Evidence map›Paper›PMID 29546689›Full record

ArticleMetabolic brain disease2018

Disruption of leptin signalling in a mouse model of Alzheimer's disease.

Anna King, Anna Brain, Kelsey Hanson, Justin Dittmann, James Vickers, Carmen Fernandez-Martos

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Leptin levels are associated with body mass index and Alzheimer's disease in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Leptin bioavailability and markers of brain atrophy and vascular injury in the middle age.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  4. Article
  5. Article
  6. A Pathophysiological Intersection of Diabetes and Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  7. Review
  8. TNF-Oxidative medicine and cellular longevity · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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 1 institution in 1 country.

Anna KingWicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Private Bag 143, Hobart, TAS, 7000, Australia.
Anna BrainWicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Private Bag 143, Hobart, TAS, 7000, Australia.
Kelsey HansonWicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Private Bag 143, Hobart, TAS, 7000, Australia.
Justin DittmannWicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Private Bag 143, Hobart, TAS, 7000, Australia.
James VickersWicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Private Bag 143, Hobart, TAS, 7000, Australia.
Carmen Fernandez-MartosWicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Private Bag 143, Hobart, TAS, 7000, Australia. Carmen.fernandezmartos@utas.edu.au.ORCID http://orcid.org/0000-0002-6387-4456
University of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of leptin signalling has been implicated as playing a role in the development of Alzheimer's disease (AD). Leptin has previously been shown to be affected by amyloid-beta (Aβ)-related signalling; however, pathways that link leptin to the disease pathogenesis have not been determined. To characterize the association between increasing age-dependent Aβ levels with leptin signalling and the vulnerable brain regions in AD, we assessed the mRNA and protein expression profile of leptin and leptin receptor (Ob-Rb) at 9 and 18-month-age in APP/PS1 mice. Immunohistochemical labelling demonstrated that leptin and Ob-Rb proteins were localised to neocortical and hippocampal neurons in APP/PS1 and wildtype (WT) mice. Neuronal leptin and Ob-Rb immunolabelling was more prominent in the neocortex of both groups at 9 month of age, while, at 18 months, labelling was reduced in the hippocampus of APP/PS1 mice relative to WT. Immunoblotting analysis demonstrated decreased hippocampal leptin levels, concomitantly with an increased Ob-Rb levels, in APP/PS1 mice compared with WT controls at 18 month of age. While no leptin mRNA was found in either of the groups analysed, Ob-Rb mRNA was significantly decreased in the hippocampus of APP/PS1 mice at both ages analysed. In addition, a significant decreased protein kinase B (Akt) activity concomitantly with an upregulation of suppressor of cytokine signaling-3 (SOCS3) and protein-tyrosine phosphatase 1B (PTP1B) transcripts was present. Thus, these results collectively indicate alterations of leptin signalling in the hippocampus of APP/PS1 mice, providing novel insights about the pathways that could link aberrant leptin signaling to the pathological changes of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalHippocampusLeptinMiceMice, TransgenicNeuronsPresenilin-1Receptors, LeptinSignal TransductionAmyloid beta-Protein PrecursorLeptinPresenilin-1Receptors, LeptinAlzheimer’s disease (AD)Amyloid-beta (Aβ)Cognitive declineLeptinLong leptin receptor (Ob-Rb)

Identifiers

PMID29546689
OpenAlexW2793187524

What OpenQuestion holds

Textmetadata
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.