Effects of Avocado Oil Supplementation on Insulin Sensitivity, Cognition, and Inflammatory and Oxidative Stress Markers in Different Tissues of Diet-Induced Obese Mice.

Obesity induces insulin resistance, chronic inflammation, oxidative stress, and neurocognitive impairment. Avocado oil (AO) has antioxidants and anti-inflammatory effects. This study evaluated the effect of AO supplementation on obese mice in the adipose tissue, muscle, liver, and hippocampus. Male C57BL/6J mice received a standard and high-fat diet (20 weeks) and then were supplemented with AO (4 mL/kg of body weight, 90 days) and divided into the following groups: control (control), control + avocado oil (control + AO), diet-induced obesity (DIO), and diet-induced obesity + avocado oil (DIO + AO) (n = 10/group). AO supplementation was found to improve insulin sensitivity and decrease hepatic fat accumulation and serum triglyceride levels in DIO mice. AO improved cognitive performance and did not affect mood parameters. Oxidative marker levels were decreased in DIO + AO mice in all the tissues and were concomitant with increased catalase and superoxide dismutase activities in the epididymal adipose tissue and quadriceps, as well as increased catalase activity in the liver. AO in obese animals further induced reductions in TNF-α and IL-1ß expressions in the epididymal adipose tissue and quadriceps. These results suggest that AO supplementation has the potential to be an effective strategy for combating the effects of obesity in rats, and human studies are needed to confirm these findings.

Physical Exercise Training Improves Judgment and Problem-Solving and Modulates Serum Biomarkers in Patients with Alzheimer's Disease.

Alzheimer's disease (AD) is characterized by progressive impairment of memory, with an etiology involving oxidative stress and inflammation. Exercise training is a safe, efficacious, and economic approach to manage neurodegenerative diseases. In AD, the biomarkers of oxidative damage to lipids, proteins, and DNA are elevated. In the present study, we aimed to evaluate whether exercise is effective in patients with AD by assessing the serum biomarkers associated with the redox status, neurotrophin levels, and inflammatory system. This nonrandomized clinical study (n = 15) involved 22 training sessions performed twice a week (60 min/session) in patients diagnosed with AD. The cognitive and self-awareness tests were performed 48 h before and after the physical training session. In patients with AD, physical training significantly improved the judgment and problem-solving domains of the memory score; however, general mental health, memory, orientation, and home/hobby domains were improved slightly, and the neurotrophin levels remained unaltered. Significantly, the markers of protein integrity also increased following exercise. Furthermore, catalase activity and ROS levels decreased, nitrite levels increased, and interleukin-4 level increased following physical training in patients with AD. Although proinflammatory cytokines remained unaltered, the levels of neuron-specific enolase, a marker of neuronal damage, decreased following exercise training in these patients. In conclusion, physical exercise training could be a safe and effective method for blocking the AD progression and improving the antioxidant capacity and anti-inflammatory system, whereas certain assessed biomarkers could be utilized to monitor AD therapy.

Gold Nanoparticles Treatment Reverses Brain Damage in Alzheimer's Disease Model.

Alzheimer's disease (AD) is characterized by amyloid (A)ß peptide accumulation and intracellular neurofibrillary tangles. New hypotheses have suggested that AD involves neuroinflammation and oxidative stress. Gold nanoparticles (AuNP) presents anti-inflammatory and antioxidant characteristics. The present study evaluated the AuNP treatment on an AD model (okadaic acid, OA). Male Wistar rats were injected intracerebroventricularly with OA (100 µg); 24 h later they were treated with 20-nm AuNP (at a dose 2.5 mg/kg) every 48 h for 21 days. The following groups were separated (n = 12/group): Sham, AuNP, OA, and OA + AuNP. OA increases Tau phosphorylation in the cortex and hippocampus, while AuNP treatment maintained it as normal. Spatial memory was impaired by OA, and AuNP treatment prevented this deficit. Neurotrophic factors (BDNF and NGF- ß) in the cortex and hippocampus were decreased by OA. The OA and OA + AuNP groups showed increased interleukin (IL)-1 ß in the hippocampus and cortex, and the AuNP group showed increased IL-1 ß in the hippocampus. In both groups, S100 levels in the cortex and hippocampus were increased by OA. IL-4 was increased in OA + AuNP animals. AuNPs prevented oxidative stress (sulfhydryl and nitrite levels) in brain structures induced by OA. Moreover, OA modulated ATP synthase activity, and AuNP maintained normal brain mitochondrial function. The antioxidant capacities were reduced by OA, and AuNP restored antioxidant status (SOD, catalase activities and GSH levels) on brain. OA-induced damage on brain tissues, and long-term AuNP treatment prevented the neuroinflammation, modulation of mitochondrial function, and impaired cognition induced by AD model, showing that AuNPs may be a promising treatment for neurodisease caused by these elements.