Evidence mapPaperPMID 40748432Full record

ReviewMolecular neurobiology2025

Obesity and Cognitive Function: Leptin Role Through Blood-Brain Barrier and Hippocampus.

Ebtesam Abdullah Al-Suhaimi, Abdullah A AlRubaish, Hanan A Aldossary, Mohamed A Homeida, Adeeb Shehzad, Abdelgadir M Homeida

Abstract readReview
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In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. 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.

Ebtesam Abdullah Al-SuhaimiVice presidency for Scientific Research and Innovation, Imam Abdulrahman Bin Faisal University (IAU), P.O. Box 1982, Dammam, 31441, Saudi Arabia. ealsuhaimi@iau.edu.sa.ORCID http://orcid.org/0000-0003-1614-0211
Abdullah A AlRubaishCollege of Medicine, Imam Abdulrahman bin Faisal University (IAU), P.O. Box 1982, Dammam, 31441, Saudi Arabia.
Hanan A AldossaryVice presidency for Scientific Research and Innovation, Imam Abdulrahman Bin Faisal University (IAU), P.O. Box 1982, Dammam, 31441, Saudi Arabia.
Mohamed A HomeidaUniversity Hospitals Cleveland Medical Center, Case Western Reserve University, 11100 Euclid Ave, Cleveland, 44106, OH, USA.
Adeeb ShehzadBiodiversity Unit, Research Center, Dhofar University, Salalah, 211, Oman.
Abdelgadir M HomeidaVice presidency for Scientific Research and Innovation, Imam Abdulrahman Bin Faisal University (IAU), P.O. Box 1982, Dammam, 31441, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The signal transduction and communication between adipose tissue-secreted adipokines and the central nervous system (CNS) are increasingly recognized for their role in metabolic and neurological regulation. This crosstalk contributes to the vulnerability of individuals with obesity to developing cognitive impairment. However, the detailed underlying molecular mechanisms through which obesity-induced peripheral changes influence blood-brain barrier (BBB) and CNS function remain under investigation. Among the key mediators of this interaction are signaling molecules (adipokines) secreted by white adipose tissue that regulate various physiological processes, including energy homeostasis, neural integrity, and immune responses. Obesity is associated with dysregulated leptin secretion due to adipose tissue dysfunction, contributing to metabolic abnormalities and hippocampal synaptic disturbances-factors that increase the risk of comorbid conditions, cognitive decline, and neurodegenerative disorders such as Alzheimer's disease. Additionally, obesity increases inflammatory molecules such as RAGE, LRP1, cytokines (IL-6 and TNF-α), leptin, insulin, and free fatty acids, which perturb amyloid-β degradation and promote accumulation in the brain while impairing brain-to-blood clearance. An electronic search was performed using Web of Science, Scopus, and PubMed to collect English-language articles published from 2010 to 2025 related to the role of leptin in obesity and neurodegenerative diseases. This study underpins recent literature on the mechanisms by which obesity-induced modulation of leptin signaling impacts cognitive decline, BBB dysfunction, and the pathogenesis of Alzheimer's disease. Thus, understanding leptin-driven mechanisms and developing targeted strategies, including leptin sensitization and BBB-protective interventions, could serve as effective therapeutic approaches to managing cognitive impairment associated with obesity.

Indexed as

Blood-Brain BarrierCognitionHippocampusLeptinObesityAnimalsHumansLeptinBlood–brain barrierCognitiveHippocampalLeptinNeuroinflammationObesity

Identifiers

What Socratic 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 Socratic graph.