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Oxytocin is a neuropeptide hormone that plays an important role in social bonding and behavior. Recent studies indicate that oxytocin could be involved in the regulation of neurological disorders. However, its role in modulating cognition in Alzheimer’s disease (AD) has never been explored. Hence, the present study aims to investigate the potential of chronic intranasal oxytocin in halting memory impairment & AD pathology in aluminum chloride-induced AD in female rats. Morris water maze was used to assess cognitive dysfunction in two-time points throughout the treatment period. In addition, neuroprotective effects of oxytocin were examined by assessing hippocampal acetylcholinesterase activity, β-amyloid 1–42 protein, and Tau levels. In addition, ERK1/2, GSK3β, and caspase-3 levels were assessed as chief neurobiochemical mediators in AD. Hippocampi histopathological changes were also evaluated. These findings were compared to the standard drug galantamine alone and combined with oxytocin. Results showed that oxytocin restored cognitive functions and improved animals’ behavior in the Morris test. This was accompanied by a significant decline in acetylcholinesterase activity, 1–42 β-amyloid and Tau proteins levels. Hippocampal ERK1/2 and GSK3β were also reduced, exceeding galantamine effects, thus attenuating AD pathological hallmarks formation. Determination of caspase-3 revealed low cytoplasmic positivity, indicating the ceasing of neuronal death. Histopathological examination confirmed these findings, showing restored hippocampal cells structure. Combined galantamine and oxytocin treatment showed even better biochemical and histopathological profiles. It can be thus concluded that oxytocin possesses promising neuroprotective potential in AD mediated via restoring cognition and suppressing β-amyloid, Tau accumulation, and neuronal death.

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The current study focused on the effect of creatine supplementation with/without exercise on the expression of genes controlling mitochondrial biogenesis in skeletal and cardiac muscles, as well as its safety profile on the liver and kidney. A total of 40 male Wister rats were included in the present study. Two unexercised groups: The control sedentary group and the sedentary creatine-treated group (n=10) were treated daily with oral creatine (0.5 g/kg per day). Two exercised groups performed swimming exercise training 5 days/week for a period of 5 weeks; The Exercise training group, and exercise training and creatine (0.5 g/kg per day) treated group. After sacrifice, blood samples, cardiac and soleus muscles were collected for assessment of mtDNA copy number, gene expression analysis and nuclear extraction for the assay of PGC-1α. The results of the current study demonstrated that, physical activity with short-term creatine supplementation increased all factors of mitochondrial biogenesis, an effect that is devoid of any kidney or liver adverse effects. Further studies are still required to explore the potential of creatine supplementation in ameliorating mitochondrial diseases, including epilepsy, skeletal and cardiac myopathies, hepatopathies and nephropathies.