970›Full record

ArticleNeuroImage. Clinical2017

APPswe/PS1dE9 mice with cortical amyloid pathology show a reduced NAA/Cr ratio without apparent brain atrophy: A MRS and MRI study.

Angela Kuhla, Claire Rühlmann, Tobias Lindner, Stefan Polei, Stefan Hadlich, Bernd J Krause, Brigitte Vollmar, Stefan J Teipel

Open access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Updates on mouse models of Alzheimer's disease.Molecular neurodegeneration · 2024
    Review
  3. Calpain-2 Mediates MBNL2 Degradation and a Developmental RNA Processing Program in Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Longitudinal [EJNMMI research · 2020
    Article
  10. Article
  11. Rodent models for Alzheimer disease.Nature reviews. Neuroscience · 2018
    Review
  12. 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.

Angela KuhlaInstitute for Experimental Surgery, Rostock University Medical Center, Rostock, Germany. Electronic address: angela.kuhla@uni-rostock.de.
Claire RühlmannInstitute for Experimental Surgery, Rostock University Medical Center, Rostock, Germany.
Tobias LindnerCore Facility Multimodal Small Animal Imaging, Rostock University Medical Center, Rostock, Germany.
Stefan PoleiCore Facility Multimodal Small Animal Imaging, Rostock University Medical Center, Rostock, Germany.
Stefan HadlichInstitute of Diagnostic Radiology and Neuroradiology, University Medicine Greifswald, Greifswald, Germany.
Bernd J KrauseDepartment of Nuclear Medicine, Rostock University Medical Center, Rostock, Germany.
Brigitte VollmarInstitute for Experimental Surgery, Rostock University Medical Center, Rostock, Germany.
Stefan J TeipelGerman Center for Neurodegenerative Diseases (DZNE) - Rostock/Greifswald, Rostock, Germany, Department of Psychosomatic Medicine, University of Rostock, Rostock, Germany.
University of Rostock · DEGerman Center for Neurodegenerative Diseases · DEUniversitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenic animal models of Aβ pathology provide mechanistic insight into some aspects of Alzheimer disease (AD) pathology related to Aβ accumulation. Quantitative neuroimaging is a possible aid to improve translation of mechanistic findings in transgenic models to human end phenotypes of brain morphology or function. Therefore, we combined MRI-based morphometry, MRS-based NAA-assessment and quantitative histology of neurons and amyloid plaque load in the APPswe/PS1dE9 mouse model to determine the interrelationship between morphological changes, changes in neuron numbers and amyloid plaque load with reductions of NAA levels as marker of neuronal functional viability. The APPswe/PS1dE9 mouse showed an increase of Aβ plaques, loss of neurons and an impairment of NAA/Cr ratio, which however was not accompanied with brain atrophy. As brain atrophy is one main characteristic in human AD, conclusions from murine to human AD pathology should be drawn with caution.

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-Protein PrecursorAnimalsAspartic AcidBrainCreatineFemaleMagnetic Resonance ImagingMagnetic Resonance SpectroscopyMiceMice, Inbred C3HMice, Inbred C57BLMice, TransgenicPresenilin-1AmyloidAmyloid beta-Protein PrecursorAspartic AcidCreatineN-acetylaspartatePresenilin-1presenilin 1, mouseAPPswe/PS1dE9 miceAβ-plaquesBrain atrophyNAA/Cr ratioNeuronal loss

Identifiers

PMID28652970
PMCPMC5476467
OpenAlexW2622277040

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.