# Behavioral, Histopathological, and Biochemical Implications of Aloe Emodin in Copper-Aβ-Induced Alzheimer’s Disease-like Model Rats

## TL;DR

Aloe emodin, a compound from rhubarb, may help treat Alzheimer’s disease by reducing brain copper levels and beta-amyloid buildup in rat models.

## Contribution

This study demonstrates aloe emodin’s novel ability to target copper-induced Aβ toxicity in Alzheimer’s disease models.

## Key findings

- Aloe emodin reduced copper accumulation and regulated Aβ metabolism in rat brain tissues.
- Treatment improved memory impairment and hippocampal nerve cell damage in model rats.
- Biochemical indicators of Aβ pathology were ameliorated by aloe emodin treatment.

## Abstract

Simultaneously inhibiting beta-amyloid protein (Aβ) aggregation and reducing metal ion overload in the brain is a promising strategy for treating Alzheimer’s disease (AD). Aloe emodin (AE) is one of the major components of the traditional Chinese medicine rhubarb. Based on its reported pharmacological effects and its structural affinity for metal ions, this study aims to explore the potential of AE in improving AD pathology. Through the injection of Aβ or copper-Aβ complex in the bilateral hippocampus of rats, we constructed two kinds of nontransgenic animal models. Behavioral tests were used to evaluate cognitive impairment, and the effects of AE on neuronal damage and Aβ deposition were measured via Nissl staining and immunohistochemistry. Furthermore, we detected copper content in the serum and brain tissues as well as some biochemical indexes of Aβ cascade pathology in the brain tissues of model rats to explore the mechanism of action. AE treatment decreased copper accumulation and regulated Aβ metabolism in the brain of model rats, thereby improving Aβ deposition, memory impairment, hippocampal nerve cell damage, and related biochemical indicators. AE ameliorated the AD pathology of the model rats by targeting copper-induced Aβ toxicity, revealing a mechanism of action by which AE may exhibit good clinical efficacy in treating AD.