Selenium ameliorates cognitive impairment through activating BDNF/TrkB pathway

Background

Alzheimer's disease (AD) is a neurodegenerative disorder that primarily affects older adults. Selenium, an essential micronutrient for humans, plays a crucial role in the body's normal physiological and metabolic processes. A long-term deficiency in selenium intake can lead to various diseases and even contribute to the ageing process. This study aims to explore the ameliorative effect of selenium on cognitive impairment in 3 × Tg-AD mice and to determine if its effects are related to the BDNF/TrkB pathway.

Methods

We employed the APP/PS1/tau 3 × Tg-AD mouse model for dietary selenium intervention. Behavioural experiments were conducted to assess learning and memory. Additionally, we measured selenium and GSH-Px levels in whole blood and brain tissue. Neuronal apoptosis in the hippocampus was observed using transmission electron microscopy. The expressions of Aβ, P-tau, BDNF, TrkB, and CREB were measured via RT-qPCR, while the expressions of Aβ, P-tau, BDNF, TrkB, p-CREB, and CREB were quantified using Western blot analysis.

Results

Our findings indicate that selenium supplementation can improve spatial learning and memory deficiencies in 3 × Tg-AD mice. Selenium supplementation increased selenium and GSH-Px levels in the brain tissue of 3 × Tg-AD mice and significantly enhanced neuronal conditions. Furthermore, the expression levels of proteins related to the BDNF/TrkB pathway significantly increased following selenium supplementation.

Conclusions

Our study demonstrates that selenium can ameliorate memory impairment in 3 × Tg-AD mice by activating the BDNF/TrkB pathway.