Evidence map›Paper›PMID 40316879›Full record

ArticleMolecular neurobiology2025

Dual Mechanism of Docosahexaenoic acid (DHA) in Alzheimer's Disease: PAD4 Inhibition and Autophagy Stimulation.

Haleh Barmaki, Alireza Nourazarian, Hadi Yousefi, Asghar Khalilnezhad, Elham Shahriyari, Fatemeh Khaki-Khatibi

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Article in Molecular neurobiology, 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

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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.

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4 · The record

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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.

Haleh BarmakiStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Alireza NourazarianDepartment of Basic Medical Sciences, Khoy University of Medical Sciences, Khoy, Iran.
Hadi YousefiDepartment of Basic Medical Sciences, Khoy University of Medical Sciences, Khoy, Iran.
Asghar KhalilnezhadDepartment of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey.
Elham ShahriyariDepartment of Medical Biology, Faculty of Medicine, Ege University, Izmir, Turkey.
Fatemeh Khaki-KhatibiStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. fatemehkhakikhatibi@yahoo.com.

Funding

Tabriz University of Medical Sciences IR.TBZMED.VCR.REC.1403.265.
6 · The paper itself

Abstract

Alzheimer's disease (AD), which affects millions globally, is marked by progressive cognitive decline and neurodegeneration driven by protein aggregation and chronic inflammation. Emerging evidence has implicated peptidyl arginine deiminase 4 (PAD4) activity and impaired autophagy as key contributors to disease progression. In this study, we explored the neuroprotective potential of DHA in an in vitro model of AD. DHA was administered before arachidonic acid (AA), a proinflammatory agent that mimics AD-like cellular stress. DHA treatment reduced PAD4 expression, enhanced autophagy-related gene expression, and attenuated inflammatory and oxidative stress markers. It also lowered amyloid-beta accumulation and preserved neuronal integrity. These outcomes suggest a potential dual mechanism by which DHA may influence Alzheimer's-related pathology via PAD4 inhibition and autophagy stimulation in vitro. While these findings offer important mechanistic insights, further validation in animal models and clinical contexts is essential before therapeutic relevance can be confirmed.

Indexed as

Alzheimer DiseaseAutophagyDocosahexaenoic AcidsProtein-Arginine Deiminase Type 4Amyloid beta-PeptidesAnimalsArachidonic AcidHumansNeuronsOxidative StressAmyloid beta-PeptidesArachidonic AcidDocosahexaenoic AcidsProtein-Arginine Deiminase Type 4Alzheimer's diseaseApoptosisAutophagyDocosahexaenoic acidNeuroinflammationPAD4

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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.