# Elucidation of the Neuroprotective Effects of Astaxanthin Against Amyloid β Toxicity in the SH-SY5Y Human Neuroblastoma Cell Line

## TL;DR

This study shows that astaxanthin, a natural compound, can protect brain cells from amyloid beta toxicity, a key factor in Alzheimer's disease.

## Contribution

The study demonstrates the neuroprotective effects of astaxanthin against amyloid β toxicity in a human neuroblastoma cell line.

## Key findings

- Astaxanthin inhibits amyloid β aggregation in a medium-dependent manner in SH-SY5Y cells.
- Astaxanthin prevents amyloid β-induced early apoptosis and restores impaired cell motility.
- Astaxanthin reduces amyloid β fibril formation around cells as shown by Thioflavin T staining.

## Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and cognitive decline, primarily due to amyloid β (Aβ) aggregation in the brain. Astaxanthin (AxN), a xanthophyll carotenoid derived from Haematococcus pluvialis, possesses antioxidant and neuroprotective properties. This study investigated the neuroprotective effects of AxN against Aβ aggregation in human neuroblastoma SH-SY5Y cells. Initially, AxN inhibited Aβ aggregation in DMEM/F12 culture medium but not in PBS, suggesting a medium-dependent effect. Using quantum dot nanoprobes, Aβ aggregation was visualized in the presence of SH-SY5Y cells. AxN treatment (0.032–20 µM) significantly reduced Aβ aggregation and accumulation on SH-SY5Y cells. AxN also prevented Aβ-induced early apoptotic cell death but was less effective against late necrosis. Furthermore, a wound-healing assay showed that AxN restored the impaired cell motility caused by Aβ aggregation. Thioflavin T staining confirmed the reduction in Aβ fibril formation around the cells following AxN treatment. In conclusion, our study suggests that AxN prevents Aβ aggregation and accumulation on the cell surface, thereby restoring cell motility and preventing early apoptosis in neuronal cells.