Evidence map›Paper›PMID 41009474›Full record

ReviewInternational journal of molecular sciences2025

The Interplay of Inflammation and Gut-Microbiota Dysbiosis in Alzheimer's Disease: Mechanisms and Therapeutic Potential.

Hanis Nabilah Abdol Samat, Nurul Nadirah Razali, Hazlina Mahadzir, Tengku Sifzizul Tengku Muhammad, King-Hwa Ling, Nur Izzati Mansor, Shahidee Zainal Abidin

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

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  11. Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  12. Antioxidant and Anti-Inflammatory Activities of Probiotic Strains.International journal of molecular sciences · 2026
    Review
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  14. 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

7 authors.

Hanis Nabilah Abdol SamatFaculty of Science and Marine Environment, Universiti Malaysia Terengganu, Kuala Nerus 21030, Terengganu, Malaysia.
Nurul Nadirah RazaliFaculty of Science and Marine Environment, Universiti Malaysia Terengganu, Kuala Nerus 21030, Terengganu, Malaysia.ORCID 0000-0002-7725-0353
Hazlina MahadzirDepartment of Medicine, Hospital Canselor Tuanku Muhriz, Faculty of Medicine, Universiti Kebangsaan Malaysia, Cheras 56000, Kuala Lumpur, Malaysia.ORCID 0000-0002-8226-9550
Tengku Sifzizul Tengku MuhammadInstitute of Climate Adaptation and Marine Biotechnology, Universiti Malaysia Terengganu, Kuala Nerus 21030, Terengganu, Malaysia.
King-Hwa LingDepartment of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang 43400, Selangor, Malaysia.ORCID 0000-0002-3968-7263
Nur Izzati MansorDepartment of Nursing, Faculty of Medicine, Universiti Kebangsaan Malaysia, Cheras 56000, Kuala Lumpur, Malaysia.
Shahidee Zainal AbidinFaculty of Science and Marine Environment, Universiti Malaysia Terengganu, Kuala Nerus 21030, Terengganu, Malaysia.ORCID 0000-0003-4458-4565

Funding

Ministry of Higher Education FRGS/1/2023/STG01/UMT/02/2
6 · The paper itself

Abstract

Alzheimer's disease (AD) represents a major global health challenge, characterised by progressive neurodegeneration that leads to cognitive decline. Inflammation is a key factor in the pathogenesis of AD, affecting both neuroinflammation and systemic inflammation. In AD, neuroinflammation is marked by the activation of microglia and the release of pro-inflammatory cytokines, which exacerbate neuronal damage and cognitive deficits. Systemic inflammation further compromises the blood-brain barrier (BBB), increasing its permeability and permitting the entry of inflammatory molecules and immune cells into the brain, thereby advancing the disease's hallmark features. Recent studies have elucidated the influence of gut microbiota dysbiosis on AD and inflammation. This imbalance is thought to be associated with alterations in the concentrations of short-chain fatty acids (SCFAs) and bile acids, which can modulate neuroinflammation and contribute to AD pathology. Additionally, imbalances in neurotransmitters resulting from gut microbiota dysbiosis can further disrupt brain function and facilitate AD progression. This review provides an overview of the hypothesis that systemic and central nervous system (CNS) inflammation, together with gut-microbiota dysbiosis, may interact to influence the development and progression of AD.

Indexed as

Alzheimer DiseaseBrain-Gut AxisDysbiosisFatty Acids, VolatileGastrointestinal MicrobiomeNeuroinflammatory DiseasesBile Acids and SaltsBlood-Brain BarrierDisease ProgressionHumansNeurotransmitter AgentsBile Acids and SaltsFatty Acids, VolatileNeurotransmitter AgentsAlzheimer’s diseasegut microbiota dysbiosisgut microbiota metaboliteneuroinflammationsystemic inflammation

Identifiers

PMID41009474
PMCPMC12469281

What Socratic holds

Textmetadata
LicenceCC BY
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.