There is a growing body of scientific research showing the link between depression and dementia in Alzheimer’s disease (AD). The chronic stress contributes to the formation of oxidative stress in the parts of the brain involved in the development of depression and AD. The scientific literature reports the significant role of antioxidants, which are highly effective in treating these diseases. In this review, we have summarized the relationship between chronic stress, oxidative stress, and the changes in the brain they cause occurring in the brain. Among all the compounds showing antioxidant properties, the most promising results in AD treatment were observed for Vitamin E, coenzyme Q10 (CoQ10), melatonin, polyphenols, curcumin, and selenium. In case of depression treatment, the greatest potential was observed in curcumin, zinc, selenium, vitamin E, and saffron.

The ketogenic diet (KD) is a high-fat, low-carbohydrate and adequate-protein diet that has gained popularity in recent years in the context of neurological diseases (NDs). The complexity of the pathogenesis of these diseases means that effective forms of treatment are still lacking. Conventional therapy is often associated with increasing tolerance and/or drug resistance. Consequently, more effective therapeutic strategies are being sought to increase the effectiveness of available forms of therapy and improve the quality of life of patients. For the moment, it seems that KD can provide therapeutic benefits in patients with neurological problems by effectively controlling the balance between pro- and antioxidant processes and pro-excitatory and inhibitory neurotransmitters, and modulating inflammation or changing the composition of the gut microbiome. In this review we evaluated the potential therapeutic efficacy of KD in epilepsy, depression, migraine, Alzheimer’s disease and Parkinson’s disease. In our opinion, KD should be considered as an adjuvant therapeutic option for some neurological diseases.

The NOP receptor, the fourth member of the opioid receptor family, is found throughout the brain and in the periphery. This receptor is particularly abundant in the trigeminal ganglia and trigeminal nucleus caudalis (TNC), regions intimately involved in cephalic pain, including migraine. Because NOP receptor activation reduces neuronal firing, we have hypothesized that a NOP receptor agonist will block migraine pain and other migraine-associated phenomena such as photophobia. Here we examined the effect of the selective NOP receptor agonist Ro 64-6198 on migraine symptoms induced by systemic administration of both acute and chronic treatment with the migraine-related peptide CGRP. A single injection of CGRP was more effective in inducing periorbital allodynia in male than female mice and this was dose-dependently blocked by Ro 64-6198 (0.3 and 1.0 mg/kg). In female mice chronic treatment (daily for four days) with CGRP induced periorbital sensitivity that lasts at least 24 h after administration and both 0.3 and 1.0 mg/kg Ro 64-6198 blocked both the acute pain and the development of chronic pain. CGRP-induced sensitivity to light (photophobia) was also reversed by 0.3 mg/kg of Ro 64-6198. Ro 64-6198 was not able to block CGRP-induced decrease in locomotion or time spent in the middle of an open field, an indication of anxiety. Finally, Ro 64-6198 also reduced cellular activation in the TNC in CGRP-treated but not vehicle-treated mice suggesting inhibition mostly of CGRP-activated cells. These results suggest that a NOP receptor agonist could be an effective treatment for migraine or other cephalic pain syndromes.