The interplay between oxidative stress and brain‐derived neurotrophic factor modulates the outcome of a saturated fat diet on synaptic plasticity and cognition

TLDR

High saturated‑fat diets lower BDNF, impairing neuroplasticity and cognition, while BDNF normally promotes synaptic function via synapsin I and CREB. The study aimed to determine whether oxidative stress mediates the impact of BDNF on synaptic plasticity and cognition in rats fed a high‑fat diet, using vitamin E as an antioxidant. Rats received a 2‑month high‑fat diet with or without 500 IU/kg vitamin E; vitamin E reduced oxidative damage and restored BDNF, synapsin I, and CREB levels. Vitamin E supplementation reduced oxidative damage, restored BDNF, synapsin I, and CREB levels, preserved their activation, and reversed high‑fat‑diet‑induced cognitive deficits, demonstrating that oxidative stress interacts with the BDNF system to modulate synaptic plasticity and cognition.

Abstract

Abstract A diet high in saturated fat (HF) decreases levels of brain‐derived neurotrophic factor (BDNF), to the extent that compromises neuroplasticity and cognitive function, and aggravates the outcome of brain insult. By using the antioxidant power of vitamin E, we performed studies to determine the role of oxidative stress as a mediator for the effects of BDNF on synaptic plasticity and cognition caused by consumption of the HF diet. Male adult rats were maintained on a HF diet for 2 months with or without 500 IU/kg of vitamin E. Supplementation of the HF diet with vitamin E dramatically reduced oxidative damage, normalized levels of BDNF, synapsin I and cyclic AMP‐response element‐binding protein (CREB), caused by the consumption of the HF diet. In addition, vitamin E supplementation preserved the process of activation of synapsin I and CREB, and reversed the HF‐impaired cognitive function. It is known that BDNF facilitates the synapse by modulating synapsin I and CREB, which have been implicated in synaptic plasticity associated to learning and memory. These results show that oxidative stress can interact with the BDNF system to modulate synaptic plasticity and cognitive function. Therefore, studies appear to reveal a mechanism by which events classically related to the maintenance of energy balance of the cell, such as oxidative stress, can interact with molecular events that modulate neuronal and behavioural plasticity.