Evidence map›Paper›PMID 39800461›Full record

ReviewThe journal of prevention of Alzheimer's disease2025

Microglial activation states and their implications for Alzheimer's Disease.

Zachary Valiukas, Kathy Tangalakis, Vasso Apostolopoulos, Jack Feehan

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The journal of prevention of Alzheimer's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing 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

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

  1. Pooled it
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  7. Investigation of the Potential Neuroprotective Mechanisms ofInternational journal of molecular sciences · 2026
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17 more citing papers are in PubMed but not listed here.

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

4 authors.

Zachary ValiukasInstitute for Health and Sport, Victoria University, 70/104 Ballarat Road, Footscray VIC 3011, Australia.
Kathy TangalakisFirst Year College, Victoria University, 70/104 Ballarat Road, Footscray VIC 3011, Australia.
Vasso ApostolopoulosSchool of Health and Biomedical Sciences, RMIT University, 220 3-5 Plenty Road, Bundoora VIC 3082, Australia. Electronic address: vasso.apostolopoulos@rmit.edu.au.
Jack FeehanSchool of Health and Biomedical Sciences, RMIT University, 220 3-5 Plenty Road, Bundoora VIC 3082, Australia. Electronic address: Jack.Feehan@rmit.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is a chronic neurodegenerative disorder characterized by the accumulation of toxic amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) of tau protein in the brain. Microglia, key immune cells of the central nervous system, play an important role in AD development and progression, primarily through their responses to Aβ and NFTs. Initially, microglia can clear Aβ, but in AD, chronic activation overwhelms protective mechanisms, leading to sustained neuroinflammation that enhances plaque toxicity, setting off a damaging cycle that affects neurons, astrocytes, cerebral vasculature, and other microglia. Current AD treatments have been largely ineffective, though emerging immunotherapies focusing on plaque removal show promise, but often overlook the role of neuroinflammation. Activated microglia display a complex range of phenotypes that can be broadly broken into pro- or anti-inflammatory states, although this dichotomy does not describe the significant overlap between states. Aβ can strongly induce inflammatory activity, triggering the production of reactive oxygen species, inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6), synapse engulfment, blood-brain barrier compromise, and impaired Aβ clearance. These processes contribute to neural tissue loss, manifesting as cognitive decline such as impaired executive function and memory. Conversely, anti-inflammatory activation exerts neuroprotective effects by suppressing inflammatory pathways and releasing neurotrophic factors that aid neuron repair and protection. Induction of anti-inflammatory states may offer a dual therapeutic approach to address both neuroinflammation and plaque accumulation in AD. This approach suggests potential strategies to modulate microglial phenotypes, aiming to restore neuroprotective functions and mitigate disease progression by simultaneously targeting inflammation and plaque pathology.

Indexed as

Alzheimer DiseaseMicrogliaAmyloid beta-PeptidesAnimalsBrainHumansNeurofibrillary TanglesNeuroinflammatory DiseasesPlaque, AmyloidAmyloid beta-PeptidesAlzheimer's DiseaseAmyloid BetaMicrogliaNeuroinflammationTau

Identifiers

PMID39800461
PMCPMC12184064

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.