Related Experiment Video
Updated: Dec 28, 2025
An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons
Published on: May 23, 2019
Melatonin affects the release of exosomes and tau-content in in vitro amyloid-beta toxicity model
Mehmet Ozansoy1, Muzaffer Beyza Ozansoy2, Burak Yulug3
1T.C. Istanbul Bahcesehir University, School of Medicine, Dept. of Physiology, Istanbul, Turkey; T.C. Istanbul Medipol University, Regenerative and Restorative Medical Research Center (REMER), Istanbul, Turkey.
Background:
Recent studies have been revealed that oxidative damage is the main cause of aging and age-related neurodegenerative diseases like Alzheimer's disease (AD). Melatonin is secreted from the pineal gland and its secretion has been found to be altered in AD. In the last decade the role of exosomes in spreading toxic proteins and inducing the propagation of diseases like AD has been discussed. However, it is not known how melatonin affects the amount of exosomes released from the cells and the content of the exosomes.
Objective:
Herein, we investigated the possible role of melatonin treatment in the releasing of exosomes and exosomal tau content in an in vitro Aβ toxicity model.
Method:
SH-SY5Y cell line was used. The optimum concentration of Aβ was determined by cell viability and cell proliferation tests. Melatonin (100 µM) was applied before and after Aβ application. Total exosomes isolated from cell culture media were immunoprecipitated. The amount of released exosomes and their tau content were analyzed by Western blots.
Results:
Our data demonstrated for the first time that melatonin treatment clearly affected the amount of released exosomes. It would decrease the amyloid beta load and toxicity by inhibiting exosome release. We also demonstated that melatonin also affected the level of tau carried by exosomes depending on whether melatonin was applied before or after Aβ application.
Conclusion:
It is considered that the effect of melatonin in the release of exosomes and exosomal tau content would contribute the development of therapeutic strategies in AD and related disorders.
Insights
Melatonin treatment impacts exosome release and tau protein content in Alzheimer's disease models. This finding suggests melatonin could be a therapeutic strategy for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Oxidative damage is a key factor in aging and neurodegenerative diseases like Alzheimer's disease (AD).
- Melatonin, a pineal gland hormone, shows altered secretion in AD patients.
- Exosomes are implicated in the spread of toxic proteins and disease propagation in AD.
Purpose of the Study:
- To investigate melatonin's effect on exosome release and exosomal tau content.
- To explore melatonin's role in an in vitro model of amyloid-beta (Aβ) toxicity.
Main Methods:
- Utilized the SH-SY5Y cell line to model Aβ toxicity.
- Determined optimal Aβ concentration via cell viability and proliferation assays.
- Applied melatonin before and after Aβ exposure, then isolated and analyzed exosomes for quantity and tau content using immunoprecipitation and Western blots.
Main Results:
- Melatonin treatment significantly altered the number of exosomes released.
- Melatonin inhibited exosome release, reducing amyloid-beta load and toxicity.
- The effect of melatonin on exosomal tau levels varied based on the timing of application relative to Aβ exposure.
Conclusions:
- Melatonin influences exosome release and their tau protein content.
- These findings may inform the development of therapeutic strategies for Alzheimer's disease and related disorders.
