"Always Look on the Bright Side of Life!" - Higher Hypomania Scores Are Associated with Higher Mental Toughness, Increased Physical Activity, and Lower Symptoms of Depression and Lower Sleep Complaints.

Background: In the present study, we explored the associations between hypomania, symptoms of depression, sleep complaints, physical activity and mental toughness. The latter construct has gained interest for its association with a broad variety of favorable behavior in both clinical and non-clinical samples. Subjects and Methods: The non-clinical sample consisted of 206 young adults (M = 21.3 years; age range: 18-24 years; 57.3% males). They completed questionnaires covering hypomania, mental toughness, symptoms of depression, physical activity, and sleep quality. Results: Higher hypomania scores were associated with higher mental toughness, increased physical activity, lower symptoms of depression and lower sleep complaints. No gender differences were observed. Higher hypomania scores were predicted by higher scores of mental toughness subscales of control and challenge, and physical activity. Conclusion: The pattern of results suggests that among a non-clinical sample of young adults, self-rated hypomania scores were associated with higher scores on mental toughness and physical activity, along with lower depression and sleep complaints. The pattern of results further suggests that hypomania traits are associated with a broad range of favorable psychological, behavioral and sleep-related traits, at least among a non-clinical sample of young adults.

Neurogenesis and increase in differentiated neural cell survival via phosphorylation of Akt1 after fluoxetine treatment of stem cells.

Fluoxetine (FLX) is a selective serotonin reuptake inhibitor (SSRI). Its action is possibly through an increase in neural cell survival. The mechanism of improved survival rate of neurons by FLX may relate to the overexpression of some kinases such as Akt protein. Akt1 (a serine/threonine kinase) plays a key role in the modulation of cell proliferation and survival. Our study evaluated the effects of FLX on mesenchymal stem cell (MSC) fate and Akt1 phosphorylation levels in MSCs. Evaluation tests included reverse transcriptase polymerase chain reaction, western blot, and immunocytochemistry assays. Nestin, MAP-2, and ß-tubulin were detected after neurogenesis as neural markers. Ten µ M of FLX upregulated phosphorylation of Akt1 protein in induced hEnSC significantly. Also FLX did increase viability of these MSCs. Continuous FLX treatment after neurogenesis elevated the survival rate of differentiated neural cells probably by enhanced induction of Akt1 phosphorylation. This study addresses a novel role of FLX in neurogenesis and differentiated neural cell survival that may contribute to explaining the therapeutic action of fluoxetine in regenerative pharmacology.

Dehydroepiandrosterone stimulates nerve growth factor and brain derived neurotrophic factor in cortical neurons.

Due to the increasing cases of neurodegenerative diseases in recent years, the eventual goal of nerve repair is very important. One approach for achieving a neuronal cell induction is by regenerative pharmacology. Nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) are neurotrophins that play roles in neuronal development, differentiation, and protection. On the other hand, dehydroepiandrosterone (DHEA) is a neurosteroid which has multiple actions in the nervous system. DHEA could be an important agent in regenerative pharmacology for neuronal differentiation during tissue regeneration. In this study, we investigated the possible role of DHEA to modulate NGF and BDNF production. The in vivo level of neurotrophins expression was demonstrated by ELISA in rat harvested brain cortex. Also neurotrophins expression after DHEA treatment was revealed by the increased neurite extension, immunostaining, and BrdU labeling in rats. Anti-NGF and anti-BDNF antibodies were used as suppressive agents on neurogenesis. The results showed that NGF and BDNF are overproduced after DHEA treatment but there is not any overexpression for NT-3 and NT-4. Also DHEA increased neurite extension and neural cell proliferation significantly. Overall, DHEA might induce NGF and BDNF neurotrophins overproduction in cortical neurons which promotes neural cell protection, survival, and proliferation.