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Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions
Min‐Young Noh, Hyuk Sung Kwon, Min‐Soo Kwon, Minyeop Nahm, Hee Kyung Jin, Jae‐sung Bae, Seung Hyun Kim. Molecular Neurodegeneration, 2025-07-10
Topic: Brain proteins, microglia and lab models
Recent advances in our understanding of non-cell-autonomous mechanisms in neurodegenerative diseases (NDDs) have highlighted microglial dysfunction as a core driver of disease progression. Conditions such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and frontotemporal dementia (FTD) share features of impaired microglial phagocytosis, chronic neuroinflammation, and metabolic dysregulation. These insights have prompted new therapeutic strategies targeting microglial function and emphasized the need for reliable biomarkers to monitor disease progression and treatment response. Well-established therapeutic targets, such as triggering receptor expressed on myeloid cells 2 (TREM2), progranulin (PGRN), and sortilin (SORT1), along with emerging candidates including LILRB4, P2Y6R, TAM receptors, and neuroinflammation-related markers, are discussed alongside novel blood, cerebrospinal fluid (CSF), and imaging biomarkers. Despite notable progress, many of these biomarkers remain restricted to preclinical studies and face translational challenges due to species-specific differences, lack of standardization, and clinical heterogeneity. Emerging technologies-including single-cell omics, spatial transcriptomics, and artificial intelligence (AI)-driven integration of multimodal data-offer new opportunities to align biomarker profiles with evolving disease states and improve patient stratification. Building on the model of companion diagnostics (CDx) in oncology, integrating multimodal biomarker strategies holds promise for guiding personalized interventions, improving clinical outcomes, and deepening our mechanistic understanding of microglial contributions across the neurodegenerative spectrum.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Noh, M., Kwon, H. S., Kwon, M., Nahm, M., Jin, H. K., Bae, J., et al. (2025). Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-025-00867-4
Vancouver
Noh M, Kwon HS, Kwon M, Nahm M, Jin HK, Bae J, et al. Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions. Molecular Neurodegeneration. 2025. doi:10.1186/s13024-025-00867-4. PMID: 40640892.
BibTeX
@article{noh2025-40640892,
author = {Noh, Min‐Young and Kwon, Hyuk Sung and Kwon, Min‐Soo and Nahm, Minyeop and Jin, Hee Kyung and Bae, Jae‐sung and Kim, Seung Hyun},
title = {{Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions}},
journal = {Molecular Neurodegeneration},
year = {2025},
doi = {10.1186/s13024-025-00867-4},
pmid = {40640892},
url = {https://doi.org/10.1186/s13024-025-00867-4}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- These insights have prompted new therapeutic strategies targeting microglial function and emphasized the need for reliable biomarkers to monitor disease progression and treatment response.
- Well-established therapeutic targets, such as triggering receptor expressed on myeloid cells 2 (TREM2), progranulin (PGRN), and sortilin (SORT1), along with emerging candidates including LILRB4, P2Y6R, TAM receptors, and neuroinflammation-related markers, are discussed alongside novel blood, cerebrospinal fluid (CSF), and imaging biomarkers.
- Despite notable progress, many of these biomarkers remain restricted to preclinical studies and face translational challenges due to species-specific differences, lack of standardization, and clinical heterogeneity.
- Emerging technologies-including single-cell omics, spatial transcriptomics, and artificial intelligence (AI)-driven integration of multimodal data-offer new opportunities to align biomarker profiles with evolving disease states and improve patient stratification.
- Building on the model of companion diagnostics (CDx) in oncology, integrating multimodal biomarker strategies holds promise for guiding personalized interventions, improving clinical outcomes, and deepening our mechanistic understanding of microglial contributions across the neurodegenerative spectrum.
Why it matters
This review discusses microglial dysfunction as a driver of several neurodegenerative diseases and lists therapeutic targets and biomarkers being studied. It notes that many biomarkers remain limited to preclinical studies and face challenges before clinical use, so no treatment is established here.
Study details
- Evidence strengthLow
How this study scored 49/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular Neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2025 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 71 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 23.7 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 5 / 6 | Cited 21.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 3 / 4 | Cited 71 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Seung Hyun Kim: h-index 63 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Hanyang University: institution h-index 548 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40640892) |
| Free to read | 2 / 2 | Free to read |
| Total | 49 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-025-00867-4
- PubMed: 40640892
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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