Betaine Induced Autophagy to Protect Neurons Against Amyloid Beta in Alzheimer’s Disease
preprint
OA: closed
Abstract
Background: Alzheimer disease is a neurodegenerative disease, which is accompanied by the accumulation of amyloid beta and tau hyper phosphorylation. The objective of this study is to investigate amyloid-beta clearance through autophagy in HMC3 cells by betaine. Methods: : In this study HMC3 cells were used. LC3, P62, p-AKT, p-MTOR, Beclin1, ATG 5, ATG 7, ATG 12 and beta-actin were studied by western blot. LC3 was studied by confocal microscopy. Neuroprotection and cell viability were assessed by MTT assay. Confocal microscopy and ELISA studied amyloid-beta clearance. Student's T-test was used to compare the treated vs untreated groups. Results: : We have identified betaine an autophagy inducer in microglia HMC3 cells. We have further tried to establish the mechanism of betaine for autophagy induction. Betaine was able to induce autophagy through the PI3K/AKT pathway. Further, we investigated the clearance of amyloid-beta by betaine through autophagy induction. Betaine was also able to reduce the toxicity of amyloid-beta in human SHSY-5Y cells. A known down of LC3 reverses the protective effect of betaine against amyloid-beta in differentiated SHSY5Y cells. Conclusion: Betaine induced autophagy, clears amyloid-beta and protects SHSY-5Y cells against amyloid-beta. Based on these data, betaine can be further studied for anti-Alzheimer therapy.
My notes (saved in your browser only)
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.
Source provenance
- europepmc
- last seen: 2026-05-19T01:45:01.086888+00:00