Evidence map›Paper›PMID 24780498›Full record

ReviewNeurobiology of disease2014

Neuroprotective effects of leptin in the context of obesity and metabolic disorders.

Cecilia Davis, Jeremy Mudd, Meredith Hawkins

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Adipokines as Immune Cell Modulators in Multiple Sclerosis.International journal of molecular sciences · 2021
    Review
  11. Metabolic Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Cecilia DavisDiabetes Research Center, Albert Einstein College of Medicine, USA.
Jeremy MuddDiabetes Research Center, Albert Einstein College of Medicine, USA.
Meredith HawkinsDiabetes Research Center, Albert Einstein College of Medicine, USA.
Albert Einstein College of Medicine · US

Funding

Role of Hepatic Fat Metabolism in Glucose EffectivenessR01DK069861 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI HAWKINS, MEREDITH A, ROUTH, VANESSA H · 2006 to 2025
$7.6M
BIOCHEMICAL MECHANISMS OF IN VIVO INSULIN RESISTANCER01DK048321 · NIDDK · YESHIVA UNIVERSITY · PI HAWKINS, MEREDITH A · 1994 to 2008
$3.1M
NIDDK NIH HHS R01 DK048321NIDDK NIH HHS R01 DK069861
6 · The paper itself

Abstract

As the population of the world ages, the prevalence of neurodegenerative disease continues to rise, accompanied by increases in disease burden related to obesity and metabolic disorders. Thus, it will be essential to develop tools for preventing and slowing the progression of these major disease entities. Epidemiologic studies have shown strong associations between obesity, metabolic dysfunction, and neurodegeneration, while animal models have provided insights into the complex relationships between these conditions. Experimentally, the fat-derived hormone leptin has been shown to act as a neuroprotective agent in various animal models of dementia, toxic insults, ischemia/reperfusion, and other neurodegenerative processes. Specifically, leptin minimizes neuronal damage induced by neurotoxins and pro-apoptotic conditions. Leptin has also demonstrated considerable promise in animal models of obesity and metabolic disorders via modulation of glucose homeostasis and energy intake. However, since obesity is known to induce leptin resistance, we hypothesize that resistance to the neuroprotective effects of leptin contributes to the pathogenesis of obesity-associated neurodegenerative diseases. This review aims to explore the literature pertinent to the role of leptin in the protection of neurons from the toxic effects of aging, obesity and metabolic disorders, to investigate the physiological state of leptin resistance and its causes, and to consider how leptin might be employed therapeutically in the prevention and treatment of neurodegenerative disease.

Indexed as

Alzheimer DiseaseAnimalsBrainDisease Models, AnimalHumansHypothalamusLeptinMiceNeuronsNeuroprotective AgentsObesityParkinson DiseaseRatsLeptinNeuroprotective AgentsDiabetesLeptinLeptin resistanceMetabolic disorderNeurodegenerationObesity

Identifiers

PMID24780498
PMCPMC12169508
OpenAlexW2020897081

What OpenQuestion holds

Textmetadata
LicenceTDM
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.