Evidence map›Paper›PMID 34476545›Full record

ArticleCellular and molecular life sciences : CMLS2021

Sex-dependent effects of amyloid precursor-like protein 2 in the SOD1-G37R transgenic mouse model of MND.

Phan H Truong, Peter J Crouch, James B W Hilton, Catriona A McLean, Roberto Cappai, Giuseppe D Ciccotosto

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

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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

6 authors at 2 institutions in 1 country.

Phan H TruongDepartment of Biochemistry and Pharmacology, The University of Melbourne, Parkville, VIC, 3010, Australia. phan.truong@florey.edu.au.ORCID http://orcid.org/0000-0002-9964-0678
Peter J CrouchDepartment of Biochemistry and Pharmacology, The University of Melbourne, Parkville, VIC, 3010, Australia.
James B W HiltonDepartment of Biochemistry and Pharmacology, The University of Melbourne, Parkville, VIC, 3010, Australia.
Catriona A McLeanAnatomical Pathology, Alfred Hospital, Melbourne, VIC, 3005, Australia.
Roberto CappaiDepartment of Biochemistry and Pharmacology, The University of Melbourne, Parkville, VIC, 3010, Australia.
Giuseppe D CiccotostoDepartment of Biochemistry and Pharmacology, The University of Melbourne, Parkville, VIC, 3010, Australia. j.ciccotosto@unimelb.edu.au.
The University of Melbourne · AUThe Alfred Hospital · AU

Funding

Motor Neurone Disease Research Institute of Australia Beryl BayleyMotor Neurone Disease Research Institute of Australia Betty LaidlawMotor Neurone Disease Research Institute of Australia Jenny Barr Smith Research Grants
6 · The paper itself

Abstract

Motor neurone disease (MND) is a neurodegenerative disorder characterised by progressive destruction of motor neurons, muscle paralysis and death. The amyloid precursor protein (APP) is highly expressed in the central nervous system and has been shown to modulate disease outcomes in MND. APP is part of a gene family that includes the amyloid precursor-like protein 1 (APLP1) and 2 (APLP2) genes. In the present study, we investigated the role of APLP2 in MND through the examination of human spinal cord tissue and by crossing APLP2 knockout mice with the superoxide dismutase 1 (SOD1-G37R) transgenic mouse model of MND. We found the expression of APLP2 is elevated in the spinal cord from human cases of MND and that this feature of the human disease is reproduced in SOD1-G37R mice at the End-stage of their MND-like phenotype progression. APLP2 deletion in SOD1-G37R mice significantly delayed disease progression and increased the survival of female SOD1-G37R mice. Molecular and biochemical analysis showed female SOD1-G37R:APLP2-/- mice displayed improved innervation of the neuromuscular junction, ameliorated atrophy of muscle fibres with increased APP protein expression levels in the gastrocnemius muscle. These results indicate a sex-dependent role for APLP2 in mutant SOD1-mediated MND and further support the APP family as a potential target for further investigation into the cause and regulation of MND.

Indexed as

Amyloid beta-Protein PrecursorAmyotrophic Lateral SclerosisAnimalsCentral Nervous SystemDisease Models, AnimalFemaleHumansMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMotor Neuron DiseaseMotor NeuronsMuscle Fibers, SkeletalNeuromuscular JunctionPhenotypeAmyloid beta-Protein PrecursorAplp2 protein, mouseSod1 protein, mouseSuperoxide Dismutase-1Amyloid precursor-like proteinAmyloid precursor proteinAmyotrophic lateral sclerosisMotor neuron diseaseSex differencesSOD1-G37R

Identifiers

PMID34476545
PMCPMC8558206
OpenAlexW3150848769

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.