Evidence map›Paper›PMID 40381069›Full record

ReviewMetabolic brain disease2025

Microglial activation as a hallmark of neuroinflammation in Alzheimer's disease.

Rasoul Ebrahimi, Shahrzad Shahrokhi Nejad, Mahdi Falah Tafti, Zahra Karimi, Seyyedeh Reyhaneh Sadr, Dana Ramadhan Hussein, Niki Talebian, Khadijeh Esmaeilpour

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Review
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  7. New Oligophenalenone Dimers fromMolecules (Basel, Switzerland) · 2026
    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

8 authors.

Rasoul Ebrahimi *School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0004-0991-7752
Shahrzad Shahrokhi Nejad *School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0002-6865-3481
Mahdi Falah Tafti *Student Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0001-6320-5466
Zahra KarimiRoss and Carol Nese College of Nursing, Pennsylvania State University, University Park, PA, USA.ORCID 0009-0000-5051-9124
Seyyedeh Reyhaneh SadrStudent Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0002-2918-9356
Dana Ramadhan HusseinSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0009-0009-9896-9752
Niki TalebianStudent Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-7304-3621
Khadijeh EsmaeilpourDepartment of Psychology, University of Toronto Mississagua, Mississauga, ON, Canada. Kh.esmaeilpour@utoronto.ca.ORCID 0000-0002-5349-9285

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglial activation has emerged as a hallmark of neuroinflammation in Alzheimer's disease (AD). Central to this process is the formation and accumulation of amyloid beta (Aβ) peptide and neurofibrillary tangles, both of which contribute to synaptic dysfunction and neuronal cell death. Aβ oligomers trigger microglial activation, leading to the release of pro-inflammatory cytokines, which further exacerbates neuroinflammation and neuronal damage. Importantly, the presence of activated microglia surrounding amyloid plaques is correlated with heightened production of cytokines such as interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α), creating a vicious cycle of inflammation. While microglia play a protective role by clearing Aβ plaques during the early stages of AD, their chronic activation can lead to detrimental outcomes, including enhanced tau pathology and neuronal apoptosis. Recent studies have highlighted the dualistic nature of microglial activation, showcasing both inflammatory (M1) and anti-inflammatory (M2) phenotypes that fluctuate based on the surrounding microenvironment. Disruption in microglial function and regulation can lead to neurovascular dysfunction, further contributing to the cognitive decline seen in AD. Moreover, emerging biomarkers and imaging techniques are unveiling the complexity of microglial responses in AD, providing avenues for targeted therapeutics aimed at modulating these cells. Understanding the intricate interplay between microglia, Aβ, and tau pathology is vital for developing potential interventions to mitigate neuroinflammation and its impact on cognitive decline in AD. This review synthesizes current findings regarding microglial activation and its implications for AD pathogenesis, offering insights into future therapeutic strategies.

Indexed as

Alzheimer DiseaseMicrogliaNeuroinflammatory DiseasesAmyloid beta-PeptidesAnimalsHumansInflammationPlaque, AmyloidAmyloid beta-PeptidesAlzheimer’s diseaseMicrogliaNeuroinflammationReview

Identifiers

PMID40381069

What OpenQuestion 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 OpenQuestion graph.