Evidence map›Paper›PMID 42943300›Full record

ReviewPharmaceuticals (Basel, Switzerland)2026

Microglial Therapeutic Potential in Alzheimer's Disease: From Phenotypic Diversity to Targeted Interventions.

Maria-Raluca Gogu, Ivona Mazarianu, Gabriela-Dumitrita Stanciu, Bogdan-Ionel Tamba, Mitica Ciorpac, Dragos-Lucian Gorgan

Abstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Maria-Raluca GoguDepartment of Biology, Faculty of Biology, Alexandru Ioan Cuza University of Iasi, 700506 Iasi, Romania.ORCID 0009-0006-0906-3499
Ivona MazarianuAdvanced Research and Development Center for Experimental Medicine "Prof. Ostin C. Mungiu", Grigore T. Popa University of Medicine and Pharmacy Iasi, 700454 Iasi, Romania.ORCID 0009-0003-6396-0105
Gabriela-Dumitrita StanciuAdvanced Research and Development Center for Experimental Medicine "Prof. Ostin C. Mungiu", Grigore T. Popa University of Medicine and Pharmacy Iasi, 700454 Iasi, Romania.ORCID 0000-0003-4440-9628
Bogdan-Ionel TambaAdvanced Research and Development Center for Experimental Medicine "Prof. Ostin C. Mungiu", Grigore T. Popa University of Medicine and Pharmacy Iasi, 700454 Iasi, Romania.ORCID 0000-0001-9868-1999
Mitica CiorpacDepartment of Biology, Faculty of Biology, Alexandru Ioan Cuza University of Iasi, 700506 Iasi, Romania.ORCID 0000-0001-5374-0908
Dragos-Lucian GorganDepartment of Biology, Faculty of Biology, Alexandru Ioan Cuza University of Iasi, 700506 Iasi, Romania.ORCID 0000-0001-6454-9092

Funding

This work was supported by a grant of the Ministry of Education and Research, CCCDI - UEFISCDI project number PN-IV-P6-6.1-CoEx-2024-0141, within PNCDI IV
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) deposition, tau pathology and cognitive decline. Increasing evidence from genetic, transcriptomic, experimental and clinical studies has identified microglia as key regulators of AD pathogenesis. Under physiological conditions, microglia maintain central nervous system homeostasis through immune surveillance, phagocytosis and neurotrophic support. However, persistent exposure to pathological stimuli promotes a shift toward dysfunctional inflammatory states that contribute to neuroinflammation, synaptic impairment, tau propagation and neurodegeneration. Recent advances have revealed substantial microglial heterogeneity, highlighting the existence of dynamic and disease stage-dependent activation states rather than fixed phenotypes. In early disease stages, microglia can promote Aβ clearance and tissue repair, whereas chronic activation may exacerbate pathological processes. These findings have driven the development of microglia-targeted therapeutic strategies aimed at enhancing protective functions while limiting maladaptive inflammatory responses. This review summarizes current knowledge regarding microglial involvement in AD and discusses emerging therapeutic approaches, ranging from immunomodulation and metabolic reprogramming to gene-based and nanotechnology-driven interventions, with a focus on their translational potential.

Indexed as

Alzheimer’s diseasedisease-associated microgliamicrogliamicroglia-targeted therapiesneurodegenerationneuroinflammationtau pathologyβ-amyloid

Identifiers

PMID42943300
PMCPMC13708539

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.