Effect of exercise on the hypothalamic-pituitary-gonadal axis in a rat model of Alzheimer's disease.

Hypothalamic-pituitary-gonadal (HPG) axis dysregulation was suggested to play a crucial role in Alzheimer's disease (AD). This study investigated the effects of exercise on HPG hormones in an AD rat model, as a possible mechanism underlying the favorable effect of exercise on AD. Forty male Wistar albino rats 2-3 months old were subdivided randomly into two groups (n = 20 each): AD group (injected intraperitoneally with aluminum chloride (70 mg/kg/day) for 6 weeks) and Control group. Each group was subdivided into exercised or non-exercised group (n = 10 each). Exercised groups were subjected to a swimming protocol (60 min/day, 5 days/week, 4 weeks). Serum HPG hormones, hippocampal ß-amyloid levels and Morris water-maze cognition were assessed. Results demonstrated higher levels of ß-amyloid, gonadotropin releasing hormone (GnRH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) together with lower testosterone levels and cognitive impairment in the AD rats compared to controls. Β-amyloid levels negatively correlated with testosterone levels and positively correlated with GnRH, LH and FSH among the AD rats. Higher testosterone and lower GnRH, LH, FSH and ß-amyloid levels, as well as cognitive improvement, were observed in the exercised compared to non-exercised AD rats, suggesting a modulatory role of exercise training on AD-associated HPG axis dysregulation.

Modulatory effects of swimming exercise against malathion induced neurotoxicity in male and female rats.

Malathion is one of the most commonly used organophosphorus (OP) pesticides. It is important to regard that exposure to OP poisoning may cause anxiety and depression. Malathion toxicity induces cholinergic symptoms. Brain-derived neurotrophic factor (BDNF) is the most profusely expressed neurotrophin in the central nervous system; it promotes the survival of neurons. Regular exercise improves brain well-being and enhances recovery from brain Injuries. It is suggested that BDNF may mediate these effects. Therefore, this study was planned to assess the modulatory effects of regular exercise performance on brain BDNF level, cholinergic activity, oxidative stress and apoptosis in male and female rats subjected to neurotoxicity induced by malathion administration. MATERIALS AND METHODS: Thirty-two adult male and thirty-two adult female albino rats were included in this study. The rats were divided into four equal groups (8rats). Control group, malathion treated group, exercised group, malathion exercised group. Acetylcholinesterase (AchE) activity, total antioxidant capacity (TAC), BDNF level and Caspase 3 activity were assessed. RESULTS: Female rats had higher baseline content of BDNF in brain homogenate than male rats. Malathion administration induced a significant decrease in BDNF level in female rats and in the total antioxidant capacity in both male and female rats. A significant elevation in caspase 3 activity was detected in the malathion treated groups, with more elevation in female rats. Swimming exercise improved BDNF level, AchE activity, and apoptosis in both male and female rats in all groups. In addition, male rats were more cholinergic system responders to regular exercise than female rats. CONCLUSION: It could be concluded that malathion induced elevation in oxidative stress and apoptosis in all rats, with reduction in BDNF level in female rats. Meanwhile, regular swimming exercise was found to improve brain health through modulation of BDNF level and cholinergic activity. It is recommended to practice regular exercise to maintain brain health. Further studies are required to clarify the involvement of sex hormones in BDNF regulation.