Evidence map›Paper›PMID 26993509›Full record

ReviewCellular and molecular neurobiology2016

Leptin Dysfunction and Alzheimer's Disease: Evidence from Cellular, Animal, and Human Studies.

Matthew J McGuire, Makoto Ishii

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 123 citations in OpenAlex.

  1. Trial
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  11. 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
  12. Review
  13. Article
  14. Review
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  16. 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
  17. Article
  18. Article
  19. Review
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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

2 authors at 1 institution in 1 country.

Matthew J McGuireFeil Family Brain and Mind Research Institute, Joan and Sanford I. Weill Medical College of Cornell University, New York, NY, 10065, USA.
Makoto IshiiFeil Family Brain and Mind Research Institute, Joan and Sanford I. Weill Medical College of Cornell University, New York, NY, 10065, USA. mishii@med.cornell.edu.ORCID http://orcid.org/0000-0003-3397-9908
Cornell University · US

Funding

Pathobiology of Hypothalamic and Metabolic Dysfunction in Normal Aging and Alzheimer's DiseaseK08AG051179 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI ISHII, MAKOTO · 2015 to 2019
$864k
NIA NIH HHS K08 AG051179
6 · The paper itself

Abstract

There is accumulating evidence from epidemiological studies that changes in body weight are associated with Alzheimer's disease (AD) from mid-life obesity increasing the risk of developing AD to weight loss occurring at the earliest stages of AD. Therefore, factors that regulate body weight are likely to influence the development and progression of AD. The adipocyte-derived hormone leptin has emerged as a major regulator of body weight mainly by activating hypothalamic neural circuits. Leptin also has several pleotropic effects including regulating cognitive function and having neuroprotective effects, suggesting a potential link between leptin and AD. Here, we will examine the relationship between leptin and AD by reviewing the recent evidence from cellular and animal models to human studies. We present a model where leptin has a bidirectional role in AD. Not only can alterations in leptin levels and function worsen cognitive decline and progression of AD pathology, but AD pathology, in of itself, can disrupt leptin signaling, which together would lead to a downward spiral of progressive neurodegeneration and worsening body weight and systemic metabolic deficits. Collectively, these studies serve as a framework to highlight the importance of understanding the molecular mechanisms underlying the body weight and systemic metabolic deficits in AD, which has the potential to open new avenues that may ultimately lead to novel therapeutic targets and diagnostic tools.

Indexed as

Alzheimer DiseaseAnimalsBody WeightDisease Models, AnimalHumansLeptinNeuroprotective AgentsTranslational Research, BiomedicalLeptinNeuroprotective AgentsAlzheimer’s diseaseAmyloidBody weightLeptinMetabolismTau

Identifiers

PMID26993509
PMCPMC4846558
OpenAlexW2300004503

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.