Evidence map›Paper›PMID 27600840›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2017

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin.

Yasaman Malekizadeh, Alison Holiday, Devon Redfearn, James A Ainge, Gayle Doherty, Jenni Harvey

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. Brain-Bone Axis in Physiological and Pathological Conditions.International journal of molecular sciences · 2025
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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

6 authors at 2 institutions in 1 country.

Yasaman MalekizadehDivision of Neuroscience, Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee, DundeeDD1 9SY, UK.
Alison HolidaySchool of Psychology and Neuroscience, St Mary's Quad, University of St Andrews, St Andrews, FifeKY16 9TS, UK.
Devon RedfearnSchool of Psychology and Neuroscience, St Mary's Quad, University of St Andrews, St Andrews, FifeKY16 9TS, UK.
James A AingeSchool of Psychology and Neuroscience, St Mary's Quad, University of St Andrews, St Andrews, FifeKY16 9TS, UK.
Gayle DohertySchool of Psychology and Neuroscience, St Mary's Quad, University of St Andrews, St Andrews, FifeKY16 9TS, UK.
Jenni HarveyDivision of Neuroscience, Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee, DundeeDD1 9SY, UK.
University of St Andrews · GBUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A key pathology of Alzheimer's disease (AD) is amyloid β (Aβ) accumulation that triggers synaptic impairments and neuronal death. Metabolic disruption is common in AD and recent evidence implicates impaired leptin function in AD. Thus the leptin system may be a novel therapeutic target in AD. Indeed, leptin has cognitive enhancing properties and it prevents the aberrant effects of Aβ on hippocampal synaptic function and neuronal viability. However, as leptin is a large peptide, development of smaller leptin-mimetics may be the best therapeutic approach. Thus, we have examined the cognitive enhancing and neuroprotective properties of known bioactive leptin fragments. Here we show that the leptin (116-130) fragment, but not leptin (22-56), mirrored the ability of leptin to promote AMPA receptor trafficking to synapses and facilitate activity-dependent hippocampal synaptic plasticity. Administration of leptin (116-130) also mirrored the cognitive enhancing effects of leptin as it enhanced performance in episodic-like memory tests. Moreover, leptin (116-130) prevented hippocampal synaptic disruption and neuronal cell death in models of amyloid toxicity. These findings establish further the importance of the leptin system as a therapeutic target in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCell DeathCognitionHippocampusHumansLeptinMemoryNeuronal PlasticityNeuronsPeptide FragmentsSynapsesAmyloid beta-PeptidesLeptinleptin (116-130)leptin 22-56Peptide FragmentsAlzheimer's diseaseAMPA receptor traffickingamyloid betaepisodic memoryhippocampussynaptic plasticity

Identifiers

PMID27600840
PMCPMC6433184
OpenAlexW2520040696

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.