Home › Research › Risk factors
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease
Guo T, Zhang D, Zeng Y, Huang TY, Xu H, Zhao Y.. Molecular neurodegeneration, 2020-07-16
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is the most common neurodegenerative disorder seen in age-dependent dementia. There is currently no effective treatment for AD, which may be attributed in part to lack of a clear underlying mechanism. Studies within the last few decades provide growing evidence for a central role of amyloid β (Aβ) and tau, as well as glial contributions to various molecular and cellular pathways in AD pathogenesis. Herein, we review recent progress with respect to Aβ- and tau-associated mechanisms, and discuss glial dysfunction in AD with emphasis on neuronal and glial receptors that mediate Aβ-induced toxicity. We also discuss other critical factors that may affect AD pathogenesis, including genetics, aging, variables related to environment, lifestyle habits, and describe the potential role of apolipoprotein E (APOE), viral and bacterial infection, sleep, and microbiota. Although we have gained much towards understanding various aspects underlying this devastating neurodegenerative disorder, greater commitment towards research in molecular mechanism, diagnostics and treatment will be needed in future AD research.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020). Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease. Molecular neurodegeneration. https://doi.org/10.1186/s13024-020-00391-7
Vancouver
Guo T, Zhang D, Zeng Y, Huang TY, Xu H, Zhao Y. Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease. Molecular neurodegeneration. 2020. doi:10.1186/s13024-020-00391-7. PMID: 32677986.
BibTeX
@article{guo2020-32677986,
author = {Guo, T. and Zhang, D. and Zeng, Y. and Huang, T. Y. and Xu, H. and Zhao, Y.},
title = {{Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease}},
journal = {Molecular neurodegeneration},
year = {2020},
doi = {10.1186/s13024-020-00391-7},
pmid = {32677986},
url = {https://doi.org/10.1186/s13024-020-00391-7}
}
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.
Key findings
- There is currently no effective treatment for AD, which may be attributed in part to lack of a clear underlying mechanism.
- Studies within the last few decades provide growing evidence for a central role of amyloid β (Aβ) and tau, as well as glial contributions to various molecular and cellular pathways in AD pathogenesis.
- Herein, we review recent progress with respect to Aβ- and tau-associated mechanisms, and discuss glial dysfunction in AD with emphasis on neuronal and glial receptors that mediate Aβ-induced toxicity.
- We also discuss other critical factors that may affect AD pathogenesis, including genetics, aging, variables related to environment, lifestyle habits, and describe the potential role of apolipoprotein E (APOE), viral and bacterial infection, sleep, and microbiota.
- Although we have gained much towards understanding various aspects underlying this devastating neurodegenerative disorder, greater commitment towards research in molecular mechanism, diagnostics and treatment will be needed in future AD research.
Why it matters
This review describes evidence for roles of amyloid beta, tau, and glial dysfunction in Alzheimer's disease and notes that there is currently no effective treatment. It discusses possible contributing factors such as genetics, aging, environment, lifestyle, APOE, infection, sleep, and microbiota, but reports no treatment, cure, or prevention.
New to this subject? Start with our plain-English guide: Risk factors, ranked →
Study details
- Evidence strengthLow
How this study scored 53/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / 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 | 2 / 5 | 2020 — within 10 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 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 988 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 123.5 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 6 / 6 | Cited 62.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 20 other studies in this library |
| Still being cited | 4 / 4 | Cited 511 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Yingjun Zhao: h-index 40 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Sanford Burnham Prebys Medical Discovery Institute: institution h-index 676 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32677986) |
| Free to read | 2 / 2 | Free to read |
| Total | 53 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-020-00391-7
- PubMed: 32677986
- 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).
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here. Showing 12 of 109.
Later studies that cite this one
20 studies in the alzhub library list this one in their references. Showing the 8 highest-scoring.
Related studies in Risk factors
Also in Risk factors
356 studies in the library are filed under Risk factors with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Risk factors hub.