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Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway
Wani A, Gupta M, Ahmad M, Shah AM, Ahsan AU, Qazi PH, Malik F, Singh G et al.. Autophagy, 2019-04-02
Topic: Brain proteins, microglia and lab models
Imbalance in production and clearance of amyloid beta (Aβ) is the primary reason for its deposition in Alzheimer disease. Macroautophagy/autophagy is one of the important mechanisms for clearance of both intracellular and extracellular Aβ. Here, through screening, we identified alborixin, an ionophore, as a potent inducer of autophagy. We found that autophagy induced by alborixin substantially cleared Aβ in microglia and primary neuronal cells. Induction of autophagy was accompanied by up regulation of autophagy proteins BECN1/Beclin 1, ATG5, ATG7 and increased lysosomal activities. Autophagy induced by alborixin was associated with inhibition of the phosphoinositide 3-kinase (PI3K)-AKT pathway. A knock down of PTEN and consistent, constitutive activation of AKT inhibited alborixin-induced autophagy and consequent clearance of Aβ. Furthermore, clearance of Aβ by alborixin led to significant reduction of Aβ-mediated cytotoxicity in primary neurons and differentiated N2a cells. Thus, our findings put forward alborixin as a potential anti-Alzheimer therapeutic lead. Abbreviations: Aβ: amyloid beta; ALB: alborixin; ATG: autophagy-related; BECN1: beclin 1; DAPI: 4, 6-diamidino-2-phenylindole; DCFH-DA: 2,7-dichlorodihydrofluorescein diacetate; fAβ: fibrillary form of amyloid beta; GFAP: glial fibrillary acidic protein; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MAP2: microtubule-associated protein 2; MTOR: mechanistic target of rapamycin kinase; PTEN: phosphatase and tensin homolog; ROS: reactive oxygen species; SQSTM1: sequestosome 1; TMRE: tetramethylrhodamine, ethyl ester.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wani, A., Gupta, M., Ahmad, M., Shah, A. M., Ahsan, A. U., Qazi, P. H., et al. (2019). Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway. Autophagy. https://doi.org/10.1080/15548627.2019.1596476
Vancouver
Wani A, Gupta M, Ahmad M, Shah AM, Ahsan AU, Qazi PH, et al. Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway. Autophagy. 2019. doi:10.1080/15548627.2019.1596476. PMID: 30894052.
BibTeX
@article{wani2019-30894052,
author = {Wani, A. and Gupta, M. and Ahmad, M. and Shah, A. M. and Ahsan, A. U. and Qazi, P. H. and Malik, F. and Singh, G. and others},
title = {{Alborixin clears amyloid-β by inducing autophagy through PTEN-mediated inhibition of the AKT pathway}},
journal = {Autophagy},
year = {2019},
doi = {10.1080/15548627.2019.1596476},
pmid = {30894052},
url = {https://doi.org/10.1080/15548627.2019.1596476}
}
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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- We found that autophagy induced by alborixin substantially cleared Aβ in microglia and primary neuronal cells.
- Autophagy induced by alborixin was associated with inhibition of the phosphoinositide 3-kinase (PI3K)-AKT pathway.
- Furthermore, clearance of Aβ by alborixin led to significant reduction of Aβ-mediated cytotoxicity in primary neurons and differentiated N2a cells.
- Thus, our findings put forward alborixin as a potential anti-Alzheimer therapeutic lead.
Why it matters
In microglia and neuronal cells, alborixin induced autophagy that cleared amyloid beta and reduced its toxicity, acting through the PI3K-AKT pathway and PTEN. This is laboratory cell work, and the authors describe alborixin only as a potential therapeutic lead, not a proven treatment, cure, or prevention.
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Study details
- Evidence strengthLow
How this study scored 44/100
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 (Autophagy) |
| Journal's citation record | 2 / 4 | Autophagy: journal h-index 240 (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 | 2019 — 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 | 5 / 7 | Cited 130 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 14.4 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 3 / 6 | Cited 7.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 3 / 4 | Cited 51 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Ajay Kumar: h-index 37 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Auburn University: institution h-index 505 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30894052) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 44 / 100 | — |
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Read the original
- DOI: 10.1080/15548627.2019.1596476
- PubMed: 30894052
- Original source →
- Free full text: PubMed Central →
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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