The rising prevalence of obesity has become a worldwide severe public health problem [1,2]. In recent years, a number of studies have demonstrated that neuronal apoptosis mediated obesity-induced cognitive dysfunction from the perspective of population and animals [3], [4], [5]. Therefore, ameliorating neuronal apoptosis is an effective measure to prevent obesity-induced cognitive dysfunction [6,7].

It has been demonstrated that oxidative stress induced by mitochondrial dysfunction is the main mechanism of apoptosis in neurons [6,8]. Besides the production of ATP, mitochondria is also the source of reactive oxygen species (ROS) and plays an essential role in keeping the balance between oxidation and antioxidation [9]. High fat diet (HFD) induces mitochondrial dysfunction, which contributes to excessive ROS production [10], [11], [12]. The excessive production of ROS activates apoptosis factor like Bak and Bax, resulting in release of cytochrome C into cytoplasm which activates caspase3 and trigger cascade reaction to cause the cell apoptosis ultimately [13,14]. In addition, excess production of ROS leads to lipid peroxidation in mitochondria and cause further mitochondrial impairment to create a vicious circle [15,16]. From the perspective of population and animal study, ameliorating mitochondrial function via adjusting mitochondrial respiratory chain, tricarboxylic acid cycle (TCA) homeostasis and mitochondrial dynamic equilibrium play a vital role in reducing oxidative damage [17], [18], [19], [20]. Therefore, improving mitochondrial function is used as a strategy to attenuate apoptosis in neurons [8,20,21].

Apple are rich in polyphenols and polysaccharides, which were proved to have a broad spectrum of biological properties [22]. Earlier, we found apple pomace polysaccharides had the effect of improving mitochondrial respiratory function, enhancing antioxidant capacity, and inhibiting oxidative stress in mice liver [17]. Moreover, apple polyphenols effectively protect neurons via alleviating and the injury of oxidative stress [23]. Recent studies demonstrated that the polyphenols and polysaccharides in young apples were much higher than those in ripe apples, and notably performed a better antioxidant capacity than ripe apples [24], [25], [26]. Hence, we hypothesized young apple powder (YAP) may prevent abnormal increased neuronal apoptosis. In another aspect, China is the world's largest apple grower and producer, producing more than half the world's apples, two million tons of young apples were produced by thinning. However, these young apples didn't get used fully and it resulted in a large amount of waste [26]. Consequently, thinned young apples have great value and potential for nutritional therapy. Despite this, whether YAP has the preventive effect on neuronal apoptosis is unclear. Based on the above research background, the present study aims to investigate the protective effect of YAP on obesity-induced neuronal apoptosis in mice cerebral cortex.