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37/100

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer's disease (AD) is the most common cause of dementia. Recent studies have revealed incontrovertible roles of astrocytes in the pathology of AD. Considering the conflicting behaviours of astrocytes in AD brain, they have been proposed to have subtypes. In this study, astrocytes from two publicly available single-nuclei transcriptome datasets were integrated to provide in-depth characterization of astrocyte subtypes in AD. Differentially expressed genes within each astrocyte subtype were analyzed by mapping them onto a human protein-protein interaction network to discover subnetworks with biologically relevant genes. Integrating single-nuclei datasets and using network-based analysis approach led to higher sensitivity in capturing AD-related genes compared to traditional approaches. One of the identified subtypes was highly representative of neurotoxic reactive astrocytes in AD. The results show that A1 reactive astrocytes could have an enhancing role for the amyloid beta and neurofibrillary tangle accumulation through MAPK10, MAPT, and TMED10, which were all found to be differentially expressed in this subtype during AD in our analysis. Moreover, single-nuclei ATAC-Seq data from the same tissue was re-analyzed to evaluate astrocyte subtypes at multi-omic level. It was found that astrocyte subtypes underwent epigenetic reprogramming during AD. Potential transcription factors were also identified for the regulation of the genes that exhibited alterations in both promoter accessibility and gene expression in AD. Comparative analysis of single-nuclei RNA-Seq and ATAC-Seq datasets showed that PTN gene, which was reported to be important for AD pathology, is likely regulated by ATF3 transcription factor in subtype-specific manner in astrocytes.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

İlgün, A., & Çakır, T. (2025). Functional Specificity of Astrocyte Subtypes in Alzheimer’s Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data. Molecular Neurobiology. https://doi.org/10.1007/s12035-025-04965-8

Vancouver

İlgün A, Çakır T. Functional Specificity of Astrocyte Subtypes in Alzheimer’s Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data. Molecular Neurobiology. 2025. doi:10.1007/s12035-025-04965-8. PMID: 40301248.

BibTeX

@article{ilgun2025-40301248,
  author  = {İlgün, Atılay and Çakır, Tunahan},
  title   = {{Functional Specificity of Astrocyte Subtypes in Alzheimer’s Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data}},
  journal = {Molecular Neurobiology},
  year    = {2025},
  doi     = {10.1007/s12035-025-04965-8},
  pmid    = {40301248},
  url     = {https://doi.org/10.1007/s12035-025-04965-8}
}

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Key findings

Recent studies have revealed incontrovertible roles of astrocytes in the pathology of AD.
Integrating single-nuclei datasets and using network-based analysis approach led to higher sensitivity in capturing AD-related genes compared to traditional approaches.
The results show that A1 reactive astrocytes could have an enhancing role for the amyloid beta and neurofibrillary tangle accumulation through MAPK10, MAPT, and TMED10, which were all found to be differentially expressed in this subtype during AD in our analysis.
Comparative analysis of single-nuclei RNA-Seq and ATAC-Seq datasets showed that PTN gene, which was reported to be important for AD pathology, is likely regulated by ATF3 transcription factor in subtype-specific manner in astrocytes.

Why it matters

Using existing single-nuclei datasets, this analysis identified an astrocyte subtype that may promote amyloid beta and neurofibrillary tangle accumulation through specific genes. This is a data analysis study, so it does not provide a treatment or prevention for Alzheimer's disease.

Study details

Evidence strengthLow

How this study scored 37/100

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 Neurobiology)
Journal's citation record	2 / 4	Molecular Neurobiology: journal h-index 176 (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	2 / 7	Cited 9 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	3.0 citations a year over 3 year(s) since 2025
Impact for its field and year	3 / 6	Cited 4.9× 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	1 / 4	Cited 9 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Tunahan Çakır: h-index 19 (OpenAlex, whole career)
Institution's track record	0 / 3	Gebze Technical University: institution h-index 219 (OpenAlex)
Multicenter collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 40301248)
Free to read	2 / 2	Free to read
Total	37 / 100	—

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