Evidence map›Paper›PMID 39441400›Full record

ArticlePsychopharmacology2025

Ferulic acid ameliorates bisphenol A (BPA)-induced Alzheimer's disease-like pathology through Akt-ERK crosstalk pathway in male rats.

Mhasen Khalifa, Rabie H Fayed, Yasmine H Ahmed, Mohamed F Abdelhameed, Ahmed F Essa, Heba M A Khalil

Abstract read
In one paragraph

Article in Psychopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Identification of chemicals targeting dementia genes and pathways in the Comparative Toxicogenomics Database.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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.

Mhasen KhalifaDepartment of Veterinary Hygiene and Management, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt. mhasenabdo@cu.edu.eg.
Rabie H FayedDepartment of Veterinary Hygiene and Management, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Yasmine H AhmedCytology and Histology Department, Faculty of Vet. Medicine, Cairo University, Giza, 12211, Egypt.
Mohamed F AbdelhameedPharmacology Department, National Research Centre, 33 El Bohouth St., Dokki, Giza, 12622, Egypt.
Ahmed F EssaDepartment of Natural Compounds Chemistry, National Research Centre, Dokki, Giza, 12622, Egypt.
Heba M A KhalilDepartment of Veterinary Hygiene and Management, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study investigated the neuroprotective effect of ferulic acid (FA) against bisphenol A (BPA) induced Alzheimer's disease-like pathology in male rats.

methodsRats were allocated into four groups, control, BPA, BPA + FA, and FA, respectively, for 40 days. Spatial working memory and recognition memory were evaluated. Moreover, the brain levels of oxidative stress biomarkers, proinflammatory cytokines, extracellular signal-regulated kinase (ERK), and phosphorylated serine/threonine protein kinase (p-Akt) were measured. We also determined the brain neuropathological protein levels, including Beta-Amyloid 1-42, total Tau (tTau), and phosphorylated Tau (pTau) proteins. Furthermore, brain levels of Acetylcholinesterase (AChE) and Beta-secretase (BACE) were assessed. Brain histological investigation and immunohistochemistry determination of glial fibrillar acidic protein (GFAP) were also performed. Moreover, docking simulation was adapted to understand the inhibitory role of FA on AChE, BACE-1, and ERK1/2.

resultsInterestingly, the BPA + FA treated group showed a reversal in the cognitive impairments induced by BPA, which was associated with improved brain redox status. They also exhibited a significant decrease in brain inflammatory cytokines, ERK, and p-Akt levels. Moreover, they revealed a decline in beta-amyloid 1-42 and a significant improvement in tTau expression and pTau protein levels in the brain tissue. Further, the brain levels of AChE and BACE were substantially reduced in BPA + FA rats. The neuroprotective effect of FA was confirmed by restoring the normal architecture of brain tissue, which was associated with decreasing GFAP.

conclusionFA could be a potent neuroprotectant agent against AD with a possible prospect for its therapeutic capabilities and nutritional supplement value due to its antioxidant and antiapoptotic properties.

Indexed as

Alzheimer DiseaseBenzhydryl CompoundsCoumaric AcidsMAP Kinase Signaling SystemNeuroprotective AgentsPhenolsAcetylcholinesteraseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsBisphenol A CompoundsBrainDisease Models, AnimalMaleMemory, Short-TermMolecular Docking SimulationAcetylcholinesteraseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesBenzhydryl Compoundsbisphenol ABisphenol A CompoundsCoumaric Acidsferulic acidNeuroprotective AgentsPhenolsProto-Oncogene Proteins c-akttau ProteinsAChEApoptosisBeta-amyloid 1–42BPAFerulic acidMolecular dockingNeurotoxicityOxidative stressPhosphorylated tau proteinTotal tau protein

Identifiers

PMID39441400
PMCPMC11861243

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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.