Evidence map›Paper›PMID 40883862›Full record

ArticleClinical chemistry and laboratory medicine2025

Cerebrospinal fluid leptin in Alzheimer's disease: relationship to plasma levels and to cerebrospinal amyloid.

Elodie Bouaziz-Amar, Jeanne Neez, Fidaa Ibrahim, Matthieu Martinet, Claire Hourregue, Julien Dumurgier, Emmanuel Cognat, Francois Mouton-Liger, Agathe Vrillon, Jacques Hugon and 2 more

Abstract read
In one paragraph

Article in Clinical chemistry and laboratory medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
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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

12 authors.

Elodie Bouaziz-AmarUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Jeanne NeezUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Fidaa IbrahimBiochemistry Department, Lariboisière Hospital GHU AP-HP.Nord, Paris, France.
Matthieu MartinetUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Claire HourregueCognitive Neurology Center, Lariboisière-Fernand Widal Hospital GHU AP-HP.Nord, Paris, France.
Julien DumurgierCognitive Neurology Center, Lariboisière-Fernand Widal Hospital GHU AP-HP.Nord, Paris, France.
Emmanuel CognatUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Francois Mouton-LigerUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Agathe VrillonUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Jacques HugonUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Claire PaquetUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.
Matthieu LilamandUniversité Paris Cité, INSERM Unit UMR S-1144, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDysregulation of brain leptin signaling contributes to Alzheimer's disease (AD) pathophysiology, but plasma leptin may not accurately reflect central nervous system activity. This study examined the correlation between plasma and cerebrospinal fluid (CSF) leptin levels and their relationship with beta-amyloid (Aβ) and tau biomarkers.

methodsCross-sectional analysis of data from cognitively impaired patients from a tertiary memory clinic. All the patients were diagnosed using CSF AD biomarkers. CSF and plasma leptin were measured using standardized immunoassays. The correlation between plasma and CSF leptin levels was studied. CSF leptin levels were compared between patients with positive AD biomarkers (A+T+N+) and neurological controls (A-T-N-). Regression analyses were performed to study the relationship between CSF leptin and CSF amyloid and tau biomarkers, with adjustment for age, gender, body mass index (BMI) and estimated glomerular filtration rate (eGFR).

resultsFinally, 140 participants were included (age 69.8 [1.1], females=47.4 %). CSF and plasma leptin were highly correlated (r=0.79, p=<0.0001). Individuals with AD CSF profile (A+T+N+) showed lower CSF leptin concentrations than their A-T-N- counterparts (74.7 [4.7] vs. 120.9 [11.9] ng/L, p<0.01) and CSF leptin remained associated with ATN profile and more specifically with the amyloid beta ratio after adjusting for confounding factors (β=-0.60, [0.73], p<0.01).

conclusionsCSF leptin levels strongly correlate with plasma leptin and are reduced in individuals with AD biomarker positivity. This suggests plasma leptin may reflect central leptin activity. Our findings support a link between leptin signaling and amyloid deposition in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesLeptinAgedAged, 80 and overBiomarkersCross-Sectional StudiesFemaleHumansMaleMiddle Agedtau ProteinsAmyloid beta-PeptidesBiomarkersLeptintau ProteinsAlzheimer’s diseasebiomarkercerebrospinal fluidleptinmetabolic dysfonction

Identifiers

PMID40883862
PMCPMC12575012

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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.