Evidence map›Paper›PMID 38292430›Full record

ArticleiScience2024

Behavioral, metabolic, and lipidomic characterization of the 5xFADxTg30 mouse model of Alzheimer's disease.

J P S Marshall, K Huynh, G I Lancaster, J Ng, J M Collins, G Pernes, A Liang, T Featherby, N A Mellet, B G Drew and 6 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-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

4 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

16 authors at 5 institutions in 1 country.

J P S MarshallBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
K HuynhBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
G I LancasterBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
J NgSchool of Health Sciences, The University of Tasmania, Launceston, TAS, Australia.
J M CollinsWicking Dementia Research and Education Centre, College of Health and Medicine, University of Tasmania, Hobart, TAS, Australia.
G PernesBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
A LiangBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
T FeatherbyThe Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia.
N A MelletBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
B G DrewBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
A C CalkinBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
A E KingWicking Dementia Research and Education Centre, College of Health and Medicine, University of Tasmania, Hobart, TAS, Australia.
P J MeikleBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
M A FebbraioMonash Institute of Pharmaceutical Sciences, Melbourne, VIC, Australia.
P A AdlardThe Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia.
D C HenstridgeBaker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Baker Heart and Diabetes Institute · AUUniversity of Tasmania · AUFlorey Institute of Neuroscience and Mental Health · AUUniversity of Melbourne · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is associated with both extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles (NFT). We characterized the behavioral, metabolic and lipidomic phenotype of the 5xFADxTg30 mouse model which contains overexpression of both Aβ and tau. Our results independently reproduce several phenotypic traits described previously for this model, while providing additional characterization. This model develops many aspects associated with AD including frailty, decreased survival, initiation of aspects of cognitive decline and alterations to specific lipid classes and molecular lipid species in the plasma and brain. Notably, some sex-specific differences exist in this model and motor impairment with aging in this model does compromise the utility of the model for some movement-based behavioral assessments of cognitive function. These findings provide a reference for individuals interested in using this model to understand the pathology associated with elevated Aβ and tau or for testing potential therapeutics for the treatment of AD.

Indexed as

Animal physiologyBehavioral neuroscienceLipidomicsNeuroscience

Identifiers

PMID38292430
PMCPMC10826307
OpenAlexW4390577190

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.