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Potential Molecular Mechanisms of Alzheimer's Disease from Genetic Studies
Nwadiugwu M, Shen H, Deng HW.. Biology, 2023-04-15
Topic: Amyloid, tau and blood-test diagnosis
The devastating effects of Alzheimer's disease (AD) are yet to be ameliorated due to the absence of curative treatment options. AD is an aging-related disease that affects cognition, and molecular imbalance is one of its hallmarks. There is a need to identify common causes of molecular imbalance in AD and their potential mechanisms for continuing research. A narrative synthesis of molecular mechanisms in AD from primary studies that employed single-cell sequencing (scRNA-seq) or spatial genomics was conducted using Embase and PubMed databases. We found that differences in molecular mechanisms in AD could be grouped into four key categories: sex-specific features, early-onset features, aging, and immune system pathways. The reported causes of molecular imbalance were alterations in bile acid (BA) synthesis, PITRM1, TREM2, olfactory mucosa (OM) cells, cholesterol catabolism, NFkB, double-strand break (DSB) neuronal damage, P65KD silencing, tau and APOE expression. What changed from previous findings in contrast to results obtained were explored to find potential factors for AD-modifying investigations.
Key findings
- We found that differences in molecular mechanisms in AD could be grouped into four key categories: sex-specific features, early-onset features, aging, and immune system pathways.
- What changed from previous findings in contrast to results obtained were explored to find potential factors for AD-modifying investigations.
Why it matters
This review pulled together studies that used single-cell or spatial genetic profiling of Alzheimer's brain tissue. It grouped the molecular differences into four areas: sex-specific features, early-onset features, aging and immune pathways, and listed reported drivers such as TREM2, PITRM1, cholesterol breakdown, tau and APOE expression. The authors offer these as leads for future disease-modifying research rather than tested treatments.
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Study details
- Study designsystematic review
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal, and it is a systematic review of all the studies on the question. Scored zero for sample size, effect reported and studied in people because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Biology) |
| Journal's citation record | 1 / 4 | Biology: journal h-index 134 (OpenAlex, 2026-10-29) |
| Study design | 12 / 12 | A systematic review of all the studies on the question |
| 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 | 3 / 5 | 2023 — within 6 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) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | 2 / 7 | Cited 7 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.4 citations a year over 5 year(s) since 2023 |
| Impact for its field and year | 2 / 6 | Cited 1.0× 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 7 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Hong‐Wen Deng: h-index 82 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Tulane University: institution h-index 735 (OpenAlex) |
| Multi-centre 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 37106802) |
| Free to read | 2 / 2 | Free to read |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Nwadiugwu, M., Shen, H., & Deng, H. W. (2023). Potential Molecular Mechanisms of Alzheimer's Disease from Genetic Studies. Biology. https://doi.org/10.3390/biology12040602
Vancouver
Nwadiugwu M, Shen H, Deng HW. Potential Molecular Mechanisms of Alzheimer's Disease from Genetic Studies. Biology. 2023. doi:10.3390/biology12040602. PMID: 37106802.
BibTeX
@article{nwadiugwu2023-37106802,
author = {Nwadiugwu, M. and Shen, H. and Deng, H. W.},
title = {{Potential Molecular Mechanisms of Alzheimer's Disease from Genetic Studies}},
journal = {Biology},
year = {2023},
doi = {10.3390/biology12040602},
pmid = {37106802},
url = {https://doi.org/10.3390/biology12040602}
}
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.